Sandwalk

NCSE v National Association of Biology Teachers

 
There's been a lot of discussion recently about the proper role of scientific organizations, such as the American Association for the Advancement of Science (AAAS), The Royal Society, and the National Academies of Science (NAS), in the conflict between science and religion. Many people, including me, think that these scientific organizations should remain neutral on the issue of possible conflict between sceince and religion.

The situation with respect to the National Center for Science Education (NCSE) is more complicated. I believe that NCSE should also avoid taking a stand in favor of some religions over others, and in favor of religious versus non-religious interpretations of the conflict.

It's worth reminding people of how this issue has played out in the past so I'm posting a brief summary of an incident that took place over ten years ago.

In 1995, the National Association of Biology Teachers issued the following statement.

The diversity of life on earth is the result of evolution: an unsupervised, impersonal, unpredictable and natural process of temporal descent with genetic modification that is affected by natural selection, chance, historical contingencies and changing environments.

A number of theologians and theistic evolutionists objected to the inclusion of "unsupervised," "impersonal," and "unpreditable" since this clearly conflicted with their religious beliefs.

In 1997, NABT reviewed their statement in light of these complaints and rejected them, voting to keep the original statement. At that point, Eugenie Scott, the Executive Director of NCSE stepped in and persuaded the teachers to drop "unsupervised" and "impersonal" from the statement.

Why did NCSE support the theologians and theistic evolutionists against the biology teachers? It's because Genie draws a line between materialistic naturalism and philosophical naturalism and she thinks the biology teachers stepped over that line (see National Association of Biology Teachers incident for a description of the event). She believes that science cannot know whether evolution is unsupervised and/or impersonal.

I suppose she would have been comfortable with the following statement ....

The diversity of life on earth is the result of evolution: a natural process of temporal descent with genetic modification that is affected by natural selection, chance, historical contingencies and changing environments. Science is unable to tell whether evolution was unsupervised and impersonal or whether it was supervised by a personal god.

That's what she and her allies really want the teachers to say even though they don't insist upon it.

I disagree. I think that scientific evidence points overwhelmingly to a life that was not designed for a purpose. I think there's no evidence whatsoever to suggest that evolution was guided and I don't think we should censor ourselves from saying this.

I think Genie and NCSE are making too big of a distinction between methodological naturalism and philosophical naturalism. Saying that there is no evidence of purpose and direction is a perfectly good methodological statement and the conclusion that, therefore, evolution is unsupervised and unguided is rational based on what we know about science.

It was wrong of NCSE to pressure the biology teachers to change their statment.

---

Read More...

Summary only...

Some scientists are astrologers, therefore science and astrology are compatible

 
Most people would laugh at you if you were to say that, "Some scientists are astrologers, therefore science and astrology are compatible." There's a serious logical flaw in that statement. It probably has a name but I can't think of it right now.

Chris Mooney sides with the accommodationists in the fight over how scientific organizations should behave Atheists for Common Cause With the Religious On Evolution. That's fine, he's entitled to his opinion.

What he's not entitled to is blatantly illogical arguments like the following.

First, I don’t see anything particularly “philosophical” about the accommodationist stance. Rather, holding that there is no necessary conflict between faith and science is an empirical matter: There are a vast number of different religions traditions in the world, and a still more vast number of ways in which different people profess and live out their faiths. In some of these traditions, and for some of these people, there is stark conflict with science; in other traditions, and for other people, there isn’t. That’s just a fact, and one that can be demonstrated simply by identifying any number of scientists who are religious, any number of religious leaders and denominations which embrace evolution, and so on.

There are religious people who are scientists. That's a fact, but it doesn't necessarily mean what Chris Mooney thinks it means.

It means the same thing as saying that some Intelligent Design Creationists are scientists. That's also a fact.

Please, let's stop using illogical arguments in this discussion. We can all agree that there are Theistic Evolutionist scientists, Young Earth Creationist scientists, Intelligent Design Creationist scientists, and scientists who believe in astrology and homeopathy. There are even scientists, as Chris knows, who deny global warming.

You can't draw any conclusion from those facts about whether science is compatible with all those beliefs.

---

[Image Credit: Astrology]

Read More...

Summary only...

Head Growth and Tail Growth

 
There are many examples of polymerization reactions in biochemistry: DNA/RNA synthesis, protein synthesis, carbohydrate synthesis and fatty acid synthesis. In some cases the polymer consists of a string of identical monomers (e.g. some carbohydrates, fatty acids) while in other cases the polymer can be a mixture of several different kinds of monomers (e.g. nucleic acids, proteins).

There are two basic strategies of polymerization: head growth and tail growth. The basic concept is often presented in the textbooks when DNA synthesis or protein synthesis is described.

I posed a simple question yesterday and got some comments on the blog and in my email [Are You as Smart as a Second Year University Student? Q6]. Some people didn't have a clue what the question was about and some people declared that the question was silly. One commenter said, "Sounds like a stupid question that has something to do with memorizing someone's silliness and nothing to do with understanding biochemistry."

Let's see if you agree that this is a silly question that has nothing to do with understanding biochemistry.

In head growth the head of the growing polymer is "activated"—it carries the energy for the addition of the next monomer. This "activation" energy is depicted below as a red bond. Each of the incoming monomers is also "activated" but the energy of the activated bond will be used for the next addition once the monomer is added to the growing polymer.

The classic example of head growth is protein synthesis. Fatty acids are also made in this way.

In tail growth the head of the growing polymer is not activated. The energy for the addition of each monomer is supplied by the incoming activated monomer.

The best examples of tail growth strategy are nucleic acid synthesis, where the activated monomers are nucleoside triphosphates, and synthesis of storage polysaccharides, where the activated monomer is UDP-glucose.

Why is it important to understand the difference between head growth and tail growth? Because one type is unidirectional whereas the other type is compatible with both lengthening and shortening of the polymer.

Let's look at the process of error correction as seen in the proofreading reaction of DNA biosynthesis. Imagine that the replication complex makes a mistake and adds the wrong nucleotide to the growing DNA molecule. The incorrect nucleotide is subsequently removed by the proofreading activity of DNA polymerase. Since DNA synthesis is a tail growth mechanism, the removal of the most recently added monomer doesn't change the chemical reactivity of the growing end of the chain so the reaction can now continue in the direction of lengthening as shown by the green check mark in the figure.

If DNA synthesis utilized a head growth mechanism, then proofreading would not have evolved since removal of the last monomer also removes the activated head of the growing chain.¹ That's why there's no proofreading in protein synthesis.

The synthesis of storage carbohydrates such as starch and glycogen doesn't involve proofreading but there's still a very good reason why the mechanism is tail growth. Recall that starch and glycogen are polymers of glucose and their role is to store glucose as a potential carbon source in time of need. When the need arises, the ends of the polysaccharide chains are nibbled back releasing glucose molecules (as glucose-6-phosphate). These molecules enter the glycolysis pathway.

The degradation reaction terminates when the immediate need for glucose has been met. Later on, in time of plenty, the starch and glycogen chains can be re-extended by adding more glucose residues. The reason why this is possible is because starch and glycogen synthesis is an example of tail growth just like nucleic acid synthesis. If nibbling the ends of the polysaccaride chains removed the activated head, as it would in the case of head growth, then the synthesis reaction could not occur. Thus, the fundamental reason why tail growth evolved in both nucleic acid synthesis and glycogen synthesis is the same.


One of the other reasons for discussing this concept in introductory biochemistry classes is that it gets students thinking about the big picture. Rather than focusing on the details of any one type of polymerization reaction they are encouraged to think about general strategies and they are stimulated to compare and contrast different types of reactions. Unfortunately this approach is rapidly disappearing from introductory biochemistry courses because they are often taught in sections where the lecturer in each section is a specialist in information flow, carbohydrate metabolism, or protein structure. These lecturers often don't know enough about the other subjects to make the relevant comparisons.

That wouldn't matter a great deal as long as the introductory biochemistry textbooks did the job for them. There are two reasons why that doesn't seem to work. First, many team-taught courses don't use a textbook because the individual experts in each section think they know everything they need to know and the students can just rely on the lecture notes.

Second, the comparative biochemistry concepts and principles are disappearing from the textbooks. This is partly because of the way courses are taught and the way students are examined—once the exam on carbohydrate metabolism is over, students don't have to remember anything about carbohydrates while preparing for the next test on lipids and membranes. It's also partly because some biochemistry courses don't cover all aspects of biochemistry in a single course. Many introductory biochemistry courses, for example, separate information flow (DNA replication, transcription, translation) from the rest of biochemistry.

Because of the negative feedback from the customers (Professors) my textbook does not mention head growth and tail growth. The concept is also missing in all of the other introductory biochemistry textbooks.

I'm putting it back in the next edition of my book even if it means losing some adoptions.

---

1. Admittedly, one could imagine evolving ways around this limitation; by re-activating the end in a separate reaction, for example.

Read More...

Summary only...

Are You as Smart as a Second Year University Student? Q6

 
Are You as Smart as a Second Year University Student?

Question 1
Question 2
Question 3
Question 4
Question 5
Today was the final exam in my introductory biochemistry course. It was kinda sad because it's the last year I'll be teaching this course.

Here's a variation on one of the questions. How many of you know the answer?

There are two basic strategies in polymerization reactions: head growth and tail growth. For each of the following polymerization reactions identify whether it is an example of head growth or tail growth.

a) DNA synthesis
b) starch synthesis
c) fatty acid synthesis
d) protein synthesis

Bonus points for Sandwalk readers if you can explain why it's important for some polymerization reactions to use a tail growth strategy.

---

Read More...

Summary only...

Monday's Molecule #119: Winners

 
The molecule is arsphenamine or Salvarsan—also known as compound 606 or "magic bullet." It is the first synthetic drug developed specifically to treat syphilis. It was discovered in Paul Ehrlich's lab in 1909. Ehrlich had already receive the Nobel Prize for his pioneering work on antibodies.

The discovery of arsphenamine was the subject of a 1940 movie called Dr. Ehrlich's Magic Bullet starring Edward G. Robinson as Dr. Ehrlich.

This week's winner is Laura Gerth of the University of Notre Dame. She identified the molecule, the Nobel Laureate, and even got the correct name of the movie! Laura has already agreed to donate her free lunch to a starving undergraduate.

The undergraduate winner is Stefan Tarnawsky of the University of Toronto. He took time off yesterday when he should have been studying for this morning's final exam in Biochemistry! I hope he didn't regret it.

---

This is a very famous molecule. There was even a Hollywood movie about it! Can you name it?

There is one Nobel Laureate who is most closely identified with this particular molecule, although it had nothing to do with the awarding of the Nobel Prize. You have to identify the Nobel Laureate and what the prize was really for.

The first person to identify the molecule and the Nobel Laureate wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first won the prize.

There are six ineligible candidates for this week's reward: Peter Horwich from Dalhousie University, Devin Trudeau from the University of Toronto, Shumona De of Dalhousie University, Maria Altshuler of the University of Toronto, Mike Fraser of Toronto, and Alex Ling of the University of Toronto.

The Canadians continue their total dominance of the rest of the world. That's as it should be.

I still have one extra free lunch donated by a previous winner to a deserving undergraduate so I'm going to continue to award an additional free lunch to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow.

Comments will be blocked for 24 hours. Comments are now open.

---

Read More...

Summary only...

Monday's Molecule #119

 
This is a very famous molecule. There was even a Hollywood movie about it! Can you name it?

There is one Nobel Laureate who is most closely identified with this particular molecule, although it had nothing to do with the awarding of the Nobel Prize. You have to identify the Nobel Laureate and what the prize was really for.

The first person to identify the molecule and the Nobel Laureate wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first won the prize.

There are six ineligible candidates for this week's reward: Peter Horwich from Dalhousie University, Devin Trudeau from the University of Toronto, Shumona De of Dalhousie University, Maria Altshuler of the University of Toronto, Mike Fraser of Toronto, and Alex Ling of the University of Toronto.

The Canadians continue their total dominance of the rest of the world. That's as it should be.

I still have one extra free lunch donated by a previous winner to a deserving undergraduate so I'm going to continue to award an additional free lunch to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow.

Comments will be blocked for 24 hours.

---

Read More...

Summary only...

Brandon Thinks I'm Illogical

 
Brandon writes on Siris: Moran and the 'Courtier's Reply'.

Larry Moran suffers what looks like a complete lapse of critical thought in a recent post on the so-called 'Courtier's Reply'. As he puts it:

Atheists and theists often discuss the existence of God. Unfortunately, these discussions often degenerate into classic Christian apologetics where the main goal of the theist is to rationalize why his or her god doesn't conflict with rationality.

Before long they are rambling on about how to resolve the problem of evil or why god doesn't reveal herself. These problems only exist once you've accepted the premise that there is a god/spirit. This sort of apologetics has nothing to do with the fundamental question of whether god exists in the first place.

Now, Moran is usually pretty reasonable; but this argument is so thoroughly absurd and irrational that he should be ashamed to have put it forward. Let's abstract from the situation a bit to show why. Take a position, A, and a contrary position, B. Now suppose that A gives an objection to B. To this objection, B responds with an argument, whether good or bad, that the objection fails. To which A replies, "This sort of apologetics has nothing to do with the fundamental question of whether B is true in the first place." But this is demonstrably false, of course; B's argument was dealing with an objection put forward by A. What A is trying to do is irrational: he's trying to rig the argument so that his objections are never answered, independently of whether they can be, by dismissing any answer that might be made to them as 'apologetics that have nothing to do' with the original question.

So it is here. The reason theists talk about the problem of evil or the problem of hiddenness is that atheists typically raise these as objections to theism.

I don't talk about the "problem of evil" when I'm discussing the possible existence of supernatural beings and neither do many other atheists.

The point of the Coutrier's Reply is that theists bring up these "problems" when they should be discussing whether gods exist.

The Courtier's Reply does not apply when atheists engage in discussions about the problem of evil or any other problem that theists have when they're trying to reconcile superstition and rationality. It only applies when theists try moving the goalposts—which they do all the time.

It's unfortunate, too, because it makes Moran seem more unreasonable than he probably is. He ends by saying that he would be happy to discuss evidence for theism. This would sound somewhat more sincere if he hadn't just finished giving an argument for why he doesn't have to listen to any responses to any objections he might raise against this purported evidence.

I said I'd be happy to discuss any evidence for the existence of a spiritual world and I stand by that statement.

Brandon, if you or anyone else wants to debate the existence of the supernatural then, by all means, give it your best shot. Give me the evidence for the existence of god(s) and I promise to listen. Maybe I misunderstood your "evidence." Are you saying that the presence of evil in the world is evidence that god(s) exist?

---

Read More...

Summary only...

Foot Soldiers and Generals

 
Richard Hoppe published the usual accommodationist drivel on The Panda's Thumb: Generals who don’t know the nature of war. Here's an excerpt ...

I’m one of the foot soldiers in this battle, a sergeant operating in a conservative rural county far from the ethereal heights of the University of Chicago. I’ve been at it (off and on, mostly on for the last 6 years) for more than 20 years. I published my first article on the political nature of the evolution/religion conflict in 1987. I am engaged at the local and state levels, the former on a weekly basis (search this blog on “Freshwater” for local stuff and see here for just one example of State BOE stuff). My political experience goes back to 1968, when I was a big city Democratic party ward officer. I have a hell of a lot better view of what’s pragmatically necessary and what is effective at the level of the local school board and the local church than Coyne can even imagine. Coyne (and Myers and Moran and Dawkins) are not engaged at that level on anything approaching a regular basis. They lead their congregations from high pulpits. They sit above the choir preaching a message that is disconnected from – indeed, sometimes antithetical to – the reality on the ground. They’re the generals who argued against air power, courtmartialed Billy Mitchell, and then watched ships sink at Pearl Harbor. Coyne wants to argue philosophy in a political war. That’s not a tactic, it’s a politically lethal red herring.

I'm not going to lower myself to defending my activities over the past forty years but I would like to say one thing—I'm very disappointed that Richard hasn't made any contribution at all to the fight in my home country, Canada. (That makes the same amount of sense as what he said about me.)

Oh, and one more thing, I wasn't alive in 1941 but many of my Canadian relatives and high school friends of my parents—who admittedly weren't generals—had already been fighting World War II for two years before Pearl Harbor.¹ Some of them were involved in a little airplane dustup called The Battle of Britain. Some of them died.

How dare Richard compare me to the American Generals and politicians who sat on their asses while Hitler overran most of Europe and brought Great Britain to its knees.

PZ Myers was as outraged as I am by Richard's childish outburst. Read PZ's reply on Pharyngula: Foot soldiers who lack vision.

What he said.

---

1. I had no idea who Billy Mitchell was until my friend Google helped out.

Read More...

Summary only...

Should Scientific Organizations Advocate Accommodationism?

 
John Wilkins has started an interesting debate on the topic of Science and religion for individuals and organisations. He starts with a couple of multiple choice questions.

Get on over to Evolving Thoughts and share your evolving thoughts on the subject. Meanwhile you can answer my own multiple choice question in the sidebar.

What should scientific organizations like AAAS and NAS say about religion?

a) that religion and science are compatible
b) that religion and science are incompatbile
c) nothing

---

Read More...

Summary only...

Science in the Media:Put Up or Shut Up

 
Kathy Sykes is a professor of sciences and society at the University of Bristol (UK). She writes about science journalism in the latest issue of New Scientist [Science in the media: Put up or shut up].

Sykes doesn't like the fact that scientists are criticizing popular science journalism. Ryan Gregory has already posted an article about this and I urge you to go to Genomicron and leave a comment on his posting: Scientists about media: put up or shut up?.

I just want to make one point. Sykes writes ...

Similarly, New Scientist recently took flak over its cover that proclaimed "Darwin was wrong". The article inside described discoveries that are leading to modifications to the theory of evolution. A cheap trick to sell magazines while giving fodder to the enemies of evolution? Sales certainly went up that week, but if more people than usual bought the magazine and read the article, more people will have found that scientists agree that Darwin was fundamentally right.

The three most important criteria for good science journalism are: accuracy, accuracy, and accuracy. Everything else is secondary.

My objection to that article in New Scientist was that it had nothing to do with Darwin. It's not a question of whether Charles Darwin was right or wrong about horizontal gene transfer and the early evolution of prokaryotes. He had absolutely nothing to say about the matter. Dragging Darwin's name into modern molecular evolution was a cheap ploy to boost sales. People reading the article would have still got the wrong impression about Darwin's contributions, even if they had ignored the cover.

The article was scientifically inaccurate because it misrepresented the state of science in 2009 [Explaining the New Scientist Cover].

---

Read More...

Summary only...

Does Intelligent Design Creationism Make Scientific Predictions?

 
It is often claimed that Intelligent Design Creationism doesn't make predictions. This is not true. IDC predicted that irreducibly complex systems could not evolve. That was a firm prediction by Michael Behe.

The prediction has been shown to be wrong. There are many natural evolutionary pathways known to give rise to irreducibly complex systems. The citric acid cycle is a clear example and so is the bacterial flagellum.

Here's another prediction, according to Barry Arrington on Uncommon Descent [FAQ4 is Open for Comment].

ID does not make scientifically fruitful predictions.

This claim is simply false. To cite just one example, the non-functionality of “junk DNA” was predicted by Susumu Ohno (1972), Richard Dawkins (1976), Crick and Orgel (1980), Pagel and Johnstone (1992), and Ken Miller (1994), based on evolutionary presuppositions. In contrast, on teleological grounds, Michael Denton (1986, 1998), Michael Behe (1996), John West (1998), William Dembski (1998), Richard Hirsch (2000), and Jonathan Wells (2004) predicted that “junk DNA” would be found to be functional.

The Intelligent Design predictions are being confirmed and the Darwinist predictions are being falsified. For instance, ENCODE’s June 2007 results show substantial functionality across the genome in such “junk DNA” regions, including pseudogenes.

Thus, it is a matter of simple fact that scientists working in the ID paradigm carry out and publish research, and they have made significant and successful ID-based predictions.

This one is more contentious. There are many scientists who think that much of what we currently call "junk DNA" actually has a function. Even though they might be atheists, their prediction is the same as the creationists.

I'm convinced that most of our genome is truly junk. I predict that the creationist prediction will turn out to be wrong. I wonder if it means that intelligent design creationism will be falsified?

---

Read More...

Summary only...

Not Me

 
Andy Thomson is a psychiatrist. He gave a talk at the Atheist Convention 2009 in Atlanta, Georgia (USA). PZ Myers thinks that Thomson's explanation of religious belief is just what he (PZ) believes.

Not me. The talk is far too adaptationist for my liking. The entire lecture is based on evolution by natural selection—the Darwinian explanation.

[Darwin's] idea gives us the only workable explanation we have for the design and architecture of the human mind.

No it isn't the only workable explanation. I believe that our present mind is also due, in part, to accidents of evolution some of which might have nothing to do with design. Some of them might even be maladaptations. The architecture of our brain is a product of evolution but not all of that evolution is adaptation by natural selection.

We have got to stop trying to explain everything as an adaptation or the consequences of an adaptation. Many, but not all, people are prone to superstitious beliefs. Much of that is due to culture and it can be changed. Our brains are not perfect. They can be tricked into believing all sorts of silly things and believing in God is just one of them. It does not deserve a special evolutionary explanation.

At some point in the near future, religion will be only a minor problem in most Western industrialized nations. Will we have psychiatrists giving lectures about how are brains are adapted to be atheists?

Of course not, just as today we don't have psychiatrists and psychologists giving lectures about how the human brain is adapted to prefer slavery or the inferiority of women. Perhaps they would have if they had lived 1000 years ago.



Watch the video starting at 27 minutes. You'll see Thomson praising research that locates thoughts like "God's Love" and "God's Anger" to specific parts of the brain. These are the same parts of the brain used in other thoughts. Presumably, they are the same parts of the brain used when thinking about being abducted by UFO's or believing in Santa Claus. That's not a big deal, is it?

So when Thomson says, that this data, "Supports theories that ground religious belief in evolved adaptive mechanisms," he could just as easily have said the same thing about UFO abductions ("The evidence support theories that ground belief in UFO abductions in evolved adaptive mechanisms.")

What is the alternative? Did anyone think that these thoughts would map to a special part of the brain that was used exclusively for thinking about God's Love?

---

Read More...

Summary only...

Evolution of the Long Distance Runner

 
Today's Toronto Star has a feature article on marathon running [Any schmo can run a marathon]. The subtitle is more informative "Humans, scientists say, are built for speed – or, at least, endurance. It's all in our shortish toes and big behind."

As one of those schmos who can't run a marathon,¹ I'm always intrigued by claims that all the rest of you have evolved over millions of years to become the perfect marathon runners. The article, by staff reporter Cathel Kelley, focuses on the claims of Daniel Lieberman, an anthropologist at Harvard University. He is one of many scientist who claim that humans are vastly superior at long distance running compared to other mammals, and even compared to our ancestors. They claim there's been selection for the ability to run long distances. Is this a reasonable explanation?

Lieberman's latest paper shows that individuals with short toes are possibly better runners than those with longer toes (Rolian et al. 2009). Since humans tend to have shorter toes than non-bipedal primates, this suggests a possible evolutionary adaptation to running.

An earlier paper promoted the idea that our gluteus maximus (GM) muscle is also an adaptation for long distance running (Lieberman et al. 2006). The closing paragraph of that second paper supports an adaptive explanation but it expresses the appropriate caveats.

Future experimental and paleontological research is necessary to clarify the functional and evolutionary history of the human GM. Based on the above results, we offer several alternative scenarios that merit further study. As noted above, one possibility is that australopithecines had an intermediate configuration of the GM (Berge, 1994Go; Berge and Daynes, 2001Go), retaining some kind of caudal portion but with a less expanded cranial portion than is evident in Homo. If so, then the caudal portion would likely have been an effective extensor of the femur during climbing and perhaps walking, and the cranial portion would have helped to stabilize the sacrum, but probably would not have been a strong trunk stabilizer. An implication of this scenario is that the expansion of the cranial portion of the GM is a derived trait of Homo that would have been selected for control of trunk flexion during endurance running (Bramble and Lieberman, 2004Go) and/or foraging (Marzke et al., 1988Go). An alternative possibility, however, is that the configuration of the GM in Australopithecus was much like that of Homo in terms of the loss of the GMIF. Either the australopithecine GM as a whole was relatively smaller, as many researchers suggest, or possibly as large as in humans (Haeusler, 2002Go). As shown above, the GM in either case is unlikely to have played much of a role in level terrain walking, and is unlikely to have been selected for running given that the genus lacks many other features associated with running capabilities (Bramble and Lieberman, 2004Go). According to this scenario, the derived anatomy of the GM in Australopithecus was probably a reconfiguration of the gluteal musculature for climbing, or a novel adaptation for foraging tasks such as digging that involve flexion of the trunk (Marzke et al., 1988Go). We cannot discount the hypothesis that expansion of the GM might have been useful for walking on uneven terrain. However, it is clear that expansion of the GM in Homo would have benefited any activity that requires trunk stabilization, especially running. Regardless of which scenario is correct, the expansion of cranial portion of the GM is a uniquely hominid characteristic, perhaps distinctive to the genus Homo, which played a vital role in the evolution of human running capabilities.

The newspaper description of the endurance running hypothesis (ERH) is a little more descriptive.

Humans' ability to run is unique among primates.

Why running? Because that's how we killed our food.

Experts call it persistence hunting. The Homo genus did not develop the most basic projectile – the spear – until 200,000-300,000 years ago. That left our ancestors equipped with little more than sharpened sticks for nearly two million years of carnivorous prehistory.

"Even middle-aged college professors can run at a speed that's above the trot-gallop transition of most animals," Lieberman says.

"Why is that important? Quadrupeds cannot pant and gallop at the same time. Their guts are too busy sloshing around like a piston. So, every 10 or 15 minutes, they overheat."

When they overheat, animals must stop to cool. But their bipedal pursuers keep on coming. After several stops and starts, the prey succumbs to heat exhaustion or its heart gives out.

This explains why they don't run the Iditarod in August.

Lieberman contends that this is the only explanation of how humans were capable of killing large game before developing projectile weapons.

"I defy most people to go out and kill a wildebeest with a wooden stick," he says.

Here's how I understand this story.

About one million years ago the entire human population was engaged in hunter-gatherer activities on the African savanna. Most of the small groups obtained a significant amount of their food by hunting large animals. The males would run after these large animals with no weapons. The animals would run away but the humans kept chasing them until the animals couldn't run any more and they dropped dead. (Presumably the wildebeests never caught on to the fact that they could just turn around and gore the pesky humans. Or maybe they couldn't because the humans could outrun them? Here's what happens when marathon-adapted humans try running with bulls.)

There was considerable variation within the human population. Some men had short toes and some men had long toes. Some men had well-developed gluteus maximus muscles and some men didn't. Presumably, the men with genetic traits that enabled them to run faster or farther than the other men got more food than their friends. Their friends either died of starvation or else they had so little meat they couldn't get a mate and reproduce.

Over time there was selection for men who could run farther and faster and humans became adapted to long-distance running. (Presumably the women were good at it as well because they inherited their genes from their fathers.)

When humans began to inhabit other locations that didn't require running, the adaptations remained because by that time all the low fitness variations had been eliminated from the population. That's why there was no loss of this ability when humans began to settle in northern forests and caves, and began to farm and create cities. We all remain well-adapted to long distance running so that, with only a little training, we could all chase down a wildebeest on the African savanna.

I assume the wildebeests just didn't evolve as quickly or they would have adapted as well.

The bison on the North American plains probably could run faster than the natives because, to the best of my knowledge, the North American natives didn't run after buffalo in order to make them die of heat exhaustion. They used sneaky tricks like forcing them to charge over cliffs. They also sneakily used bows and arrows. The natives only started chasing buffalo when horses became available, which is very strange since humans are better at long-distance running than horses—or so the story goes.

One of the problems with evolutionary psychology is that the psychologists claim to know exactly what human societies were like one million years ago. That's one of the problems with the endurance running hypothesis as well. It is based on the assumption that we know how primitive societies obtained food (by running after large animals on the savanna). In fact, we don't know if this is true and we don't even know what percentage of the species might have adopted this lifestyle.

---

1. Because my toes are too long.

[Image Credit (upper): Constantina Dita-Tomescu]

Lieberman, D.E., Raichlen, D.A., Pontzer, H., Bramble, D.M., and Cutright-Smith, E. (2006) The human gluteus maximus and its role in running. Journal of Experimental Biology 209:2143-2155. [DOI: 10.1242/jeb.02255]

Rolian, C., Lieberman, D.E., Hamil, J., Scott, J.W., and Werbel, W. (2009) Walking, running and the evolution of short toes in humans. Journal of Experimental Biology 212:713-72. [DOI: 10.1242/jeb.019885]

Read More...

Summary only...

A Horse of a Different Color

 
John Hawks continues to post interesting articles on his blog and he continues his policy of not allowing comments. I want to ask a question about his latest posting [A horse of a different color] so I'm asking it here.

John is referring to a short paper on the evolution of coat colors in horses. Apparently, the analysis of DNA from ancient fossil horses reveals that most of them were bay in color. The chestnut coat color wasn't detected until about nine thousand years ago.

The authors of the paper claim there is no evidence for selection of coat color in horses prompting the following comment by John Hawks.

The pigment-altering mutations at these genes do not all show statistical signs of selection in contemporary samples of horses. But they aren't there in the ancient horses. That's the best evidence of selection you could possibly have. Message: tests of selection on contemporary samples are weak, particularly for loci with rare alleles or more than two alleles.

John, if I understand you correctly, you're saying that as long as an allele wasn't detectable in ancient populations but is detectable today then random genetic drift is ruled out.

That doesn't make sense to me. Perhaps you could explain? There must be more to your statement than that.

---

Read More...

Summary only...

On the Existence of God and the Coutier's Reply

 
Atheists and theists often discuss the existence of God. Unfortunately, these discussions often degenerate into classic Christian apologetics where the main goal of the theist is to rationalize why his or her god doesn't conflict with rationality.

Before long they are rambling on about how to resolve the problem of evil or why god doesn't reveal herself. These problems only exist once you've accepted the premise that there is a god/spirit. This sort of apologetics has nothing to do with the fundamental question of whether god exists in the first place.

PZ Myers invented the parable of The Courtier's Reply to describe this situation.¹ Rather than address the burning question—is the Emperor wearing any clothes?—the believers will complain that you don't understand the latest fashion.

They say you can't have a serious discussion about the existence of god because you aren't versed in the sophisticated arguments of Christian apologetics. In other words, you have to be intimately familiar with all the ways of rationalizing superstitious belief in god before challenging the very existence of god.²

It's amazing how few theists get the point. The latest person to demonstrate a fundamental misunderstanding of simple logic is Joe Hinman at Atheistwatch. Hinman has a Master's degree in Theology and he is currently studying for a Ph.D. in the history if ideas. He exposes himself by complaining about Anti-Intellectual Tendencies in Atheism.

So What this courtier's reply is saying is that if the skeptic says stupid things about theology and demonstrates that he knows nothing about it and the theist says "O your criticism is invalid because you don't understand what you are criticizing" then all the atheist has to do is say "that's the courtiers reply" and the theist is supposed to go "O my God, I've violated a law of logic!" and give up and stop believing in God. But in realty it's into a log of logic, I never heard it in a logic class.It's not in a logic text book, and the meaning of it is silly. I'ts just saying 'You can't point out my ignorance of theology because I will not allow theology to have any kind of validity or importance and religious people may not not any sort of human dignity." That's all it's saying. It's nothing more than anti-intellectual stupidity.

...

This anti-intellectual tendency is not confined to this one tactic. The new tactick, which I have noticed for a few years now, is to deny any sort of discipline of scholarship that has developed within the theological community. So any self defense that a believer could make is automatically suspect and wrong merely becasue it is theological. But then one wonders how the skeptics knowledge that theology is all bull shit could ever have developed in the first place? When we consider the history of Biblical scholarship it becomes clear that the atheists are merely arguing in a circle.

The history of scholarship shows us that it was not invented in answer to pressing atheist attacks on the bible.

Bingo! Christian apologetics was developed by people who believe in god. They needed to explain why their beliefs seem inconsistent with the real world. Many of these rationalizations are extremely "sophisticated" as you might expect since the problem is difficult.

I don't give a damn about those rationalizations no matter how many books have been written. Atheists don't have a problem with evil or sin or life after death or the resurrection. It's only theists who have a problem.

If Joe Hinman wants to explain why he is a theist then I'd be happy to discuss that topic. What's his best evidence for the existence of a spiritual world?

---

1. Also see The Emperor's New Clothes and the Courtier's Reply.

2. It's like saying that you have to learn how to cast a horoscope before you can question astrology.

Read More...

Summary only...

Can watery asteroids explain why life is 'left-handed'?

 
It's time to re-visit the so-called "racemization" or "chirality" problem. The "problem" is thought to be the absolute preference for left-handed amino acids in living organisms.

Naturally occurring amino acids are racemic mixtures of both L- and D-amino acids. How did life come to select only one of the two possible stereoisomer for making proteins?

Sandwalk readers will know that I prefer an evolutionary explanation. In the beginning there were only a small number of amino acids that combined to make catalytically active peptides. One of these might have been glycine, which doesn't have L- and D- forms. Glycine might have formed spontaneously from acetate or glycerol.

Next came other simple amino acids whose biosynthesis might have been assisted by short polyglycine peptides with a few other naturally occurring amino acids. The peptides are biological catalysts, like modern enzymes only less efficient. It's possible that the primitive pathway might have favored the synthesis of amino acids like L-alanine and/or L-serine. (Many enzymatically catalyzed pathways are stereospecific—they make only one of the two possible forms.) The accumulation of L-alanine and L-serine could have been entirely by accident. It could just as easily have been D-alanine and D-serine.

Once the simple amino acids started to accumulate by biosynthesis, additional pathways started to evolve and more amino acids were added to the mix. These additional amino acids were all derived from the simple ones so they too were exclusively L- forms. Eventually life evolved from this chemical mixture and all the pathways were making the same form of amino acid. This process would have had to take place in a "warm little pond" in order to produce appropriate concentrations of the amino acids (and other things).

According to this scenario, the exclusive presence of L-amino acids instead of D-amino acids is just an accident. The fact that all amino acids are of the same form as the first ones is just a consequence of the fact that more complicated pathways started with the first ones as precursors.

Is there another theory? Yes there is. Some people think that life began in a soup containing all twenty or so common amino acids. They believe that all these amino acids formed spontaneously by chemical reactions rather than by the evolution of primitive catalysts from simple peptides.

Some people believe that the amino acids, and other chemicals, formed in outer space and they were delivered to Earth in meteorites. There has long been evidence that meteorites contain amino acids, lending support to this explanation.

Does this solve the chirality problem? No, it doesn't, because the amino acids found in meteorites are mixtures of L- and D-forms. People who support the idea that all twenty amino acids were present from the beginning would have to account for the selection of only one form from the mixture. Since this is highly unlikely, most favor a solution where some form of chemical synthesis preferentially results in a huge excess of left-handed amino acids. So far no example of such a reaction has been found.

On the other hand, there are hints that such a chemical reaction might be possible. There are 74 different amino acids in the Murchison meteorite and all of them are racemic mixtures (L- + D- forms). But in some cases there's a slight excess of the L- form of the amino acid suggesting that chemical formation of amino acids in outer space may favor the left-handed version—the same version that's found in living cells.

A recently published paper shows that the slight excess of one amino acid, isovaline, is enhanced by formation in liquid water (Glavin and Dworkin, 2009), giving rise to a press release that was reported in New Scientist as Watery asteroids may explain why life is 'left-handed'.

The scientific paper examines the chirality of amino acids found in several different meteorites. The main finding is that there's an excess of L-isovaline over D-isolvaline in most samples. The excess can be as high as 18%. Most other amino acids have equal amounts of the L- and D-forms.

Isovaline is not one of the naturally occurring amino acids found in protein and the difference is significant. All 20 of the common amino acids have a structure like that shown on the left of the figure below. The central carbon atom (called the α-carbon) is attached to an amino group (—NH₃⁺) and a carboxyl group (—COO^-). The carboxyl group makes it an acid and that's why these compounds are called amino acids.

Each carbon atom can have four covalent bonds. In the standard amino acids one of the other groups is always a hydrogen atom (—H). The other is a side chain shown as "R" in the figure. If the four groups bound to the α-carbon atom are different then the amino acid will exist in two different forms; L- and D-.¹


The simplest amino acid is glycine where the R group is just a hydrogen atom. Thus, glycine is not a chiral compound and there's no such thing as L-glycine or D-glycine. All other natural amino acids are chiral.

Valine has a R group consisting of a branched 3-carbon chain. Isovaline, which is not a natural amino acid, is quite different. The hydrogen group found in all the standard amino acids is replaced by a methyl group (—CH₃).

Why is this important? It's important for two reasons. First, because isolvaline is extremely rare on Earth you can be confident that the meteorite isn't contaminated by isovaline from living organisms. Second, all amino acids will spontaneously undergo racemization, or conversion of L- forms into D- forms and vice versa. Over million of years this reaction will lead to equal amounts of the two forms. With amino acids like isovaline, where there are four large chemical groups bound to the α-carbon atom, the rate of this reaction is very slow (billions of years rather than 10 million years).

The paper by Glavin and Dworkin suggests that there may be natural chemical processes leading to an increase of one stereoisomer over the other and this natural preference for L-amino acids may be the reason why life selected the L- forms over the D- forms. Because isovaline is so stable it may preserve the original bias that has been lost in the case of the other amino acids.

In order for extraterrestrial organic matter to have fueled the origin of life, a lot of meteorites carrying organic matter had to arrive on the primitive Earth. The problem of amino acid concentrations and stabiltity were discussed in a classic paper by Jeffrey Bada published in 1991.

Some of his calculations are worth remembering.

The current flux of extraterrestrial organic material is about 3 × 10⁸ grams per year from cosmic dust and micrometeorites. About 1% of this is amino acids and most of them are not the ones found in living organisms. This should give rise over time to a concentration in the oceans of about 0.1 nM (10^-10 M). That's is not sufficient for life to have originated.

The flux in the past was almost certainly much greater and lots of organic material might have been delivered by large meteorites; however, it's unlikely that amino concentrations in the oceans could ever have been more than 10-100 pM for all amino acids combined.

Most amino acids will spontaneously degrade over time. There's a window of opportunity that only lasts about 10 million years because in that time all the water in the oceans will pass through hydrothermal vents and the high temperature will destroy most chemicals—including amino acids.

Bada concludes with ...

There are no known effective abiotic processes for generating chiral amino acids, which suggests that on the early Earth, only racemic amino acids would have existed. Because of the problem of racemization, it is likely that only after biotic protein synthesis became an efficeint process in the evolution of early life could the chirality of amino acids be maintained in proteins. Instead of amino acid chirality preceding the origin of life, it may have developed after life was well established, and possibly in close association with the origin of protein biosynthesis. As to why the protein amino acids consist only of the L-enantiomers, it is probably just a matter of chance.

The important lesson here is that there are several different scenarios leading to the preference for L- amino acids. It's wise to keep in mind that abiotic (chemical) synthesis of amino acids with a bias for the L- forms is not the only possibility.

---

1. It's better to call these L- and D- forms of the amino acids rather than "left-handed" and "right-handed." The "handedness" refers to the direction in which the stereoisomers rotate polarized light and in modern terminology there is no obligatory connection between the L- designation and the optical activity. As it turns out, most of the L-amino acids are also l-amino acids (levorotary = left-handed) actually d-amino acids (dextrorotary = right-handed), but there are some exceptions. L-cysteine, for example, is "right-handed" truly "left-handed" (see Specific Rotation and Temperature Coefficients of Amino Acids). Thanks to DK (see comments) for correcting my earlier mistake.

Bada, J. (1991) Amino acid cosmogeochemistry. Phil trans. R. Soc. Lond. 333:349-358.

Glavin, D.P. and Dworkin, J.P. (2009) Enrichment of the amino acid l-isovaline by aqueous alteration on CI and CM meteorite parent bodies. Proc. Natl. Acd. Sci. (USA) 106: 5487-5492 [DOI: 10.1073/pnas.0811618106]

Read More...

Summary only...

Nobel Laureate: Sir Paul Nurse

 

The Nobel Prize in Physiology or Medicine 2001

"for their discoveries of key regulators of the cell cycle"

Sir Paul M. Nurse (1949 - ) won the Noble Prize in 2001 for his contributions to understanding the regulation of gene expression in yeast cells. His co-recipients were Leland Hartwell and Tim Hunt.

A major part of most signaling pathways is the phosphorylation of proteins. The attachment of a phosphate group to a protein can convert it from an active state to an inactive state, or vice versa. Enzymes that catalyze phosphorylations are called "kinases" and one of the most common kinases is cyclin-dependent kinase or CDK. The activity of the kinase is itself regulated by proteins called cyclins.

Cyclins are produced at various stages of the cell cycle as it progresses from a growth state through mitosis and cell division as shown below in the press release. Paul Nurse's contribution to understanding the cell cycle was to characterize the cyclin-dependent kinase.

THEME:
Nobel Laureates

Press Release

Summary

All organisms consist of cells that multiply through cell division. An adult human being has approximately 100 000 billion cells, all originating from a single cell, the fertilized egg cell. In adults there is also an enormous number of continuously dividing cells replacing those dying. Before a cell can divide it has to grow in size, duplicate its chromosomes and separate the chromosomes for exact distribution between the two daughter cells. These different processes are coordinated in the cell cycle.

This year's Nobel Laureates in Physiology or Medicine have made seminal discoveries concerning the control of the cell cycle. They have identified key molecules that regulate the cell cycle in all eukaryotic organisms, including yeasts, plants, animals and human. These fundamental discoveries have a great impact on all aspects of cell growth. Defects in cell cycle control may lead to the type of chromosome alterations seen in cancer cells. This may in the long term open new possibilities for cancer treatment.

Leland Hartwell (born 1939), Fred Hutchinson Cancer Research Center, Seattle, USA, is awarded for his discoveries of a specific class of genes that control the cell cycle. One of these genes called "start" was found to have a central role in controlling the first step of each cell cycle. Hartwell also introduced the concept "checkpoint", a valuable aid to understanding the cell cycle.

Paul Nurse (born 1949), Imperial Cancer Research Fund, London, identified, cloned and characterized with genetic and molecular methods, one of the key regulators of the cell cycle, CDK (cyclin dependent kinase). He showed that the function of CDK was highly conserved during evolution. CDK drives the cell through the cell cycle by chemical modification (phosphorylation) of other proteins.

Timothy Hunt (born 1943), Imperial Cancer Research Fund, London, is awarded for his discovery of cyclins, proteins that regulate the CDK function. He showed that cyclins are degraded periodically at each cell division, a mechanism proved to be of general importance for cell cycle control.

One billion cells per gram tissue

Cells having their chromosomes located in a nucleus and separated from the rest of the cell, so called eukaryotic cells, appeared on earth about two billion years ago. Organisms consisting of such cells can either be unicellular, such as yeasts and amoebas, or multi-cellular such as plants and animals. The human body consists of a huge number of cells, on the average about one billion cells per gram tissue. Each cell nucleus contains our entire hereditary material (DNA), located in 46 chromosomes (23 pairs of chromosomes).

It has been known for over one hundred years that cells multiply through division. It is however only during the last two decades that it has become possible to identify the molecular mechanisms that regulate the cell cycle and thereby cell division. These fundamental mechanisms are highly conserved through evolution and operate in the same manner in all eukaryotic organisms.

The phases of the cell cycle

The cell cycle consists of several phases (see figure). In the first phase (G1) the cell grows and becomes larger. When it has reached a certain size it enters the next phase (S), in which DNA-synthesis takes place. The cell duplicates its hereditary material (DNA-replication) and a copy of each chromosome is formed. During the next phase (G2) the cell checks that DNA-replication is completed and prepares for cell division. The chromosomes are separated (mitosis, M) and the cell divides into two daughter cells. Through this mechanism the daughter cells receive identical chromosome set ups. After division, the cells are back in G1 and the cell cycle is completed.

The duration of the cell cycle varies between different cell types. In most mammalian cells it lasts between 10 and 30 hours. Cells in the first cell cycle phase (G1) do not always continue through the cycle. Instead they can exit from the cell cycle and enter a resting stage (G0).

Cell cycle control

For all living eukaryotic organisms it is essential that the different phases of the cell cycle are precisely coordinated. The phases must follow in correct order, and one phase must be completed before the next phase can begin. Errors in this coordination may lead to chromosomal alterations. Chromosomes or parts of chromosomes may be lost, rearranged or distributed unequally between the two daughter cells. This type of chromosome alteration is often seen in cancer cells.

It is of central importance in the fields of biology and medicine to understand how the cell cycle is controlled. This year's Nobel Laureates have made seminal discoveries at the molecular level of how the cell is driven from one phase to the next in the cell cycle.

Cell cycle genes in yeast cells

Leland Hartwell realized already at the end of the 1960s the possibility of studying the cell cycle with genetic methods. He used baker's yeast, Saccharomyces cerevisiae, as a model system, which proved to be highly suitable for cell cycle studies. In an elegant series of experiments 1970-71, he isolated yeast cells in which genes controlling the cell cycle were altered (mutated). By this approach he succeeded to identify more than one hundred genes specifically involved in cell cycle control, so called CDC-genes (cell division cycle genes). One of these genes, designated CDC28 by Hartwell, controls the first step in the progression through the G1-phase of the cell cycle, and was therefore also called "start".

In addition, Hartwell studied the sensitivity of yeast cells to irradiation. On the basis of his findings he introduced the concept checkpoint, which means that the cell cycle is arrested when DNA is damaged. The purpose of this is to allow time for DNA repair before the cell continues to the next phase of the cycle. Later Hartwell extended the checkpoint concept to include also controls ensuring a correct order between the cell cycle phases.

A general principle

Paul Nurse followed Hartwell's approach in using genetic methods for cell cycle studies. He used a different type of yeast, Schizosaccharomyces pombe, as a model organism. This yeast is only distantly related to baker's yeast, since they separated from each other during evolution more than one billion years ago.

In the middle of the 1970s, Paul Nurse discovered the gene cdc2 in S. pombe. He showed that this gene had a key function in the control of cell division (transition from G2 to mitosis, M). Later he found that cdc2 had a more general function. It was identical to the gene ("start") that Hartwell earlier had identified in baker's yeast, controlling the transition from G1 to S.

This gene (cdc2) was thus found to regulate different phases of the cell cycle. In 1987 Paul Nurse isolated the corresponding gene in humans, and it was later given the name CDK1 (cyclin dependent kinase 1). The gene encodes a protein that is a member of a family called cyclin dependent kinases, CDK. Nurse showed that activation of CDK is dependent on reversible phosphorylation, i.e. that phosphate groups are linked to or removed from proteins. On the basis of these findings, half a dozen different CDK molecules have been found in humans.

The discovery of the first cyclin

Tim Hunt discovered the first cyclin molecule in the early 1980s. Cyclins are proteins formed and degraded during each cell cycle. They were named cyclins because the levels of these proteins vary periodically during the cell cycle. The cyclins bind to the CDK molecules, thereby regulating the CDK activity and selecting the proteins to be phosphorylated.

The discovery of cyclin, which was made using sea urchins, Arbacia, as a model system, was the result of Hunt's finding that this protein was degraded periodically in the cell cycle. Periodic protein degradation is an important general control mechanism of the cell cycle. Tim Hunt later discovered cyclins in other species and found that also the cyclins were conserved during evolution. Today around ten different cyclins have been found in humans.

The engine and the gear box of the cell cycle

The three Nobel Laureates have discovered molecular mechanisms that regulate the cell cycle. The amount of CDK-molecules is constant during the cell cycle, but their activities vary because of the regulatory function of the cyclins. CDK and cyclin together drive the cell from one cell cycle phase to the next. The CDK-molecules can be compared with an engine and the cyclins with a gear box controlling whether the engine will run in the idling state or drive the cell forward in the cell cycle.

A great impact of the discoveries

Most biomedical research areas will benefit from these basic discoveries, which may result in broad applications within many different fields. The discoveries are important in understanding how chromosomal instability develops in cancer cells, i.e. how parts of chromosomes are rearranged, lost or distributed unequally between daughter cells. It is likely that such chromosome alterations are the result of defective cell cycle control. It has been shown that genes for CDK-molecules and cyclins can function as oncogenes. CDK-molecules and cyclins also collaborate with the products of tumour suppressor genes (e.g. p53 and Rb) during the cell cycle.

The findings in the cell cycle field are about to be applied to tumour diagnostics. Increased levels of CDK-molecules and cyclins are sometimes found in human tumours, such as breast cancer and brain tumours. The discoveries may in the long term also open new principles for cancer therapy. Already now clinical trials are in progress using inhibitors of CDK-molecules.

The different phases of the cell cycle. In the first phase (G1) the cell grows. When it has reached a certain size it enters the phase of DNA-synthesis (S) where the chromosomes are duplicated. During the next phase (G2) the cell prepares itself for division. During mitosis (M) the chromosomes are separated and segregated to the daughter cells, which thereby get exactly the same chromosome set up. The cells are then back in G1 and the cell cycle is completed.

This year's Nobel Laureates, using genetic and molecular biology methods, have discovered mechanisms controlling the cell cycle. CDK-molecules and cyclins drive the cell from one phase to the next. The CDK-molecules can be compared with an engine and the cyclins with a gear box controlling whether the engine will run in the idling state or drive the cell forward in the cell cycle.

---

[Photo Credit: Havard University]

The images of the Nobel Prize medals are registered trademarks of the Nobel Foundation (© The Nobel Foundation). They are used here, with permission, for educational purposes only.

Read More...

Summary only...

It's a Beauty Pageant - What Did you Expect?

 
I think it's safe to assume that most of you don't watch beauty pageants. However, I think it's also a safe bet that you've seen excerpts from at least one or two while you were waiting for M*A*S*H or Star Trek reruns to begin.

Remember the impromptu speeches where the contestants showed us why "intelligent" and "beauty queen" don't belong together in the same sentence? Some of the responses have become classics. It's what we expect from women who enter beauty contests. What's the big deal?

According to The Chicago Sun-Times, during the latest Miss America contest one of the contestants, Miss Arizona, was asked "Do you think the U.S. should have universal health care as a right of citizenship? Why or why not?"

Her response was, "I think this is an issue of integrity regardless of which end of the political spectrum that I stand on. I've been raised in a family to know right from wrong, and politics, whether or not you fall in the middle, the left or the right, it's an issue of integrity, whatever your opinion is and I say that with the upmost conviction."

Right. That's exactly why most of us don't pay any attention to these shows. The only surprise here is that she didn't mention world peace or freedom.

The blogosphere is all aglow over the response of Miss California.

What's the problem? Were you expecting an intelligent answer from someone with a fake smile and ten pounds of makeup?

Here's another quote on the same topic. Can you guess who said it?¹

"I'm a Christian. And so, although I try not to have my religious beliefs dominate or determine my political views on this issue, I do believe that tradition, and my religious beliefs say that marriage is something sanctified between a man and a woman."

Here's two more people who have announced on television that they are personally opposed to gay marriage. They are a little bit more important than Miss California.

---

1. Barack Obama during an inteview with the Chicago Daily Tribune, as reported on about.com: Lesbian Life.

Read More...

Summary only...

Facts Supporting Intelligent Design Creationism?

 
We all know that the Intelligent Design Creationist movement consists almost exclusively of attacks on science. The idea seems to be that if you can cast doubt on evolution then this is evidence in favor of God.

Some unnamed Professor has challenged students to come up with facts that support Intelligent Design Creationism. The only criterion is; "fact can be any observation in biology that is substantiated by publication in a scientific journal,"

Casey Luskin attempts to meet the challenge over on the Discovery Institute propaganda site, Evolution News & Views: Helping Students Answer a Professor's Challenge to "Find a Fact" That Supports Intelligent Design (Part 2).

Here's a list of "scientific" publications submitted by Luskin. I haven't read all of them but, of the ones I've read, there isn't a single one containing a fact that supports the existence of God, let alone evidence that he/she designed anything at all. Furthermore, many of them aren't from a scientific journal. It looks like Casey Luskin has goofed, once again.

Let me know if any of these publications contain evidence of Intelligent Design Creationism. Is this the best they can do? (I've put asterisks in front of the ones I've read.)

*Douglas D. Axe, "Extreme Functional Sensitivity to Conservative Amino Acid Changes on Enzyme Exteriors," Journal of Molecular Biology, Vol. 301:585-595 (2000)

*Douglas D. Axe, "Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds," Journal of Molecular Biology, 1-21 (2004)

*Michael Behe, Darwin's Black Box: The Biochemical Challenge to Evolution (Free Press, 1996)

*Michael J. Behe & David W. Snoke, "Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues," Protein Science, Vol 13:2651-2664 (2004)

Geoff Brumfiel, “Outrageous Fortune,” Nature, Vol. 439: 10-12 (Jan. 5, 2006)

Bract, "Inventions, Algorithms, and Biological Design," in Progress in Complexity, Information, and Design (Vol. 1.1, 2002)

*William A. Dembski, The Design Inference: Eliminating Chance Through Small Probabilities (Cambridge University Press, 1998)

a. William A. Dembski and Robert J. Marks II, “Conservation of Information in Search: Measuring the Cost of Success” (In publication, 2009)

b. William A. Dembski and Robert J. Marks II, “The Search for a Search: Measuring the Information Cost of Higher Level Search” (In publication, 2009)

*William Dembski and Jonathan Wells, The Design of Life: Discovering Signs of Intelligence in Living Systems, (FTE, 2008) (see www.thedesignoflife.net)

*Wayt T. Gibbs, “The Unseen Genome: Gems among the Junk,” Scientific American (November, 2003)

Guillermo Gonzalez and Jay Wesley Richards, The Privileged Planet: How our Place in the Cosmos is Designed for Discovery, (Regnery, 2004)

*Graham Lawton, "Why Darwin was wrong about the tree of life," New Scientist (January 21, 2009)

Hiroaki Kitano, ”Systems Biology: A Brief Overview,” Science, Vol. 295: 1662-1664 (March 1, 2002)

Wolf-Ekkehard Lönnig, "Dynamic genomes, morphological stasis, and the origin of irreducible complexity," in Dynamical Genetics pp. 101-119 (Valerio Parisi, Valeria De Fonzo, and Filippo Aluffi-Pentini eds., 2004)

Casey Luskin, “Human Origins and Intelligent Design,” Progress in Complexity and Design, (Vol 4.1, November, 2005)

Casey Luskin, "Intelligent Design Has Scientific Merit in Paleontology," part of the "Does Intelligent Design Have Merit?" debate at OpposingViews.com (September, 2008)

*Wojciech Makalowski, “Not Junk After All,” Science, Vol. 300(5623) (May 23, 2003)

Stephen C. Meyer, Marcus Ross, Paul Nelson & Paul Chien, "The Cambrian Explosion: Biology's Big Bang," in Darwinism, Design, and Public Education (John A. Campbell and Stephen C. Meyer eds., Michigan State University Press, 2003)

*a. Stephen C. Meyer, “The Cambrian Information Explosion,” in Debating Design (edited by Michael Ruse and William Dembski; Cambridge University Press 2004)

b. Stephen C. Meyer, “The origin of biological information and the higher taxonomic categories,” Proceedings of the Biological Society of Washington, Vol. 117(2):213-239 (2004)

Scott A. Minnich & Stephen C. Meyer, “Genetic analysis of coordinate flagellar and type III regulatory circuits in pathogenic bacteria,” in Proceedings of the Second International Conference on Design & Nature, Rhodes Greece (M.W. Collins & C.A. Brebbia eds., 2004)

Paul Nelson and Jonathan Wells, “Homology in Biology,” in Darwinism, Design, and Public Education, (Michigan State University Press, 2003)

*Richard v. Sternberg, "On the Roles of Repetitive DNA Elements in the Context of a Unified Genomic– Epigenetic System," Annals of the New York Academy of Sciences, Vol. 981: 154–188 (2002)

J.T. Trevors and D.L. Abel, "Chance and necessity do not explain the origin of life," Cell Biology International, Vol. 28: 729-739 (2004)

D. L. Abel & J. T. Trevors, “Self-organization vs. self-ordering events in life-origin models," Physics of Life Reviews, Vol. 3: 211–228 (2006)

Øyvind Albert Voie, "Biological function and the genetic code are interdependent," Chaos, Solitons and Fractals, Vol. 28:1000–1004 (2006)

Jonathan Wells, "Using Intelligent Design Theory to Guide Scientific Research" Progress in Complexity, Information, and Design (Vol. 3.1.2, November 2004)

Jonathan Wells, "Do Centrioles Generate a Polar Ejection Force?," Rivista di Biologia / Biology Forum, Vol. 98:71-96 (2005)

---

Read More...

Summary only...

The Trouble with NCSE

 
I am a member of National Center for Science Education (NCSE). That does not mean I agree with everything they do. My biggest bone of contention is over their accommodationist tactics [National Academies: Science, Evolution and Creationism, Appeasers, Spaghetti Monsters, and NCSE].

I don't like the fact that NCSE cozies up to theistic evolutionists like Ken Miller and Francis Collins while, at the same time, actively distancing itself from vocal atheist scientists like Richard Dawkins. I think NCSE shouldn't takes side and shouldn't promote the idea that science and religion are compatible.

Jerry Coyne agrees. He has published a lengthy essay on his blog where he takes NCSE to task [Truckling to the Faithful: A Spoonful of Jesus Helps Darwin Go Down]. I have warned many people at NCSE that they risk losing the support of non-theist scientists but, for the most part, they think the risk is worth it.

I wonder if they still think that way?

---

Read More...

Summary only...

How to Evaluate Genome Level Transcription Papers

 
It's often very difficult to evaluate the results of large-scale genome studies. Part of the problem is that the technology is complicated and the controls are not obvious. Part of the problem is that the results depend a great deal on the software used to analyze the data and the limitations of the software are often not described.

But those aren't the only problems. We also have to take into consideration the biases of the people who write the papers. Some of those biases are the same ones we see in other situations except that they are less obvious in the case of large-scale genome studies.

Laurence Hurst has written up a nice summary of the problem and I'd like to quote from his recent paper (Hurst, 2009).

In the 1970s and 80s there was a large school of evolutionary biology, much of it focused on understanding animal behavior, that to a first approximation assumed that whatever trait was being looked at was the product of selection. Richard Dawkins is probably the most widely known advocate for this school of thought, John Maynard Smith and Bill (WD) Hamilton its main proponents. The game played in this field was one in which ever more ingenious selectionist hypotheses would be put forward and tested. The possibility that selection might not be the answer was given short shrift.

By contrast, during the same period non-selectionist theories were gaining ground as the explanatory principle for details seen at the molecular level. According to these models, chance plays an important part in determining the fate of a new mutation – whether it is lost or spreads through a population. Just as a neutrally buoyant particle of gas has an equal probability of diffusing up or down, so too in Motoo Kimura's neutral theory of molecular evolution an allele with no selective consequences can go up or down in frequency, and sometimes replace all other versions in the population (that is, it reaches fixation). An important extension of the neutral theory (the nearly-neutral theory) considers alleles that can be weakly deleterious or weakly advantageous. The important difference between the two theories is that in a very large population a very weakly deleterious allele is unlikely to reach fixation, as selection is given enough opportunity to weed out alleles of very small deleterious effects. By contrast, in a very small population a few chance events increasing the frequency of an allele can be enough for fixation. More generally then, in large populations the odds are stacked against weakly deleterious mutations and so selection should be more efficient in large populations.

In this framework, mutations in protein-coding genes that are synonymous – that is, that replace one codon with another specifying the same amino acid and, therefore, do not affect the protein – or mutations in the DNA between genes (intergene spacers) are assumed to be unaffected by selection. Until recently, a neutralist position has dominated thinking at the genomic/molecular level. This is indeed reflected in the use of the term 'junk DNA' to describe intergene spacer DNA.

These two schools of thought then could not be more antithetical. And this is where genome evolution comes in. The big question for me is just what is the reach of selection. There is little argument about selection as the best explanation for gross features of organismic anatomy. But what about more subtle changes in genomes? Population genetics theory can tell you that, in principle, selection will be limited when the population comprises few individuals and when the strength of selection against a deleterious mutation is small. But none of this actually tells you what the reach of selection is, as a priori we do not know what the likely selective impact of any given mutation will be, not least because we cannot always know the consequences of apparently innocuous changes. The issue then becomes empirical, and genome evolution provides a plethora of possible test cases. In examining these cases we can hope to uncover not just what mutations selection is interested in, but also to discover why, and in turn to understand how genomes work. Central to the issue is whether our genome is an exquisite adaption or a noisy error-prone mess.

Sandwalk readers will be familiar with this problem. In the context of genome studies, the adaptationist approach is most often reflected as a bias in favor of treating all observations as evidence of functionality. It you detect it, then it must have been selected. If it was selected, it must be important.

As Hurst points out, the real question in evaluating genome studies boils down to a choice between an exquisitely adapted genome or one that is messy and full of mistakes. The battlefields are studies on the frequency of alternative splicing, transcription, the importance of small RNAs, and binding sites for regulatory proteins.

Let's take transcription studies as an example.

Consider, for example, the problem of transcription. Although maybe only 5% of the human genome comprises genes encoding proteins, the great majority of the DNA in our genome is transcribed into RNA [1]. In this the human genome is not unusual. But is all this transcription functionally important? The selectionist model would propose that the transcription is physiologically relevant. Maybe the transcripts specify previously unrecognized proteins. If not, perhaps the transcripts are involved in RNA-level regulation of other genes. Or the process of transcription may be important in keeping the DNA in a configuration that enables or suppresses transcription from closely linked sites.

The alternative model suggests that all this excess transcription is unavoidable noise resulting from promiscuity of transcription-factor binding. A solid defense can be given for this. If you take 100 random base pairs of DNA and ask what proportion of the sequence matches some transcription factor binding site in the human genome, you find that upwards of 50% of the random sequence is potentially bound by transcription factors and that there are, on average, 15 such binding sites per 100 nucleotides. This may just reflect our poor understanding of transcription factor binding sites, but it could also mean that our genome is mostly transcription factor binding site. If so, transcription everywhere in the genome is just so much noise that the genome must cope with.

There is no definitive solution to this conflict. Both sides have passionate advocates and right now you can't choose one over the other. My own bias is that most of the transcription is just noise—it is not biologically relevant.

That's not the point, however. The point is that as a reader of the scientific literature you have to make up your mind whether the data and the interpretation are believable.

Here's two criteria that I use to evaluate a paper on genome level transcription.

1. I look to see whether the authors are aware of the adaptation vs noise controversy. If they completely ignore the possibility that what they are looking at could be transcriptional noise, then I tend to dismiss the paper. It is not good science to ignore alternative hypotheses. Furthermore, such papers will hardly ever have controls or experiments that attempt to falsify the adaptationist interpretation. That's because they are unaware of the fact that a controversy exists.¹


2. Does the paper have details about the abundance of individual transcripts? If the paper is making the case for functional significance then one of the important bits of evidence is reporting on the abundance of the rare transcripts. If the authors omit this bit of information, or skim over it quickly, then you should be suspicious. Many of these rare transcripts are present in less that one or two copies per cell and that's perfectly consistent with transcriptional noise—even if it's only one cell type that's expressing the RNA. There aren't many functional roles for an RNA whose concentration is in the nanomole range. Critical thinkers will have thought about the problem and be prepared to address it head-on.

---

1. Or, maybe they know there's a controversy but they don't want you to be thinking about it as you read their paper. Or, maybe they think the issue has been settled and the "messy" genome advocates have been routed. Either way, these are not authors you should trust.

Hurst, L.D. (2009) Evolutionary genomics and the reach of selection. Journal of Biology 8:12 [DOI:10.1186/jbiol113]

Read More...

Summary only...

Monday's Molecule #118: Winners

 
UPDATE: The molecule is cyclin-dependent kinase 2 (CDK2), a protein involved in signaling [PDB 1b38]. The Nobel Laureate is Paul Nurse.

This week's winners are Mike Fraser of Toronto and Alex Ling of the University of Toronto.

---

This is a very famous protein but most of you won't be able to identify it from the structure alone. You'll need a hint of some sort.

Letting you know that the ligands are Mg²⁺ and adenosine-5′-triphosphate might not be enough so I'll also tell you that one of the authors on the structure paper was M.E. Noble.

There is one Nobel Laureate who is most closely identified with the function of this particular molecule, although that scientist was NOT the first to identify it. You have to identify the Nobel Laureate who got the prize for working out the function of the protein.

The first person to identify the molecule and the Nobel Laureate wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first won the prize.

There are six ineligible candidates for this week's reward: Bill Chaney of the University of Nebraska, Elvis Cela from the University of Toronto, Peter Horwich from Dalhousie University, Devin Trudeau from the University of Toronto, Shumona De of Dalhousie University, and Maria Altshuler of the University of Toronto.

I note that Canadians are trouncing the rest of the world. That's as it should be.

I still have one extra free lunch donated by a previous winner to a deserving undergraduate so I'm going to continue to award an additional free lunch to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow.

Comments will be blocked for 24 hours. Comments are now open.

---

Read More...

Summary only...

Sequenced genomes contain thousands of "unknown" genes

 
The total number of genes in the human genome has dropped from the initial estimates of 30-35,000 to about 25,000. Of these, more than 4,000 encode functional RNAs, leaving about 20,500 protein-encoding genes in the human genome [Humans Have Only 20,500 Protein-Encoding Genes].

Up to 40% of these protein-encoding genes are "unknown" in the sense that no function has been assigned to their protein products. In the jargon of genomics, the genes are "unannotated," meaning that nobody has assigned a function to the gene in the human genome database (Reichardt, 2007).

That means 8,000 unknown genes. About 1000 of these genes are "orphan" genes—genes that have no homologues in other species, including chimpanzees (Clamp, 2007).

Humans aren't unique. All sequenced eukaryotic genomes have a high percentage (~30-40%) of "unknown" protein-encoding genes.

A new paper in PLoS One looks at the "unknown" genes in the filamentous fungus Neurospora crassa (pink bread mold) (Kasuga et al. 2009). The Neurospora genome has about 9,000 protein-encoding genes and more than half of them have not been annotated. They are the "unkown" genes.

The genomes of about 40 different species of fungus have been sequenced and many of these are filamentous fungi related to Neuropsora. What this means is that it's possible to compare the Neurospora genes to those in many different genomes from closely related species; those that are part of the same family (less closelyrelated); part of the same phylum; and distantly related. You can't do such an extensive study with human genomes because there aren't very many mammalian genomes that have been sequenced and carefullyannotated. A draft sequence of the chimpanzee genome, for example, has been published but it is neither complete nor reliable enough for genomic comparisons. The only other primate genome is from macaque (Rhesus monkey) and that's far from finished. (The human and mouse genomes are the only ones listed as "complete" on the NCBI/Entrez website.)

The question is: are the unknown genes confined to Neurospora and its close relatives? If so, it would suggest that new genes have evolved within the past several million years and that's why we don't know their function.

Kasuga et al. created six sets of genes ...

1. Genes with homologs in distantly related eukaryotes and possibly prokaryotes. These are ancient genes.
2. Genes that are only found in fungi and not in plants or animals or protists (Dikarya).
3. Genes found only in Ascomycetes.
4. Genes confined to the Pezizomycotina clade to which Neurospora belongs.
5. Genes found only in Neurospora.
6. Others: genes that are found in some of the first groupings but not in all the smaller grouping.

The classification depends on the similarity cutoff. If the lowest cutoff is 25% sequence identity, then there will be more homologs in the eukarote or prokaryote class than if the cutoff is raised to 35%. The distibution of the various classes at each of three minimum sequence identify cutoffs is shown in their second figure.


Taking the 30% threshold numbers (middle group), it looks like there are 2,358 highly conserved genes with homologs in distantly related eukaryotes and prokaryotes. In contrast, there are 2,219 genes that don't have homologs in any other species. These are the orphan genes in Neurospora.

You might expect that most of the unknown/unannotated genes would be confined to Neurospora and closely related species. You might expect that highly conserved genes would be more likely to have been identified. That's partly true. Here are the numbers.


Only 16.5% of the highly conserved genes are mystery genes of unknown function. While this is much lower that the total (56%), it's still surprising that so many of the core genes remain unidentified. Presumably they are doing something very important. There are dozens of thesis projects available for talented graduate students who want to make a valuable contribution to biology.

It's not a surprise that 94% of the orphans are unannotated. These genes are likely to be new genes that have evolved recently in Neurospora and they would be expected to carry out unusual reactions that aren't found in other species. These "genes" are also the ones most likely to be artifacts (false positives) of the gene searching software. They may not be genes at all.

---

[Image Credit: Neurospora-National Institute of General Medical Sciences]

Clamp, M., Fry, B., Kamal, M., Xie, X., Cuff, J., Lin, M.F., Kellis, M., Lindblad-Toh, K. and Lander, E.S. (2007) Distinguishing protein-coding and noncoding genes in the human genome. Proc. Natl. Acad. Sci. (USA) 104:19428-19433. [DOI 10.1073/pnas.0709013104]

Kasuga, T., Mannhaupt, G., and Glass, N.L. (2009) Relationship between Phylogenetic Distribution and Genomic Features in Neurospora crassa. PLoS ONE 4(4):e5286. [DOI:10.1371/journal.pone.0005286]

Reichardt, J.K.V. (2007) Quo vadis, genoma? A call to pipettes for biochemists. Trends in Biochemical Sciences (TIBS) 32:529-530. [DOI:10.1016/j.tibs.2007.10.001]

Read More...

Summary only...

Conservative Spin

 

Canadian Cynic has built a career out of keeping an eye on The Blogging Tories. Every now and then CC comes up with something that makes you scratch your head and ask, "Can The Blogging Tories really be that stupid?"

Here's a posting from ErwinGerrits.com that will answer the question.

Funny how the current deficit budget is now universally referred to as “The Conservative Deficit”, even after this current budget was forced upon us by the Liberals, NDPers and the bloc-heads after a mid-winter stand-off on the Governour General’s front stoop. As I recall, the Conservative’s Economic Update, brought forward in December, did not make us go into a deficit at all. It was after the three stooges reared their ugly heads and blackmailed the country, that the current deficit budget was tabled.

---

Read More...

Summary only...

International team cracks mammalian gene control code

 
International team cracks mammalian gene control code

Stop the presses! Revise the textbooks! John Mattick and his collaborators have discovered how genes are controlled in mammals.

Anyone who knows Mattick's past history will know what's coming—Mattick overthrew the Central Dogma of Molecular Biology over six years ago (Mattick, 2003; Mattick, 2004).^1,2

An international consortium of scientists, including researchers from The University of Queensland (UQ), have probed further into the human genome than ever before.

They have discovered how genes are controlled in mammals, as well as the tiniest genetic element ever found.

Their discoveries will be published in three milestone papers in leading journal Nature Genetics.

---

1. See Basic Concepts: The Central Dogma of Molecular Biology for the truth about the Central Dogma.

2. See Greg Laden Gets Suckered by John Mattick for an example of how easy it is to get fooled by John Mattick.

Mattick, J.S. (2003) Challenging the dogma: the hidden layer of non-protein-coding RNAs in complex organisms. BioEssays 25:930-939

Mattick, J.S. (2004) The hidden genetic program of complex organisms. Sci. Am. 291:60-67.

Read More...

Summary only...

Idiot America?

 
Oh dear, my accommodationist friends aren't gonna like this.

From the amazon.com site ....

The Culture Wars Are Over and the Idiots Have Won

A veteran journalist's acidically funny, righteously angry lament about the glorification of ignorance in the United States.

In the midst of a career-long quest to separate the smart from the pap, Charles Pierce had a defining moment at the Creation Museum in Kentucky, where he observed a dinosaur. Wearing a saddle.... But worse than this was when the proprietor exclaimed to a cheering crowd, “We are taking the dinosaurs back from the evolutionists!” He knew then and there it was time to try and salvage the Land of the Enlightened, buried somewhere in this new Home of the Uninformed.

With his razor-sharp wit and erudite reasoning, Pierce delivers a gut-wrenching, side-splitting lament about the glorification of ignorance in the United States, and how a country founded on intellectual curiosity has somehow deteriorated into a nation of simpletons more apt to vote for an American Idol contestant than a presidential candidate.

With Idiot America, Pierce's thunderous denunciation is also a secret call to action, as he hopes that somehow, being intelligent will stop being a stigma, and that pinheads will once again be pitied, not celebrated.

I can't wait for the sequel—Idiot Canada.

---

[Hat Tip: Canadian Cynic]

Read More...

Summary only...

Bob McDonald Explains why Canadian Scientists Are Upset

 
Bob McDonald is the host of Quirks & Quarks on CBC radio. He has a blog and here's part of what he posted on Friday [Another Earth Day, Canadian scientists concerned].

While people around the globe celebrate the beauty of our planet on Earth Day, April 22nd, scientists in Canada are concerned that government funding is heading in the wrong direction to provide sensible solutions to environmental problems. More than 2000 scientists from across the country have signed an open letter to Prime Minister Harper and the Leader of the Opposition, expressing concerns over cuts to basic science research. It’s basic science that takes the pulse of the planet.

The scientists are concerned that government money is overlooking vital areas. For example, the current Conservative budget allocates $2 billion for university infrastructure - in other words, renovations to aging buildings. But those funds come with a catch. They must be matched with private funding, something everyone is having trouble finding during these tough economic times. Keeping roofs on buildings is important, but if there are no scientists to work in them, what’s the point?

The Canada Foundation for Innovation, a major source of science funding, did receive $740 million, but it also comes with that match-funding hook. The other funding agencies, the Natural Sciences and Engineering Research Council and the Canadian Institutes of Health Research, have had their budgets cut back, while Genome Canada was essentially ignored.

The rest of the government’s support for science is going towards the automotive industry, carbon sequestration, biofuels and scholarships for business students. In other words, applied science is taking precedent over basic science.

While we do need both, when it comes to the environment, the two types of science are often at loggerheads.

Politicians like to support applied science because it leads to jobs and products, such as more efficient cars or new wireless devices. Basic science, on the other hand, can’t promise an immediate economic return because it simply looks at nature to understand how things work - and more importantly these days, how things are changing. As we’ve seen with climate change, basic scientists have been out in the field watching ice caps disappear before their eyes, carbon dioxide levels rise and climate patterns shift. At the same time, those dealing with the technology at the heart of the problem resist the basic science to keep the current systems in place.

---

[Hat Tip: T. Ryan Gregory]

Read More...

Summary only...

Monday's Molecule #118

 
This is a very famous protein but most of you won't be able to identify it from the structure alone. You'll need a hint of some sort.

Letting you know that the ligands are Mg²⁺ and adenosine-5′-triphosphate might not be enough so I'll also tell you that one of the authors on the structure paper was M.E. Noble.

There is one Nobel Laureate who is most closely identified with the function of this particular molecule, although that scientist was NOT the first to identify it. You have to identify the Nobel Laureate who got the prize for working out the function of the protein.

The first person to identify the molecule and the Nobel Laureate wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first won the prize.

There are six ineligible candidates for this week's reward: Bill Chaney of the University of Nebraska, Elvis Cela from the University of Toronto, Peter Horwich from Dalhousie University, Devin Trudeau from the University of Toronto, Shumona De of Dalhousie University, and Maria Altshuler of the University of Toronto.

I note that Canadians are trouncing the rest of the world. That's as it should be.

I still have one extra free lunch donated by a previous winner to a deserving undergraduate so I'm going to continue to award an additional free lunch to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow.

Comments will be blocked for 24 hours.

---

Read More...

Summary only...

Agnotology

 
A reader (David) posted a comment about my recent Denyse O'Leary quotation. He alerted me to a new word: agnotology [Comments].

The Wikipedia entry is informative [agnolology agnatology] but there's lots more to learn about this word. Everyone is agreed that the word was invented by Robert Proctor a Standford University Professor who studies the history of science. Everyone is agreed that it refers to the study of ignorance, or why we don't know certain things. But there's more to it than that ....


Here's an excerpt from an article by Clive Thompson in WIRED magazine [Clive Thompson on How More Info Leads to Less Knowledge].

Normally, we expect society to progress, amassing deeper scientific understanding and basic facts every year. Knowledge only increases, right?

Robert Proctor doesn't think so. A historian of science at Stanford, Proctor points out that when it comes to many contentious subjects, our usual relationship to information is reversed: Ignorance increases.

He has developed a word inspired by this trend: agnotology. Derived from the Greek root agnosis, it is "the study of culturally constructed ignorance."

As Proctor argues, when society doesn't know something, it's often because special interests work hard to create confusion. Anti-Obama groups likely spent millions insisting he's a Muslim; church groups have shelled out even more pushing creationism. The oil and auto industries carefully seed doubt about the causes of global warming. And when the dust settles, society knows less than it did before.

"People always assume that if someone doesn't know something, it's because they haven't paid attention or haven't yet figured it out," Proctor says. "But ignorance also comes from people literally suppressing truth—or drowning it out—or trying to make it so confusing that people stop caring about what's true and what's not."

This is an important insight. It's not something that we didn't know already but it's good to emphasize the concept and give it a name.

Creationism is an excellent example. It's not just that creationists fail to understand science, it's also that they are being actively lied to in an attempt to spread ignorance. In other words, there are people who deliberately spread misinformation in order to oppose knowledge.

If we are going to fight creationism we have to do more than just teach evolution in the schools. If we do that then we are just barely holding our own against the people who spread ignorance. At best, students will be aware of a conflict between what they learn in school and what they learn everywhere else.

In order to fight the spread of ignorance we have to take on the liars directly and show why they are lying. They need to be discredited and exposed. Unfortunately, many of the enemy are "Christians" and Christians get special protection in our society. You can criticize astrology and quackary but not religion.

That has to change. Perhaps we can lump them all under the term "agnotology" and treat them all the same?

---

Read More...

Summary only...

And Now for a Little Comic Relief

 
It's been a few weeks since my last humorous posting so at the start of a new week I thought I'd give you something to laugh about.

Here's a few words from Denyse O'Leary.

The reason so many of us have risen up against Darwinism is not that we think natural selection never occurs but that we have never accepted - without evidence - the idea that it produces a high level of information (and that was Darwin's argument) And - as Mike Behe shows in Edge of Evolution, it doesn't.

It is amazing what people who get tenure at prestigious universities are willing to support without evidence. Including "chance" as a key explanation of high levels of information, which we must all know is completely untrue.

If you doubt that, try throwing the bag of Scrabble letters around the room and reassembling them randomly, and see what happens.

---

Read More...

Summary only...

Modified Bases in DNA

 
Adenine: from the Greek adenas "gland": first isolated from pancreatic glands (1885)

Cytosine: derived from cyto- from the Greek word for "receptacle," refering to cells (1894)

Guanine: originally isolated from "guano" or bird excrement (1850)

Thymine: first isolated from thymus glands (1894)

(source Horton et al. 2006)Bacterial genomes contain a number of unusual bases in addition to the classic adenine (A), cytosine (C), guanine (G), and thymine (T). The most common of the unusual bases are 5-methylcytosine, N⁴-methylcytosine, and N⁶-methyladenine (Erlich et al. 1987).

Bacteriophage DNA, especially the DNA of bacteriophage T4 and its close relatives, can contain 5-hydroxymethylcytosine. The base is usually glycoslylated in normal phage. (A sugar group is attached to the hydroxymethyl group.)

Many of these modified bases serve to protect DNA from restriction endonucleases—enzymes that cleave foreign DNA at specific sites. The restriction endonucleases act on bacteriophage (virus) DNA preventing it from replicating inside the bacterial cell [see Restriction, Modification, and Epigenetics].

If bacteriophage modify their nucleotides at the site of cleavage, they will escape the defenses of the bacterial cell. Of course, bacteria that make restriction endonucleases have to protect their own DNA or else they will be committing suicide. That's why their genomes have modified nucleotides.

Many other modified bases have been found in DNA but they are quite rare. Examples are uracil, α-putrescinylthymine, and 5-dihydroxypentyluracil.


Eukaryotic DNA doesn't have as many modified bases. In fact, 5-methylcytosine is the only one that's common in all eukaryotes. N⁶-methyladenine is known to exist in protist and plant DNA and it is thought to exist at low levels in mammalian DNA as well (Ratel et al. 2006). The presence of hydroxymethycytosine has been reported in various animals as far back as 1972 (Penn et al. 1972).


Now Kriaucionis and Heintz (2009) have re-discovered hydroxymethylcytosine in mammalian DNA. Their paper appears in the latest issue of Science. Apparently the modified nucleotide is found in certain brain cells. Their result confirms the work done by Penn et al. (1972), a result that had not been confirmed in several other studies. This makes hydroxymethylcytosine the seventh modified base in eukaryotic DNA—unless there are some that I don't know about.

The problem with the press release is that it doesn't put the discovery in the proper context.

ScienceDaily (Apr. 17, 2009) — Anyone who studied a little genetics in high school has heard of adenine, thymine, guanine and cytosine – the A, T, G and C that make up the DNA code. But those are not the whole story. The rise of epigenetics in the past decade has drawn attention to a fifth nucleotide, 5-methylcytosine (5-mC), that sometimes replaces cytosine in the famous DNA double helix to regulate which genes are expressed. And now there's a sixth: 5-hydroxymethylcytosine.

In experiments to be published online April 16 by Science, researchers reveal an additional character in the mammalian DNA code, opening an entirely new front in epigenetic research.

We aren't told that the sixth nucleotide is actually N⁶-methhyladenine. We aren't told that many other modified bases have been discovered in bacteria, including hydroxylmethylcytosine. And we aren't told that the authors actually cite earlier work showing the presence of hydroxymethylcytosine in mammalian DNA.

That's a shame. The authors are quoted in the press release. They should have made more of an effort to ensure that it was scientifically accurate.

---

Ehrlich, M., Wilson, G.G., Kuo, K.C., and Gehrke. C.W. (1987) N4-methylcytosine as a minor base in bacterial DNA. J Bacteriol. 169:939-943. [Journal of Bacteriology]

Kriaucionis, S. and Heintz, N. (2009) The Nuclear DNA Base 5-Hydroxymethylcytosine Is Present in Purkinje Neurons and the Brain. Science Published Online April 16, 2009 [DOI: 10.1126/science.1169786]

Penn, N.W., Suwalski, R., O'Riley, C., Bojanowski, K. and Yura, R. (1972) The presence of 5-hydroxymethylcytosine in animal deoxyribonucleic acid. Biochem J. :781–790. [Biochem. J.]

Ratel, D., Ravanat, J.L., Berger, F., and Wion, D. (2006) N6-methyladenine: the other methylated base of DNA. Bioessays :309-15. [PubMed

Read More...

Summary only...

Dancing in Antwerp's Train Station

 
I have a confession to make. Ms. Sandwalk and I, along with four other couples we've known for many years, are learning how to do ballroom line dances. It's so much fun.

Perhaps that's why this video makes me smile. It's a promotion by a Belgian TV show that's looking for a "Maria" to play the lead in "The Sound of Music." I hope my daughter—who lives in Belgium— never hears about it 'cause she already knows all the words to every song in the musical.

UPDATE: Some people may not know about the T-Mobile add in the Liverpool Street Station in London [T-Mobile Dance].

---

P.S. My dancing group is almost as good as these guys. Maybe we should do a performance in Union Station in downtown Toronto?

[Hat Tip: GrrlScientist]

Read More...

Summary only...

Jerry Coyne's View of Evolutionary Psychology

 
You'll have to read Evolutionary psychology: the adaptive significance of semen flavor to find out what Coyne thinks of evolutionary psychology. I think he's captured the essence of the movement.

---

P.S. I was looking for an appropriate illustration of the behavior that Coyne describes. Turns out that if you enter the appropriate term in your Google search box, you'll find quite a few photographs out there on the internet. I decided not to use any of them but the search was interesting.

Read More...

Summary only...

Do You Want to Know the Sequence of Your Genome?

 
It's very likely that each one of us carries several recessive lethal alleles and many alleles that make us more susceptible to various diseases. You can count on it.

Do you want to know which of the many known deleterious alleles you have in your genome? That's one of the questions asked in an article published in The Economist: Getting Personal.

Though he has the world’s most advanced gene-sequencing technology at his fingertips, Dr Altshuler refuses to get his own genome sequenced: “If someone gave it to me on a CD, I’d refuse to look at the disc. The information is meaningless.” Bill Gates agrees. He has not had his genome sequenced either, nor does he plan to, though after a moment’s reflection he adds, “unless I find out I have cancer.”

Keep in mind that there's nothing much you can do if you find out that you have a predisposition for cancer or some other disease, like Alzheimer's. You can change your lifestyle but it's not clear whether that will change the probabilities significantly. Furthermore, there are so many claims out there about how to prevent disease that you'll never be sure you're doing the right thing.

And what do you do if you want to have children with someone who also knows their genome sequence? Figure out the probabilities that your children will not inherit any of your bad alleles. Is that a responsibility that you want? Why?

I'm with David Altshuler on this one and so was John Hawks until recently. Now John is changing his mind—Turning ACGT into poetry. Part of my problem is that I don't feel very comfortable seeking advice from a for-profit company when it comes to interpreting my genome sequence. But we won't have much choice; there's absolutely no way that the average person is going to be able to do the interpretation, so they will have to pay for it. And they'll have to get an update every few years as we learn more about human genes. (Whole genome interpretation is not a service that will be covered by socialized medicine.)

Do you want to know the sequence of your genome? Assuming that you can afford the sequencing cost, how do you intend to use the information and how will you interpret it?

---

Read More...

Summary only...

Sign the Open Letter

 
Are you a Canadian scientist who is upset about cuts to research funding by the current government? Read the Open letter to the Prime Minister and Leader of the opposition and add your name to the list of over 2000 scientists.

---

Read More...

Summary only...

Proportional Representation Is about to Pass in British Columbia

 
The Single-Transferable Vote (STV) is a system where each voting district (riding/constituency) has multiple members. You vote for several candidates by ranking them from most preferred to least preferred. If a candidate gets more than the minimum number of votes needed for election then the "surplus" votes are transferred to the second choice candidates.

If, after transferring "surplus" votes, there are still candidates to be elected, then the candidate with the lowest number of votes is eliminated and the votes are transferred to the voter's next choice. This process of elimination and transfer continues until the required number of candidates are elected [BC-STV].

The system was chosen by a non-partisan citizens' assembly.

A majority of voters in British Columbia voted in favor of this form of proportional representation in the last referendum but they failed to get the 60% majority required to change the voting system. It looks like they will succeed on May 12th, making British Columbia the first province to abolish the old first-past-the-post system and adopt a form of proportional representation.

I'm certain that Ontario won't be far behind. We lost the vote for proportional representation last time but that was probably because the general public didn't understand it. That, plus the fact that many prominent newspaper columnists and editors lied made untrue statements about the dangers of proportional representation. They didn't understand it either.

April 15, 2009
FOR IMMEDIATE RELEASE
Poll: 65 per cent of British Columbians support BC-STV
Younger voters overwhelming in their support

Vancouver, B.C. – The numbers are in and British Columbia voters are giving a big thumbs up to electoral reform with 65 per cent saying they will vote for BC-STV in the upcoming referendum on May 12. That is the top line result of a major survey conducted by Angus Reid Strategies. Support for a new way of electing our MLAs is particularly strong among younger voters – those 18 to 34 – at 74 per cent.

“The survey results indicate that British Columbians and particularly younger voters are ready to embrace a new electoral system in British Columbia,” said Catherine Rogers, vice president, Angus Reid Strategies. “A large majority are looking for electoral change and want an electoral system that is fair and that elects MLAs who are more accountable to them.”

When presented with the question that will appear on the ballot, 65 per cent said yes to BC-STV while only 35 per cent chose to keep the current first-past-the post system. Angus Reid Strategies conducted the online survey March 9 to 12 and polled 702 British Columbians across the province. While support for BC-STV continues to grow, awareness of the upcoming referendum is at 44 per cent.

---

Read More...

Summary only...

The 50 Most Brilliant Atheists of All Time

 
The 50 Most Brilliant Atheists of All Time

Congratulations to Jodie Foster (#46) who's a lot more attractive than atheist #45 who, in turn, is a heck of a lot prettier than #37.

1. Democritus
2. Diagoras of Melos
3. Epicurus
4. Theodorus the Atheist
5. Andrew Carnegie
6. Ivan Pavlov
7. Sigmund Freud
8. Clarence Darrow
9. Richard Strauss
10. Bertrand Russell
11. Jawaharlal Nehru
12. Linus Pauling
13. Paul Dirac
14. Ayn Rand
15. Katherine Hepburn
16. Jacques Monod
17. Subrahmanyan Chandresekhar
18. Alan Turing
19. Francis Crick
20. Claude Shannon
21. Richard Feynman
22. Noam Chomsky
23. James D. Watson
24. Peter Higgs
25. Warren Buffet
26. John Searle
27. Steven Weinberg
28. Carl Sagan
29. David Suzuki
30. George Carlin
31. Bruce Lee
32. Leonard Susskind
33. Stephen Jay Gould
34. Richard Dawkins
35. Daniel Dennett
36. Stephen Hawking
37. Mick Jagger
38. Richard Leakey
39. David Gilmour
40. Brian Eno
41. David Sloan Wilson
42. Steve Wozniak
43. Douglas Adams
44. Steven Pinker
45. PZ Myers
46. Jodie Foster
47. Russell T Davies
48. David Chalmers
49. Sean Carroll
50. Mark Zuckerberg

---

Read More...

Summary only...

G T C A

 
Just when I've (almost) mastered Y M C A, along comes a new challenge.

---

Read More...

Summary only...

Summer Course on Intelligent Design Creationism

 
You can sign up for a full week course on Intelligent Design Creationism at the Discovery Institute in Seattle, Washington (USA) [Deadline Nears for Summer Seminars on Intelligent Design]. It runs from July 10 - 18, 2009 and it's free.

The course is open to any student ... almost. There are a few small hurdles that have to be jumped in order to qualify.

1. A copy of your resume;
2. A letter of recommendation from an ID-friendly source;
3. A copy of your academic transcript;
4. A short (one page) statement of your interest in ID within your field of study.

If anyone wants to attend I'd be happy to write a letter of recommendation.

---

Read More...

Summary only...

Christine Hurley - The Flamboyant Psychic

 
Back in October 2007, I posted a short message about a psychic who was arrested for fraud. I linked to Mike's Weekly Skeptic Rant because he had an interesting multiple choice question [see Psychic Arrested in Calgary].

A Calgary psychic named Christine Hurley posted a comment where she claimed to be as interested as the rest of us in weeding out psychic frauds. (Yes, I do see the irony.)

Since then, she has posted several more comments designed to promote her "skills" in psychic reading. You can benefit from her psychic powers by charging $120 to your credit card for a 30 minute phone reading [Christine Hurley: Prices]. An even better bargain is one hour on the phone for $150!

I'm not exactly sure how this works. Presumably Ms. Hurley will tell you all the important things you need to know in the first 30 minutes. Maybe there are some interesting details that require another half hour.

Read the comments and testimonials that are accumulating at Psychic Arrested in Calgary. It's really amazing to see how some people can be completely duped by Christine Hurley into believing that she has psychic powers.

I wonder why she spends so much time collecting $120 (CDN) from her suckers clients when she could "easily" pocket $1,000,000 (US) in James Randi's One Million Dollar Paranormal Challenge? Does anyone know why she hasn't collected the prize? As a true psychic she must know how Randi's test is going to turn out.

---

[Photo Credit: Bryan Schlosser, The Leader-Post]

Read More...

Summary only...

The Evolution Conspiracy

 
The Evolution Conspiracy is a book by Lisa Shiel. I'd never heard of her until a few days ago but some of you might know her because she's a fan of bigfoot. She has a masters degree in library science.

You can't buy the book until next September but you can read all the rave reviews of this unpublished book on Lisa's website: The Evolution Conspiracy. You can also get an inkling of what the book is about by reading her promotional material. Here's an excerpt ...

Evolution.

One word, deceptive in its simplicity, has transformed the way we look at ourselves and everything around us. Once thought of as unique, man has become one of the animals with no special claim on the planet. As children, few of us question what we learn in biology class about the origins of life and the position man holds in the hierarchy. Science textbooks present evolution as fact—indisputable, inevitable, and incomprehensible to everyone outside the exalted few with PhDs in the appropriate fields.

That’s why this book promotes one key premise—anyone can understand evolution.

That's refreshing. Anyone can understand evolution. Anyone, that is, except Lisa Shiel. Her stupidity and ignorance are on display in the comments she's making on science blogs and on her own website. By her own admission she is dropping comments on all the evolution blogs in order to promote her book [Banned by Evolutionists! Can You Handle It?].

The purpose of this posting is to help give her as much publicity as possible in order to expose her as just another kook who has no idea what evolution is all about.

Here's an example from a posting she made on April 7th: You Can’t Tell a Species by Its Cover.

The theory of evolution involves numerous complicated and confounding strands—almost as many strands, I dare say, as DNA itself. Charles Darwin posited that natural selection drives the evolution of species, and this idea has become the cornerstone of evolutionary theory. In natural selection, traits that seem beneficial are preserved in a species while undesirable traits gradually disappear. Because natural selection cannot account for all adaptations, scientists devised the theory of genetic drift, in which changes occur at random.

Yet no one has ever reproduced the creation of a species via either natural selection or genetic drift; in fact, no one has ever demonstrated scientifically that one species evolves into another. If a theory must adhere to the scientific method to remain a scientific theory, then evolution has failed the test. The scientific method requires repeated testing, and the ability to reproduce results.

Now toss into this mess the recent discovery that some species “evolve” genetically while remaining unchanged anatomically. Scientists at Massey University in New Zealand have found that a reptile called the tuatara differs genetically from its 8,000-year-old ancestors, while retaining the same anatomical makeup and outward appearance. The tuatara’s DNA changes make it the Speedy Gonzales of genetic evolution. According to Axel Meyer of Germany’s University of Konstanz, the discovery suggests “a real disconnect” can exist between genetic and anatomical evolution.

Finally, consider the recent discovery that cryptic species can fool us too—two creatures look identical, but their DNA identifies them as different species. Perhaps the fossilized tuatara aren’t really tuatara after all…

Evolution: The unscientific scientific theory.

Makes you wonder if Lisa Shiel has even read her own book—a book that presumably explains evolution correctly. There are so many factual and conceptual errors in this short posting that it catapults Lisa into contention for the most ignorant IDiot award. And that's saying a lot 'cause the competition is fierce.

Anyway, the bottom line is that there's nothing to see here folks. You can move along to other books and other blogs. Lisa even makes Denyse O'Leary look good.

---

Read More...

Summary only...

Nobel Laureate: Max Theiler

 

The Nobel Prize in Physiology or Medicine 1951

"for his discoveries concerning yellow fever and how to combat it"

Max Theiler (1899 - 1972) won the Noble Prize in 1951 for his work on combating yellow fever.

Theiler's most important contribution was the discovery of a variant of the yellow fever virus that did not cause the disease in humans. When injected into healthy patients, this variant produced immunity to the normal disease-producing virus.

This discovery was not immediately useful since attenuated virus from mice was more effective in producing immunity—a result also discovered by Theiler. The Nobel Committee felt that Theiler had made a significant contribution to understanding viral diseases.

One gets the impression from reading the presentation speech that Theiler was also being recognized as a representative of work done by the Rockefeller Foundation.

THEME:
Nobel Laureates

The significance of Max Theiler's discovery must be considered to be very great from the practical point of view, as effective protection against yellow fever is one condition for the development of the tropical regions - an important problem in an overpopulated world. Dr. Theiler's discovery does not imply anything fundamentally new, for the idea of inoculation against a disease by the use of a variant of the etiologic agent which, though harmless, produces immunity, is more than 150 years old. Jenner used a natural virus variant, cowpox virus, against smallpox, and Pasteur produced a similar variant of the rabies virus by repeated passage through animals. So far there have been only a few successful attempts to master a disease by such measures, but Dr. Theiler's discovery gives new hope that in this manner we shall succeed in mastering other virus diseases, many of which have a devastating, effect and against which we are still entirely powerless. Max Theiler, therefore, has rendered mankind such a service as Nobel made a condition for the awarding of this prize.

Dr. Theiler. For a period of almost forty years the International Health Division of the Rockefeller Foundation has carried on very comprehensive and fruitful work in combating yellow fever and extending our knowledge of it. Among the many who have made their contributions, you take an especially prominent place, because you have made their contributions profitable and because you have opened the way to greater understanding of the epidemiology of the disease and to an effective prophylaxis against it. The Caroline Institute esteems your research work so highly, not the least for its practical value, that it has found it proper to award this year's Nobel Prize in Physiology or Medicine to you.

I ask you, Dr. Theiler, to receive the prize from the hands of His Majesty, our gracious King.

---

[Photo Credit: ©Bettmann/CORBIS, Rights Managed, Corbis]

The images of the Nobel Prize medals are registered trademarks of the Nobel Foundation (© The Nobel Foundation). They are used here, with permission, for educational purposes only.

Read More...

Summary only...

Gary Goodyear's Letter to Nature

 
Canadian government reaffirms support for science and discovery

Sir

You report researchers' concerns about the Canadian government's support for science in two recent News stories (Nature 457, 646; 2009 and Nature 458, 393; 2009). As Minister of State for Science and Technology, I can say that, despite the global economic situation, the government of Canada remains committed to innovation and discovery. We have increased funding to researchers, both in universities and in the private sector.

In the past three years, for example, we have significantly increased the budgets of federal granting councils, increased scholarships through the Canada Graduate Scholarships Program, and increased the Industrial Research Assistance Program for small and medium-sized businesses. The Budget 2009 announcements include Can$750 million (US$590 million) for the Canada Foundation for Innovation to attract and retain world-leading researchers, and a Can$2-billion infrastructure programme. The government has also put in place two five-year funding agreements with Genome Canada that are worth Can$240 million, to support large-scale, world-class research.

Your readers should therefore rest assured that the government of Canada will continue to fund research for the benefit of all scientists and Canadians.

Isn't it strange that basic science researchers are upset about the fact that funding to the major granting councils has been cut for the next three years?

Either the researchers are correct, and Canadian basic research is in trouble, or Gary Goodyear is correct and the Conservatives are doing a fine job.

I know who is telling the truth.

---

Read More...

Summary only...

Do Science and Religion Conflict in Louisiana?

 
The National Center for Science Education reports on the results from a recent poll in Louisiana [Polling Evolution in Louisiana]. Respondents were asked the following question.

Do you think the scientific theory of evolution is well supported by evidence and widely accepted within the scientific community, or that it is not well supported by evidence and many scientists have serious doubts about it?

39% answered "yes" and 21% didn't know. 40% said that evolution is not well supported by evidence and/or is not accepted by the scientific community.

Let's dismiss the 21% who didn't know the answer. That leaves almost 80% of the population who see no conflict between science and religion. Half of them probably believe in a God who accepts evolution and the other half of them think that the scientists reject evolution, which maked science compatible with creationism.

That's pretty amazing, and scary, when you think about it.

---

Read More...

Summary only...

Teabagging

 
Today is April 15th. It's a significant day in America because income taxes are due. It's also the day when some people are protesting taxes by having "teabagging" parties. If you don't live in the USA, or watch American television, you've probably never heard of "teabagging." Here's a quick summary from a show that I watched on MSNBC.

Listen for Lawrence O'Donnell, who explains the importance of socialism in America. According to O'Donnell, America is like all other Western industrialized nations. It has a mixed economy (capitalism and socialism).

I agree with that. I don't agree with his claim that, compared to all other nations, American probably has the best mix of socialism and capitalism.

---

Read More...

Summary only...

Monday's Molecule #117: Winners

 
UPDATE: The molecule is yellow fever virus.

The Nobel Laureate is Max Theiler.

This week's winner is Maria Altshuler of the University of Toronto.

---

Today's "molecule" is fairly complex for a "molecule" but not quite as complex as a living cell. You have to identify the particular type of "molecule" that's shown here but it will be too hard to do that without some clues. One of the clues is the connection to a Nobel Laureate. The other one is cleverly hidden in the bottom part of this posting.

The first person to identify the "molecule" and the Nobel Laureate wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first won the prize.

There are seven ineligible candidates for this week's reward: Dima Klenchin from the university of Wisconsin, Alex Ling from the University of Toronto, Bill Chaney of the University of Nebraska, Elvis Cela from the University of Toronto, Peter Horwich from Dalhousie University, Devin Trudeau from the University of Toronto, and Shumona De of Dalhousie University

Dima and Bill have donated their free lunch to a deserving undergraduate so I'm going to continue to award an additional free lunch to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow.

Comments will be blocked for 24 hours. Comments are now open.

---

Read More...

Summary only...

Child Abuse and the Anti-Vaccination Movement

 
I was attending the Center for Inquiry 12th World Congress in Washington last weekend and I happened to catch a re-broadcast of a Larry King show on the "dangers" of vaccinating children. It was an appropriate reminder of the lack of rationalism in our society.

Normally I'm fairly tolerant of people who reject standard medicine. In fact, society might actually benefit when these stupid people are eliminated by succumbing to various diseases. That's what the Darwin awards are for.

But this case is different. These adults are not putting themselves at risk—they are endangering their children.

If you stop vaccinating your children you are putting them at risk for many deadly diseases. Some of your children will die. If everyone stops vaccinating children then millions of children will die. How can anyone in their right mind think that vaccinations are so dangerous that the risk is worth it?

I'm not surprised that movie actors and average citizens are kooks. I am surprised that normally responsible TV networks like CNN contribute to potential child abuse. But I'm absolutely shocked that there are physicians who go along with the kooks.

One of those physicians is Dr. Bernadine Healy who appears in this CNN clip. I was astonished to hear her advocate more studies, lending credibility to the claims that vaccinations cause autism and other diseases. Bernadine Healy is a Republican who was the head of the National Institutes of Health under George H.W. Bush. She was removed when Clinton took over the Presidency in 1993.

Healy's defense of the anti-vaccination movement did not ring true. Her "statistics" didn't sound reasonable to me but I was in no position to refute them directly. Fortunately Orac has taken up the task at Bernadine Healy: Flirting with the anti-vaccine movement. Thanks Orac.

You know we're in trouble when the media and former NIH directors can't tell the difference between science and superstition.

This reminds me of the debate over the fluoridation of water back in the 1950's. There were kooks who warned us that fluoridation was dangerous and that it was a communist plot.

---

Read More...

Summary only...

Dying for Love in Afghanistan

 
It's been eight years since coalition forces "liberated" Afghanistan. Here's the result: Taleban 'kill love affair couple'.

Mr Azad said: "An unmarried young boy and an unmarried girl who loved each other and wanted to get married had eloped because their families would not approve the marriage."

Officials said the couple were traced by militants after they tried to go to Iran. They were made to return to their village in Khash Rod district. [Nimroz province, south-west Afghanistan - see map]

"Three Taleban mullahs brought them to the local mosque and they passed a fatwa (religious decree) that they must be killed. They were shot and killed in front of the mosque in public," the governor said. ...

Extrajudicial "honour killings" have been widely carried out in Afghanistan since then by conservative families angered by a relative who has brought them shame - usually by refusing to marry a chosen partner.

The Taleban have widened their influence over the past three years and now control many remote districts where there are not enough coalition forces to establish a permanent presence.

The people of Afghanistan should make up their own minds about whether this sort of behavior is tolerable. We cannot do it for them. As long as the country is semi-united in repulsing foreign invaders it will put off the social reforms that could bring it into the 21st century.

It's time to leave and let them face up to, and solve, their own internal problems. No people in the world would tolerate a foreign army from a different culture coming in and telling them how to behave—even if they suspected that their behavior was immoral.

Imagine that the USA was invaded and conquered by a European army who insisted that gays be allowed to marry, socialized medicine is begun, the metric system is imposed, proportional representation becomes the law, and capital punishment is abolished. Would those changes be welcomed by Americans who all of a sudden recognize that the foreigners are correct? Or would the changes be resisted even more fiercely because advocating change means siding with the enemy?

---

[Hat Tip: Pharyngula]

Read More...

Summary only...

Wild chimpanzees exchange meat for sex

 
I don't know if it's true that Wild chimpanzees exchange meat for sex but I know some vegetarians who may find it interesting.

Wild female chimpanzees copulate more frequently with males who share meat with them over long periods of time, according to a study led by researchers from the Max Planck Institute for Evolutionary Anthropology in Germany, published in the open-access, peer-reviewed journal PLoS ONE April 8.

It probably works for humans as well.

I'm going out to buy some steaks for dinner.

The original paper is Gomes and Boesch (2009)

---

Gomes, C.M. and Boesch, C. (2009) Wild Chimpanzees Exchange Meat for Sex on a Long-Term Basis. PLoS ONE 4(4): e5116. DOI:10.1371/journal.pone.0005116

Read More...

Summary only...

Which Gas Is Cheapest?

 
Here's three photographs of gas station signs. The one on the left was taken in Mississauga, Ontario, Canada and the two on the right were taken in Bethesda, Maryland, USA. The Bethesda gas stations are one block apart.

Assuming that the photos were taken on the same day (Wednesday, April 8, 2009), which station has the cheapest gas if you pay by credit card?

---

Read More...

Summary only...

A Breakthrough in Gene Expression?

 
When we teach protein synthesis in undergraduate molecule biology classes we cover the main mechanisms regulating the rate of translation.

One of them is the influence of codon bias among synonymous codons. We've known for 35 years that rare codons are translated more slowly that the common codons. Highly expressed genes have a pronounced codon bias in favor of the most common codons. As a result of this phenomenon, it is not true that every codon for leucine, for example, is equal. Some are better than others in some genes. Synonymous codons are not always neutral in their effect. (For a complete description of this phenomenon see: Silent Mutations and Neutral Theory.)

We also teach about the influence of messenger RNA secondary stucture. The classic examples in the E. coli ribosomal protein genes are in all the textbooks, as are the examples of attentuation—especially in the Trp operon. Again, this stuff was standard fair in textbooks and courses beginning in the 1970's.

A press release caught my eye: Penn biologists discover how 'silent' mutations influence protein production. "Cool," I thought, "maybe this is something that I'll have to put into the next edition of my textbook."

Here's the breakthrough.

For biologists, these results fundamentally change the understanding of the role of synonymous mutations, which were previously considered evolutionarily neutral. ....

The silent mutations changed the amount of fluorescent protein by as much as 250-fold, without changing the properties of the protein. Codon bias, the probability that one codon of three adjacent nucleotides will code for one amino acid over another, was previously thought to be the cause for protein expression variance, but it did not correlate with gene expression in these experiments.

"At first we were stumped," Plotkin said. "How were the silent mutations influencing protein levels? Eventually, we looked at mRNA structure and discovered that this was the underlying mechanism."

Imagine that. They've rediscovered what most of my students have been taught for 35 years!

---

[Image Credit: The figure is from page 706 of my textbook. Similar figures are in all biochemistry and molecular biology textbooks. The figure shows the secondary mRNA structure around the initiation codon of the S7 ribosomal protein gene in E. coli. The secondary structure inhibits translation initiation. Although in this case the actual codons are not involved in the formation of double-stranded regions, in other cases they are.]

Read More...

Summary only...

Monday's Molecule #117

 
Today's "molecule" is fairly complex for a "molecule" but not quite as complex as a living cell. You have to identify the particular type of "molecule" that's shown here but it will be too hard to do that without some clues. One of the clues is the connection to a Nobel Laureate. The other one is cleverly hidden in the bottom part of this posting.

The first person to identify the "molecle" and the Nobel Laureate wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first won the prize.

There are seven ineligible candidates for this week's reward: Dima Klenchin from the university of Wisconsin, Alex Ling from the University of Toronto, Bill Chaney of the University of Nebraska, Elvis Cela from the University of Toronto, Peter Horwich from Dalhousie University, Devin Trudeau from the University of Toronto, and Shumona De of Dalhousie University

Dima and Bill have donated their free lunch to a deserving undergraduate so I'm going to continue to award an additional free lunch to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow.

Comments will be blocked for 24 hours.

---

Read More...

Summary only...

Down with Darwinism!

 
I've been fuming ever since hearing Michael Ruse speak on Friday night. It's a crying shame that the skeptics at the 12th World Congress had to get their information about evolution from him.

One of the things I detest about Michael Ruse is his insistence on using the word "Darwinism" to describe evolutionary biology. As most of you know I am not a Darwinist.

Adam M. Goldstein at Evolution:Education and Outreach reminds us that we should all stop using the word "Darwinism" when we are trying to educate people about evolutionary biology [Give the old man a break, and let’s stop it with “Darwinism”].

---

[Hat Tip: Stranger Fruit]

Read More...

Summary only...

The New Skeptics

 
The next generation of skeptics/atheists is well represented at the CFI World Congress in Washington.

Meet Derek Rodgers (left), a computer science student at Dalhousie University in Halifax, Nova Scotia (Canada) and Jason Ball (right), a political science/history and philosophy of science student at Melborne University (Australia). Jason might be taking a course from John Wilkins next term. I expressed my sympathy. :-)

Visit the Dalhousie Atheists and Young Australian Skeptics to see what these leaders of the future are doing today.

---

Read More...

Summary only...

A Night at the Newseum

 
Okay, so technically it wasn't a "night" at the Newseum—it was most of a day. Ms. Sandwalk and I had a wonderful time at the Newseum. It's on Pensylvania, just one block from the Mall and right next door to the Canadian embassy.

If you're in Washington you must go to the Newseum.

---

Read More...

Summary only...

Michael Ruse: 90% 0f Scientists Are Selectionists

 
I'm at the Center for Inquiry 12th World Congress in Washington D.C.

Last night I attended a session on "The Influence of Darwin." The four panelists were: Michael Ruse, a philosopher, Barbara Forrest, a philosopher, David Contosta, a historian, and Edward Tabash, a lawyer.

Ruse presented his usual distorted view of evolutionary biology only this time he added a comment in his defense. He said, "90% of scientists are selectionists, and the other 10% are selectionists 90% of the time." This was obviously a response to people who have criticized Ruse for being too much of an adaptationist.

Incidentally, Ruse made it clear that he is an atheist, even though he is strongly opposed to the idea that science/evolution leads to a loss of faith. I mention this because I've seen numerous references to Ruse implying that he is religious.

I asked the panel why there was no scientist on the panel and whether they thought that they could represent science accurately. I added, provocatively, that in my opinion three of the four panelists did not do a good job of describing science

The panel didn't think this was problem. I assume Darwin had a great influence on law, philosophy, and history but not much of an influence on science.

---

Read More...

Summary only...

Twisted Tree of Life Award #3

 
Jonathan Eisen at The Tree of Life has just awarded his third Twisted Tree of Life Award. And well-deserved it is.

---

Read More...

Summary only...

New Breakthrough in Evolution Theory

 
Imagine a culture of yeast cells growing in a medium where sucrose is the only carbon source. Sucrose isn't the preferred carbon source for yeast but yeast can handle it if need be. Cells secrete an enzyme called invertase that breaks down sucrose to glucose and fructose


The products of the reaction, glucose and fructose, can be taken up by the cell or they may diffuse away before being taken up. Molecules produced by the invertase from one cell can be absorbed by a neighboring cell.

As the concentration of free glucose and fructose rises in the medium, cells that lack the ability to synthesize and secrete invertase may survive. Thus invertase negative mutants may accumulate because they don't need to make their own invertase in order to have a source of carbon. In game theory, such mutants are called "cheaters."

Hands up, all you people who think that the existence of a stable equilibrium of cheaters and cooperators is a new discovery in evolutionary theory.

Right, it's not.

The editors of Nature think it is, so they published the paper from the Dept. of Physics at MIT (Gore et al., 2009).

The MIT PR department thought it was revolutionary enough to warrant a press release that was picked up by ScienceDaily [Cooperative Behavior Meshes With Evolutionary Theory].

One of the perplexing questions raised by evolutionary theory is how cooperative behavior, which benefits other members of a species at a cost to the individual, came to exist.

Cooperative behavior has puzzled biologists because if only the fittest survive, genes for a behavior that benefits everybody in a population should not last and cooperative behavior should die out, says Jeff Gore, a Pappalardo postdoctoral fellow in MIT's Department of Physics.

Gore is part of a team of MIT researchers that has used game theory to understand one solution yeast use to get around this problem. The team's findings, published in the April 6 online edition of Nature, indicate that if an individual can benefit even slightly by cooperating, it can survive even when surrounded by individuals that don't cooperate.

In short, the study offers a concrete example of how cooperative behaviors can be compatible with evolutionary theory.

I agree that this is an interesting example but I don't think the public is well served by presenting it as a new contribution to evolutionary theory. The public is entitled to think that evolutionary biologists must be really stupid if they've never thought of this before.

They (the public) would be really confused if they happened to read the Wikipedia entry on John Maynard Smith (1920 - 2004).

There are no references to Maynard Smith's work in the citations at the end of the Nature paper, although there is a reference to "Smith, J.M." who wrote the book Evolution and the Theory of Games.

---

Gore, J., Youk, H., and van Oudenaarden A. (2009) Snowdrift game dynamics and facultative cheating in yeast. Nature advance online publication 6 April 2009. [DOI: doi:10.1038/nature07921]

Read More...

Summary only...

What Stephen Harper Said in 1997

 
I don't know where Canadian Cynic gets all this stuff but he has just posted a link to a speech by Stephen Harper in 1997 [CTV.ca].

It's worth reading the entire speech if you can stomach it. If you can't, then try this little excerpt.

OTTAWA -- The text from a speech made by Stephen Harper, then vice-president of the National Citizens Coalition, to a June 1997 Montreal meeting of the Council for National Policy, a right-wing U.S. think tank, and taken from the council's website:

Ladies and gentlemen, let me begin by giving you a big welcome to Canada. Let's start up with a compliment. You're here from the second greatest nation on earth. But seriously, your country, and particularly your conservative movement, is a light and an inspiration to people in this country and across the world.

Now, having given you a compliment, let me also give you an insult. I was asked to speak about Canadian politics. It may not be true, but it's legendary that if you're like all Americans, you know almost nothing except for your own country. Which makes you probably knowledgeable about one more country than most Canadians.

But in any case, my speech will make that assumption. I'll talk fairly basic stuff. If it seems pedestrian to some of you who do know a lot about Canada, I apologize.

I'm going to look at three things. First of all, just some basic facts about Canada that are relevant to my talk, facts about the country and its political system, its civics. Second, I want to take a look at the party system that's developed in Canada from a conventional left/right, or liberal/conservative perspective. The third thing I'm going to do is look at the political system again, because it can't be looked at in this country simply from the conventional perspective.

First, facts about Canada. Canada is a Northern European welfare state in the worst sense of the term, and very proud of it. Canadians make no connection between the fact that they are a Northern European welfare state and the fact that we have very low economic growth, a standard of living substantially lower than yours, a massive brain drain of young professionals to your country, and double the unemployment rate of the United States.

In terms of the unemployed, of which we have over a million-and-a-half, don't feel particularly bad for many of these people. They don't feel bad about it themselves, as long as they're receiving generous social assistance and unemployment insurance.

---

Read More...

Summary only...

2009 Canada Gairdner Awards

 
The 2009 Canada Gairdner Award recipients were announced last week. Each awardee gets $100,000 (CDN). The winners are ...

Richard Losick: "for the discovery of mechanisms that define cell polarity and asymmetric cell division, processes key in cell differentiation and in the generation of cell diversity"

Kazutoshi Mori: "for the dissection and elucidation of a key pathway in the unfolded protein response which regulates protein folding in the cell"

Nubia Muñoz: "for her epidemiological studies that defined the essential role of the human papilloma virus in the etiology of cervical cancer on a global level which led to the development of successful prophylactic vaccines"

David Sackett: "for his leadership in the fields of clinical epidemiology and evidence-based medicine, which have had major impacts internationally in applied clinical research and in the practice of medicine"

Lucy Shapiro: "for the discovery of mechanisms that define cell polarity and asymmetric cell division, processes key in cell differentiation and in the generation of cell diversity"

Peter Walter: "for the dissection and elucidation of a key pathway in the unfolded protein response which regulates protein folding in the cell"

Shinya Yamanaka: "for his demonstration that the key transcription factors which specify pluripotency may become reprogrammed somatic cells to pluripotent stem cells"

The awards will be presented next October at the University of Toronto. Since this is the 50th anniversary of the Gairdner Awards there will be quite a gathering. You should plan on being here.

This year The Gairdner Foundation is celebrating its 50th Anniversary in spectacular fashion.

Between March and November we will hold 7 major international symposia across the country, in Vancouver, Edmonton, Ottawa, Toronto (York), Sherbrooke, Montreal and Halifax (see under Events). The finale will occur in Toronto, where we will host 50 past Gairdner recipients, including 22 Nobel Laureates, from Oct 28-30. This will be by far the largest gathering of the world's top scientists ever held in Canada. We will also introduce the 2009 Canada Gairdner Award recipients.

Canada Gairdner Laureates will participate in lectures, panel discussions, public forums, interviews and informal talks with academics, researchers, biotech and pharma companies, government leaders, graduate and postgraduate students, high school students, the media and interested members of the general public. With the exception of the social events, all the programs will be free and open to anyone who wants to share in the excitement of leading edge biomedical science.

The 50th Anniversary will be a spectacular culmination of everything The Gairdner Foundation has achieved in becoming Canada's premier international prize, and one of the top three biomedical prizes in the world. It will be a vehicle to raise awareness of the fascinating world of biomedical science and its importance to lives.

---

Read More...

Summary only...

Nobel Laureates: Mario Capecchi, Martin Evans, and Oliver Smithies

 

The Nobel Prize in Physiology or Medicine 2007

"for their discoveries of principles for introducing specific gene modifications in mice by the use of embryonic stem cells"

Mario R. Capecchi (1937 - ), Sir Martin J. Evans (1941 - ), and Oliver Smithies (1925 - ) won the Noble Prize in 2007 for developing techniques to transform embryonic stem cells with foreign genes integrated at a specific place in the genome, then using those cells to make transgenic mice.

The Press Release describing this work is a well-written description of how the techniques was developed.

This is how to make knock-out mice.
THEME:
Nobel Laureates

Summary

This year's Nobel Laureates have made a series of ground-breaking discoveries concerning embryonic stem cells and DNA recombination in mammals. Their discoveries led to the creation of an immensely powerful technology referred to as gene targeting in mice. It is now being applied to virtually all areas of biomedicine – from basic research to the development of new therapies.

Gene targeting is often used to inactivate single genes. Such gene "knockout" experiments have elucidated the roles of numerous genes in embryonic development, adult physiology, aging and disease. To date, more than ten thousand mouse genes (approximately half of the genes in the mammalian genome) have been knocked out. Ongoing international efforts will make "knockout mice" for all genes available within the near future.

With gene targeting it is now possible to produce almost any type of DNA modification in the mouse genome, allowing scientists to establish the roles of individual genes in health and disease. Gene targeting has already produced more than five hundred different mouse models of human disorders, including cardiovascular and neuro-degenerative diseases, diabetes and cancer.

Modification of genes by homologous recombination

Information about the development and function of our bodies throughout life is carried within the DNA. Our DNA is packaged in chromosomes, which occur in pairs – one inherited from the father and one from the mother. Exchange of DNA sequences within such chromosome pairs increases genetic variation in the population and occurs by a process called homologous recombination. This process is conserved throughout evolution and was demonstrated in bacteria more than 50 years ago by the 1958 Nobel Laureate Joshua Lederberg.

Mario Capecchi and Oliver Smithies both had the vision that homologous recombination could be used to specifically modify genes in mammalian cells and they worked consistently towards this goal.

Capecchi demonstrated that homologous recombination could take place between introduced DNA and the chromosomes in mammalian cells. He showed that defective genes could be repaired by homologous recombination with the incoming DNA. Smithies initially tried to repair mutated genes in human cells. He thought that certain inherited blood diseases could be treated by correcting the disease-causing mutations in bone marrow stem cells. In these attempts Smithies discovered that endogenous genes could be targeted irrespective of their activity. This suggested that all genes may be accessible to modification by homologous recombination.

Embryonic stem cells – vehicles to the mouse germ line

The cell types initially studied by Capecchi and Smithies could not be used to create gene-targeted animals. This required another type of cell, one which could give rise to germ cells. Only then could the DNA modifications be inherited.

Martin Evans had worked with mouse embryonal carcinoma (EC) cells, which although they came from tumors could give rise to almost any cell type. He had the vision to use EC cells as vehicles to introduce genetic material into the mouse germ line. His attempts were initially unsuccessful because EC cells carried abnormal chromosomes and could not therefore contribute to germ cell formation. Looking for alternatives Evans discovered that chromosomally normal cell cultures could be established directly from early mouse embryos. These cells are now referred to as embryonic stem (ES) cells.

The next step was to show that ES cells could contribute to the germ line (see Figure). Embryos from one mouse strain were injected with ES cells from another mouse strain. These mosaic embryos (i.e. composed of cells from both strains) were then carried to term by surrogate mothers. The mosaic offspring was subsequently mated, and the presence of ES cell-derived genes detected in the pups. These genes would now be inherited according to Mendel’s laws.

Evans now began to modify the ES cells genetically and for this purpose chose retroviruses, which integrate their genes into the chromosomes. He demonstrated transfer of such retroviral DNA from ES cells, through mosaic mice, into the mouse germ line. Evans had used the ES cells to generate mice that carried new genetic material.

Two ideas come together – homologous recombination in ES cells

By 1986 all the pieces were at hand to begin generating the first gene targeted ES cells. Capecchi and Smithies had demonstrated that genes could be targeted by homologous recombination in cultured cells, and Evans had contributed the necessary vehicle to the mouse germ line – the ES-cells. The next step was to combine the two.

For their initial experiments both Smithies and Capecchi chose a gene (hprt) that was easily identified. This gene is involved in a rare inherited human disease (Lesch-Nyhan syndrome). Capecchi refined the strategies for targeting genes and developed a new method (positive-negative selection, see Figure) that could be generally applied.

Birth of the knockout mouse – the beginning of a new era in genetics

The first reports in which homologous recombination in ES cells was used to generate gene-targeted mice were published in 1989. Since then, the number of reported knockout mouse strains has risen exponentially. Gene targeting has developed into a highly versatile technology. It is now possible to introduce mutations that can be activated at specific time points, or in specific cells or organs, both during development and in the adult animal.

Gene targeting is used to study health and disease

Almost every aspect of mammalian physiology can be studied by gene targeting. We have consequently witnessed an explosion of research activities applying the technology. Gene targeting has now been used by so many research groups and in so many contexts that it is impossible to make a brief summary of the results. Some of the later contributions of this year's Nobel Laureates are presented below.

Gene targeting has helped us understand the roles of many hundreds of genes in mammalian fetal development. Capecchis research has uncovered the roles of genes involved in mammalian organ development and in the establishment of the body plan. His work has shed light on the causes of several human inborn malformations.

Evans applied gene targeting to develop mouse models for human diseases. He developed several models for the inherited human disease cystic fibrosis and has used these models to study disease mechanisms and to test the effects of gene therapy.

Smithies also used gene targeting to develop mouse models for inherited diseases such as cystic fibrosis and the blood disease thalassemia. He has also developed numerous mouse models for common human diseases such as hypertension and atherosclerosis.

In summary, gene targeting in mice has pervaded all fields of biomedicine. Its impact on the understanding of gene function and its benefits to mankind will continue to increase over many years to come.

---

[Photo Credits: Mario Capecchi: Reuters,DayLife, Sir Martin J. Evans: Reuters, DayLife, Oliver Smithies: University of North Carolina, Chapel Hill.]

The images of the Nobel Prize medals are registered trademarks of the Nobel Foundation (© The Nobel Foundation). They are used here, with permission, for educational purposes only.

Read More...

Summary only...

On the Evolution of Bacterial Chromosomes

 

This is a story about two cultures; the old biologists who grew up with the 'phage group and bacterial genetics, and the younger biologists who didn't.

It's also a story about science journalism and the reporting of science in the 21st century.

We've known about plasmids in bacteria for a very long time. Plasmids are small circular DNA molecules that carry a number of genes, such as those for antibiotic resistance, or sex. Some of them are present in multiple copies while others are present in only a single copy. In the case of single-copy plasmids, their replication is coupled to that of the chromosome and the daughter plasmids segregate to the daughter cells just like the newly replicated chromosomes do.

Genes can hop from chromosomes to plasmids and back again. This phenomenon was discovered in the 1950's by Jacob and Adelberg (1959). Several well-known plasmids carrying certain chromosomal genes were studied, including a famous one known as F-lac—an F plasmid containing the lac operon.

By the time the first E. coli Bible was published in 1987, there were dozens and dozens of examples of gene transfer between chromosomes and plasmids (Holloway and Low, 1987).

During the 1970s and 80s, the DNA contents of many difference species of bacteria were published. It soon became apparent that certain classes of bacteria (e.g. Rhizobiaceae) contained large plasmids called megaplasmids. Sometimes it was difficult to tell the difference between a plasmid and a chromosome (bacterial chromosomes are usually circular).

As a general rule, plasmids were dispensable. The bacteria could be "cured" of a plasmid and still survive. When the plasmid acquired essential genes, as they did from time to time, they became chromosomes. Some species of bacteria had two or more chromosomes. It was part of general knowledge that plasmids could evolve into chromosomes as described in a 1998 review by Moreno.

Animal intracellular Proteobacteria of the alpha subclass without plasmids and containing one or more chromosomes are phylogenetically entwined with opportunistic, plant-associated, chemoautotrophic and photosynthetic alpha Proteobacteria possessing one or more chromosomes and plasmids. Local variations in open environments, such as soil, water, manure, gut systems and the external surfaces of plants and animals, may have selected alpha Proteobacteria with extensive metabolic alternatives, broad genetic diversity, and more flexible and larger genomes with ability for horizontal gene flux. On the contrary, the constant and isolated animal cellular milieu selected heterotrophic alpha Proteobacteria with smaller genomes without plasmids and reduced genetic diversity as compared to their plant-associated and phototrophic relatives. The characteristics and genome sizes in the extant species suggest that a second chromosome could have evolved from megaplasmids which acquired housekeeping genes. Consequently, the genomes of the animal cell-associated Proteobacteria evolved through reductions of the larger genomes of chemoautotrophic ancestors and became rich in adenosine and thymidine, as compared to the genomes of their ancestors. Genome organisation and phylogenetic ancestor-descendent relationships between extant bacteria of closely related genera and within the same monophyletic genus and species suggest that some strains have undergone transition from two chromosomes to a single replicon. It is proposed that as long as the essential information is correctly expressed, the presence of one or more chromosomes within the same genus or species is the result of contingency. Genetic drift in clonal bacteria, such as animal cell-associated alpha Proteobacteria, would depend almost exclusively on mutation and internal genetic rearrangement processes. Alternatively, genomic variations in reticulate bacteria, such as many intestinal and plant cell-associated Proteobacteria, will depend not only on these processes, but also on their genetic interactions with other bacterial strains.

Given this context, I was interested in a recent press release: Evolutionary origin of bacterial chromosomes revealed. "Hmmm," I thought., "I wonder what new mechanism has been discovered?"

Imagine my surprise to read ...

Most bacteria have only one chromosome. The Rhizobiaceae is an unusual bacterial family in that all of its members have either two chromosomes or one chromosome and very large plasmids. Until this study, it was not clear how such multichromosomal architectures had evolved.

João Setubal, associate professor at the Virginia Bioinformatics Institute and the Department of Computer Science at Virginia Tech, commented: "Thanks to the efforts of the Agrobacterium Genome Sequence Consortium and the wider research community, we have sufficient sequence data available from different bacterial species to allow the inference of a general model for bacterial genome evolution. It appears that the transfer of genes from chromosomes to large plasmids mediates second chromosome formation."

That's not new. The idea that large megaplasmids in Rhizobiaceae could become plasmids by acquiring essential genes has been around for three decades, at least. Surely these workers known their history? The press release must be an exaggeration of what's in the paper.

So I looked up the paper (Slater et al., 2009). These workers sequenced the genomes of a number of related bacterial species containing chromosomes and plasmids. They announce the "surprising" discovery that genes can transfer between chromosomes and plasmids.

While it has long been known that gene transfer can occur between organisms, the picture that emerges from our study shows a group characterized by composite genomes in which genes of all classes are not only migrating between organisms, but also intracellularly among chromosomal and plasmid replicons.

It sounds like they never heard of F-lac or any of the other F′ or R′ plasmids. It sounds like they are completely unaware to the fact that transfer of genes from chromosomes to plasmids is an old established fact.

The authors propose a "general model for bacterial genome evolution" in which plasmids evolve into chromosomes.

This is not an isolated phenomenon. There seem to be lots of cases where today's scientists are unaware of the history of their field. A consequence of this ignorance is that the wheel is being constantly reinvented, with all the associated hype of a modern breakthrough.

Another example is the recent "discovery" of regulatory RNAs. Bacterial and 'phage examples have been known for forty years.

Why is this happening? Why do reviewers let it pass?

---

[Image Credit: Jessica Snyder Sachs]

Holloway, B. and Low, K.B. (1987) F-Prime and R-Prome Factors. in Escherichia coli and Salmonella typhimurium: Cellular and Molecular Biology. F.C. Neidhardt ed. vol.2.

Jacob, F. and Adelberg, E.A. (1959) Transfer of Genetic Characters by Incorporation in the Sex Factor of Escherichia coli. Comptes Rendus 249:189-191.

Moreno, E. (1998) Genome evolution within the alpha Proteobacteria: why do some bacteria not possess plasmids and others exhibit more than one different chromosome? FEMS Microbiol 22(4):255-275. [PubMed]

Slater, S.C., Goldman, B.S., Goodner, B., Setubal, J.C., Farrand, S.K., Nester, E.W., Burr, T.J., Banta, L., Dickerman, A.W., Paulsen, I., Otten, L., Suen, G., Welch, R., Almeida, N.F., Arnold, F., Burton, O.T., Du, Z., Ewing, A., Godsy, E., Heisel, S., Houmiel, K.L., Jhaveri, J., Lu, J., Miller, N.M., Norton, S., Chen, Q., Phoolcharoen, W., Ohlin, V., Ondrusek, D., Pride, N., Stricklin, S.L., Sun, J., Wheeler, C,, Wilson, L,, Zhu, H., and Wood, D.W. (2009) Genome Sequences of Three Agrobacterium Biovars Help Elucidate the Evolution of Multi-Chromosome Genomes in Bacteria. J. Bacteriol. 2009 Feb 27. [Epub ahead of print] [PubMed] [DOI: 10.1128/JB.01779-08]

Read More...

Summary only...

How to Prevent Evolution in Mosquitos

 
A paper in PLoS Biology discusses How to Make Evolution-Proof Insecticides for Malaria Control. The idea is to develop drugs that only kill mosquitoes after they've reproduced. That way the population can't evolve resistance to the drug.

What's interesting about this paper is the response of two different bloggers. On adaptationist, Jerry Coyne's blog, guest writer Matthew Cobb thinks it's a great idea [Of mosquitoes and the menopause]. In fact he links his discussion of the paper to the well-known adaptationist explanation of menopause.

The pluralist, Ryan Gregory, is much more skeptical, pointing out that evolution is smarter than you are ["Evolution-proof"?].

Grab your popcorn and enjoy the fight. My money's on Gregory.

---

Read More...

Summary only...

Monday's Molecule #116: Winners

 
UPDATE:The photographs of the mouse embryos are from a paper by Kothary et al. (1989). This was a study where a lacZ (β-galactosidase) gene under the control of a strong, ubiquitously competent promoter was introduced into mouse zygotes. When the gene was induced (right) the presence of β-galactosidase was detected by a blue color assay. The foreign gene is induced in almost every tissue.

These sorts of experiments in construction of transgenic mice were later extended by the work of Nobel Lauteates Mario Capecchi, Martin Evans, and Oliver Smithies who developed techniques for using embryonic stem cells.

Several people guessed the Nobel Laureates but only two people provided an explanation of the "molecule." Dima Klenchin, who is ineligible, was the only one to pick up on the hint and find the 1989 paper.

The winner is Shumona De of Dalhousie University.

---

If you look closely you'll realize that these mouse embryos aren't really "molecules" in any meaningful sense of the word "molecule." That doesn't matter 'cause I still want you to identify what's going on here. This is the first time that I've resorted to using photographs from my previous life—shows you how desperate I'm getting!

The images are supposed to remind you of the work of some Nobel Laureates. See if you can guess who they are.

The first person to identify the photographs and the Nobel Laureates wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first won the prize.

There are eight ineligible candidates for this week's reward: David Schuller of Cornell University, Adam Santoro of the University of Toronto, Dima Klenchin from the university of Wisconsin, Alex Ling from the University of Toronto, Bill Chaney of the University of Nebraska, Elvis Cela from the University of Toronto, Peter Horwich from Dalhousie University, and Devin Trudeau from the University of Toronto.

Dima and Bill have donated their free lunch to a deserving undergraduate so I'm going to continue to award an additional free lunch to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow.

Comments will be blocked for 24 hours. Comments are now open.

---

Kothary, R., Clapoff, S., Darling, S., Perry, M.D., Moran, L.A., Rossant, J. (1989) Inducible expression of an hsp68-lacZ hybrid gene in transgenic mice. Development. 105:707-14. [PDF]

Read More...

Summary only...

Applying to NSERC? Everyone gets a grant!

 
According to a study done by Richard Gordon and Bryan J. Poulin, Cost of the NSERC Science Grant Peer Review System Exceeds the Cost of Giving Every Qualified Researcher a Baseline Grant. (NSERC is Canada's funding agency for non-medical science research.)

Using Natural Science and Engineering Research Council Canada (NSERC) statistics, we show that the $40,000 (Canadian) cost of preparation for a grant application and rejection by peer review in 2007 exceeded that of giving every qualified investigator a direct baseline discovery grant of $30,000 (average grant). This means the Canadian Federal Government could institute direct grants for 100% of qualified applicants for the same money. We anticipate that the net result would be more and better research since more research would be conducted at the critical idea or discovery stage. Control of quality is assured through university hiring, promotion and tenure proceedings, journal reviews of submitted work, and the patent process, whose collective scrutiny far exceeds that of grant peer review. The greater efficiency in use of grant funds and increased innovation with baseline funding would provide a means of achieving the goals of the recent Canadian Value for Money and Accountability Review. We suggest that developing countries could leapfrog ahead by adopting from the start science grant systems that encourage innovation.

This sounds like a good idea to me. Thanks to Bora Zivkovic of A Blog Around the Clock for finding the paper.

---

Read More...

Summary only...

Royal Protocol

 
Ever country has a protocol officer and part of their job is to specify how one is supposed to treat the Head of State. In America, for example, you must always refer to the President as Mr. President and unelected cabinet ministers are addressed as Mr./Madam Secretary [Office of the Chief of Protocol].

Visiting Heads of State are expected to conform to American protocol and when the President visits another country he is expected to conform to their rules of protocol. That's how international diplomacy works. It's a system that has evolved over several centuries to try and makes things easier when two different countries communicate. The idea is for countries to respect each other.

Postdiluvian at The Unexamined Life doesn't think that Americans need to respect the protocols and traditions of a foreign country [Is it OK to hug the Queen?]. Now, as it turns out, Michelle's hug was a breach of protocol but not that big a deal, even in England. It would be comparable to someone forgetting to say "Mr. President" when addressing Barack Obama.

That doesn't justify this kind of response ....

Now here’s the bottom line: you can have your “Queen” as a powerless (and utterly pointless) figurehead if you like. She can even keep her massive wealth that somehow came into her family’s possession over the centuries. But if you ever start this bullshit about “Royal Protocol” again, or whether or not it’s okay for people to touch her, you will be removing yourself from the realm of the Serious and joining the realm of Laughingstock, much like the concept of Monarchy did ages ago.

Americans often wonder why they have so much trouble making friends in "foreign" countries. I can't imagine why.

---

Read More...

Summary only...

Five Against One

 
It's sounds so unfair. Four Christians against one lone atheist. If you add in the moderator it's five against one.

But the atheist is Christopher Hitchens so they didn't have a chance.¹

Next time they should try half a dozen Christians—and they should look for ones that are smart.²

Christian Book Expo 2009

---

1. Actually, if you watch the "debate" you'll realize that Hitchens didn't need to do or say anything. Every single one of their arguments for the existence of God has been refuted dozens of times. It's like a kindergarten class in Christian apologetics. Most of the time I wish Hitchens had kept his mouth shut.

2. Assuming that ....

[Hat Tip: Friendly Atheist]

Read More...

Summary only...

What Is Epigenetics?

 
Berger et al. (2009) attempt to define epigenetics.

"An epigenetic trait is a stably heritable phenotype resulting from changes in a chromosome without alterations in the DNA sequence."

Sounds good to me. Just about anything wold be better than the kitchem sink definition proposed by Eva Jablonka [Epigenetics at SEED].

The main examples are "DNA methylation, histone modifications, histone variants, and nucleosome positioning." These are chromosomal alterations that are passed on to daughter cells following cell division by mitosis or meiosis.

Although the Berger et al. don't mention it, these epigenetic signals are all reversible. I still don't find the term useful. It's far more accurate to refer to each of the individual examples by name and the field is regulation of gene expression.

---

Berger, S.L., Kouzarides, T., Shiekhattar, R., and Shilatifard, A. (2009) An operational definition of epigenetics. Genes & Dev. 23:781-783. [DOI: 10.1101/gad.1787609]

[Hat Tip: Hopeful Monster]

Read More...

Summary only...

Monday's Molecule #116

 
If you look closely you'll realize that these mouse embryos aren't really "molecules" in any meaningful sense of the word "molecule." That doesn't matter 'cause I still want you to identify what's going on here. This is the first time that I've resorted to using photographs from my previous life—shows you how desperate I'm getting!

The images are supposed to remind you of the work of some Nobel Laureates. See if you can guess who they are.

The first person to identify the photographs and the Nobel Laureates wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first won the prize.

There are eight ineligible candidates for this week's reward: David Schuller of Cornell University, Adam Santoro of the University of Toronto, Dima Klenchin from the university of Wisconsin, Alex Ling from the University of Toronto, Bill Chaney of the University of Nebraska, Elvis Cela from the University of Toronto, Paul Horwich from Dalhousie University, and Devin Trudeau from the University of Toronto.

Dima and Bill have donated their free lunch to a deserving undergraduate so I'm going to continue to award an additional free lunch to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow.

Comments will be blocked for 24 hours.

---

Read More...

Summary only...

Religion Wars: Linux and Mac vs. Rationalism

 
Greg Linux is disappointed that the Confliker virus didn't do more damage on April 1st [Did Conflicker Flop? Yes. Why? Nobody knows].

I wasn't worried because I checked all five of my computers and not one them were infected. If they had been, it was very easy to get rid of the worm. My Linux machine didn't have the worm either.

That doesn't stop Greg from offering this advice ...

Experts expect that the worm is going to re-awaken at some time in the future and possibly actually do something. In the mean time, you may want to get rid of it if is on your system.

If you run Windows, the best way to get rid of the computer is to get a Mac or a Linux computer. There are probably other ways to do this but I don't really care. If you are running Linux, this worm can't directly affect you.

Sheesh, those religious nuts sure can be silly.

---

Read More...

Summary only...

The End of Christian America?

 
The number of Americans who don't identify with a religion has increased from 8% in 1990 to 15% today. This is encouraging but it doesn't quite mean that the battle between rationalism and superstition has been won.

Nevertheless, the fact that a national magazine could publish an article like "The End of Christian America" is an indication that the debate is on.

If North American societies become much less religious—like those in Europe—then most of the major problems with creationism will go away. Maybe then we can concentrate on promoting good science education. That's why some of us would rather put our efforts into promoting rationalism over superstition rather than defending specific creationist attacks on schools.

Both approaches are needed but those who advocate the compatibility of science and superstition are not helping.

---

[Hat Tip: Hemant Mehta who has some interesting comment.]

Read More...

Summary only...

Last Week's Scientific Breakthroughs

 
This are stories from the past week that would make good topics for discussion. I don't have time so I'll leave it up to you.

Scientists Find 'Baffling' Link between Autism and Vinyl Flooring

Masturbation could bring hay fever relief for men

New research shows lower educational outcomes for survivors of childhood cancer

6 out of every 10 university students present mathematical anxiety or fear of this subject

Humanoid Robot Helps Scientists To Understand Intelligence

Omega-3 kills cancer cells

How probiotics can prevent disease

UBC study first to show evolution's impact on ecosystems

UT Southwestern researchers reveal how the brain processes important information

Your oral health is connected to your overall health

Penn researchers demonstrate a new model for drug discovery with a fluorescent anesthetic

Humans May Be Losers If Technological Nature Replaces The Real Thing, Psychologists Warn

Milkshakes Are Medicine For Anorexic Teens In Family-based Outpatient Therapy

Hermit Arthropods 500 Million Years Ago?

Alzheimer's Disease Linked To Mitochondrial Damage

Robot Scientist Becomes First Machine To Discover New Scientific Knowledge

Virus-built Battery Could Power Cars, Electronic Devices

Athletic Ability May Lie in a Single Gene

---

Read More...

Summary only...

Washington D.C.

 
In a few days I'll be on my way to Washington (Bethesda, actually) to attend the Center for Inquiry World Congress 2009. Let me know if you'll be there and we can meet up.

Here are the main events ....

Thursday April 9, evening: Panel: The Influence of Darwin

Friday April 10, afternoon: Science and Public Policy

Friday April 10, 5:45pm: James Randi: Search for the Chimera

Saturday April 11, morning: Skepticism and Science

Saturday April 11, 5pm: Special Feature: Separation of Church and State

Sunday April 12, morning: Secularism Around the World

---

Read More...

Summary only...

Darwin Rocks

 
Watch this video about evolution and see if you can figure out what's going on. You can check your answer here.

In the fight to increase scientific literacy, I'm not sure if this contribution is useful, useless, or counter-productive but I'm leaning toward counter-productive.

---

[Hat Tip: John Dennehy, who leans toward the "useful" point of view.]

Read More...

Summary only...

Will Universities Survive?

 
Believe it or not, there are supposedly intelligent people out there who think the internet will replace universities.¹ It didn't take Sean Caroll very long to come up with some excelent reasons why this ain't gonna happen [Will the Internet Replace Universities?].

Let me add one more—research experience. You can't learn what it's like to work in a research lab if you're sitting at your desk in the suburbs.

Why do I get the feeling that most people don't understand what a university is supposed to be like? Is it true that most people think of universities just as places where you come and listen to lectures and then go home?

---

1. Back in 1970 their parents were convinced that television would mean the end of universities as we know them.

Read More...

Summary only...

Electronic Textbooks

 
There's an article in this week's issue of Nature on The textbook of the future.

Most of the article is about a Kindle version of science textbooks.

Another drawback of current e-readers is that they have small black-and-white displays, just a little larger than 9 by 12 centimetres. This makes them unsuited to most science textbooks, which typically have large pages and colourful graphics. "The market is not likely to expand until the e-readers improve," says Hegarty.

Publishers are experimenting with ways of delivering their textbooks electronically (e.g. CourseSmart) but there are still problems to be solved.

Competing ideas, such as Wiki's that replace textbooks, have a long way to go before they become a threat to the textbook market [Wikibooks: Biochemistry]. Besides, there are other problems that need to be solved.

For now these free textbooks remain a cottage industry, says Esposito. Wikipedia-like volunteer efforts are much better suited to self-contained modules that are small enough for an individual to see through from A to Z. But a textbook demands a coherent overall structure and coordination between sections. That is why creating one has always been a major undertaking, demanding long-term commitments by publishers — who need to make a profit — and by authors who usually want to be paid for their effort.

Still, perhaps 'free' and 'profitable' need not be a contradiction in terms. One group of veteran textbook publishing executives is trying to put open textbooks on a solid commercial footing. In 2007 they created Flat World Knowledge, based in Nyack, New York, and in January 2009 rolled out the first of the 21 textbooks they have in development so far. The texts are written by some 40 domain experts who will be paid 20% of royalties. The company also plans to make its content available via Kindle and other e-readers. All its content will be free to reuse for non-commercial purposes under a creative commons licence.

Eric Frank, Flat World's co-founder, says that the strategy is to attract greater use by giving the e-textbooks away — the initial targets are the high-volume texts for first-year students — and then look for profit from students' purchase of print-on-demand versions at $29.95 for black and white, and $59.95 for colour. Students can copy and use the electronic content in any way they wish, says Frank. "Cheap prices are the most effective digital-rights management," he says. "We want to avoid a digital-rights war with students." The company also hopes to make money by licensing its content to commercial companies, such as distance-learning outfits and course-management software firms.

I think there's going to be a way to make cheaper electronic versions of textbooks and still compensate the people who do all the work. I'm not sure how it's going to work but I'd love to put my book on a website where I can make changes quickly and get instant feedback from the users.

---

Read More...

Summary only...

James Lunney: Creationist, Chiropractor, Conservative

 
Meet Dr. James Lunney a chiropractor and a Conservative Party Member of Parliament for Nanaimo-Alberni in British Columbia.

"Dr." Lunney recently made a fool of himself by making the following statement in the House of Commons as reported in Maclean's magazine [James Lunney v. Evolution].

Mr. Speaker, recently we saw an attempt to ridicule the presumed beliefs of a member of this House and the belief of millions of Canadians in a creator. Certain individuals in the media and the scientific community have exposed their own arrogance and intolerance of beliefs contrary to their own. Any scientist who declares that the theory of evolution is a fact has already abandoned the foundations of science. For science establishes fact through the study of things observable and reproducible. Since origins can neither be reproduced nor observed, they remain the realm of hypothesis.

In science, it is perfectly acceptable to make assumptions when we do not have all the facts, but it is never acceptable to forget our assumptions. Given the modern evidence unavailable to Darwin, advanced models of plate techtonics, polonium radiohalos, polystratic fossils, I am prepared to believe that Darwin would be willing to re-examine his assumptions.

The evolutionists may disagree, but neither can produce Darwin as a witness to prove his point. The evolutionists may genuinely see his ancestor in a monkey, but many modern scientists interpret the same evidence in favour of creation and a creator.

PZ Myers is making fun of Canada by posting Lunney's remarks on Pharyngula. He's right. We deserve it. Lunney is a genuine kook who quite obviously wouldn't know real science if it bit him on the backbone.

Listen up, all you people who live on Vancouver Island! Don't send this guy back to Ottawa after the next election or you're going to look very silly.

---

Read More...

Summary only...

March on Sandwalk

 
Bora's doing it and Greg Laden is doing it. They're revisiting their posts from last month.

Now I'm doing it too.

Last month Sandwalk attracted 107,747 page views and 75,156 visits from all over the world. That's a new record. I posted 123 times.



The month began with an account of my streetcar ride and the atheist sign campaign in Toronto [The Streetcar We Desire]. I also celebrated the 35th anniversary of my thesis defense.

There were three debates that took up a lot of posting time.

One of them was about positive selection in humans, especially the idea that human evolution might have accelerated in the past 10,000 years. I tried to explain why some of the data looks suspicious in Signals of Positive Selection in Humans?.

We also talked a lot about the quality of science journalism. The two topics were combined when I reviewed SEED magazine's coverage of a recent book on accelerated human evolution [SEED Reviews The 10,000 Year Explosion].

The third debate was about Canada's science minister, Gary Goodyear, and the fact that he is a creationist [Gary Goodyear "Clarifies" His Stance on Evolution].

I'm pretty proud of this posting: Casey Luskin on Junk DNA and Junk RNA. It generated some comments and got a mention on several blogs.

Speaking of comments, one other posting caught the attention of Sandwalk readers and stimulated comments. You were interested to know why I Hate Cilantro/Coriander!.

In terms of most popular postings there was nothing in March that's going to make the top 20 postings. I still get a lot of traffic from people who want to learn about The Genetics of Eye Color from a posting in February 2007. Another popular posting is The Genetics of ABO Blood Types, also from February 2007.

As usual, there were lots of people who tried to guess Monday's molecule. There are a small number of regulars who get most of the prizes, The rest of you are going to have to be faster. I think I'll try and post much earlier in the day to give my European readers a better chance. We don't need to worry about giving the Australians a chance 'cause they probably wouldn't win anyway! :-)

We had an interesting group of Nobel Laureates. These postings always get looked at but nobody leaves comments. I guess there isn't much to say. The most interesting Nobel Laureates from my perspective were Frederick Banting and J.J.R. Macleod because they're from the University of Toronto. Several of the recent prize winners were controvesial, especially Selman Waksman.

Does anyone have suggestions for future postings?

---

Read More...

Summary only...

A field guide to misunderstandings about open access

 
Want to find out what Open Access is really all about? Read A field guide to misunderstandings about open access.

Do you think that articles in open access journals aren't peer reviewed? Think again.

Do you think that all open access journals charge huge publication fees? Wrong.

Do you think that open access journals are lower quality? Nope.

---

[Hat Tip: Bora Zivkovic: A Blog Around the Clock]

Read More...

Summary only...

Dynamic Genomes

 
There may have been a time in the past when scientists imagined a static genome that only changed slowly over millions of years. However, beginning in the 1960's we began to see the genome as a much more dynamic entity. The first evidence of this kind of genome came with the discovery of huge amounts of variation between individuals in a species.

This was followed by the discovery of transposons and junk DNA. We began to see genomes as rather sloppy DNA molecules with lots of pieces hopping in and out on a timescales of generations. We began to realize that many genomes were full of pseudogenes.

Chromosomal rearrangements such as inversions, duplications, and translocations were documented. In mammals, many of them were associated with cancer, thalassemias, and other diseases but the general impression was that these rearrangements of genetic material were quite common. Indeed, some non-disease examples began to accumulate in the literature. Clear evidence of normal rearrangements associated with regulation and development—including mating type switching in yeast, immunoglobulin rearrangements in mammals, chorion gene amplification in Drosophila, and antigenic variation in trypanosomes—reinforced the idea that the genome was not static.

Most of this information was incorporated into the textbooks. For example, by the early 1980's Benjamin Lewin' textbook Genes had an entire group of chapters under the heading "The Dynamic Genome: DNA in Flux."

We soon learned about the expansion and contraction of repetitive sequences in the human genome. These observations eventually gave rise to DNA fingerprinting whereby every individual could be uniquely identified by variations in the genome.

By the early 1990's the concept of the dynamic genome had become so widely entrenched among molecular biologists that when Singer and Berg published "Genes and Genomes" they felt obliged to inject a note of caution. While genomes are dynamic at the scale of species evolution, the typical genome of an individual is not subject to significant rearrangements.

Outside of molecular biology, the idea that genomes were flexible never seemed to catch on. Most people thought of genomes as relatively static entities that didn't change much over millions of years. In part, they adopted this position because they still placed a great deal of emphasis on the power of natural selection. If genomes were well-adapted then why would they change? Part of the skepticism about junk DNA stems from the belief that selection will eliminate useless DNA.

Recent developments have stirred many people to re-think their concept of genomes. For example, Sandra Porter of Discovering Biology in a Digital World recently asked, "What if everything you thought you knew about the genome was wrong?."

To the extent that such questions acquaint people with the concept of a dynamic genome, they are good. On the other hand, if such questions lead to the unthinking acceptance of alternative splicing, superabundant transcription, and a plethora ot RNAs, they are bad.

---

Read More...

Summary only...

Handel's Messiah

 
One year Ms. Sandwalk took the entire family to see a full performance of Handel's Messiah. It was agony, except for one brief part of the performance where we all got to stand up. Ms. Sandwalk thought it was wonderful but, remember, she also likes some country music.

My children still talk about it. I guess it's one of those "experiences" that contribute to character building, or something.

Now there's an explanation in New Scientist: How misery inspired Handel's Messiah. I knew there had to be a reason.

---

Read More...

Summary only...

Monday's Molecule #115: Winners

 
UPDATE: The molecule is indigotin or indigo dye [2,2’-Bis(2,3-dihydro-3- oxoindolyliden)]. The Nobel Laureate is Johann Friedrich Wilhelm Adolf von Baeyer.

This week's only winner is Alex Ling from the University of Toronto.

The winners this week are Pete Horwich from Dalhousie University and Devin Trudeau from the University of Toronto.

---

Identify this molecule and explain why it is useful. You must supply the common name and the formal IUPAC name.

I'm looking for the Nobel Laureate whose name is associated with this molecule.

The first person to identify the molecule and the Nobel Laureate wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first won the prize.

There are seven ineligible candidates for this week's reward: Maria Altshuler of the University of Toronto, David Schuller of Cornell University, Adam Santoro of the University of Toronto, Dima Klenchin from the university of Wisconsin, Alex Ling from the University of Toronto, Bill Chaney of the University of Nebraska, and Elvis Cela from the University of Toronto.

Dima and Bill have donated their free lunch to a deserving undergraduate so I'm going to continue to award an additional free lunch to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow. I reserve the right to select multiple winners if several people get it right.

Comments will be blocked for 24 hours. Comments are now open.

---

Read More...

Summary only...

Nobel Laureate: Adolf von Baeyer

 

The Nobel Prize in Chemistry 1905.

"in recognition of his services in the advancement of organic chemistry and the chemical industry, through his work on organic dyes and hydroaromatic compounds"


Johann Friedrich Wilhelm Adolf von Baeyer (1835 - 1917) won the Nobel Prize in Chemistry for his work on the preparation of organic dyes from coal tar.

His most notable achievement was the synthesis of indigo dye and determination of its structure. A cheap industrial synthesis of indigo was soon developed, freeing Europe from its dependence on indigo from India.

He was also the first person to synthesize phenolphthalein, the well-known acid or base indicator.

The presentation speech highlights the importance of the relationship between basic science and industry.
THEME:
Nobel Laureates

The complex and unique composition of indigo, however, made this also one of the hardest of tasks. Here there could be no question of one of those casual discoveries, which by happy accident seem to achieve half the work. Years of work were required for even von Baeyer's acumen and experimental skill to achieve the necessary insight into the pigment's chemical composition and to be able to manufacture it from simpler constituents. Even after the purely scientific part of the work had been completed it still took a number of years to make the results obtained from research applicable to technology.

Von Baeyer succeeded in producing indigo synthetically in three principal ways, namely from ortho-nitrophenylacetic acid, from ortho-nitrocinnamic acid and from ortho-nitrobenzaldehyde and acetone. This paved the way for the reproduction of indigo from raw material obtainable without much difficulty from coal tar. And if the problem of producing indigo industrially has now been solved from the technical as well as the economic point of view, this is entirely due to von Baeyer's basic work in the fields in question.

---

The images of the Nobel Prize medals are registered trademarks of the Nobel Foundation (© The Nobel Foundation). They are used here, with permission, for educational purposes only.

Read More...

Summary only...

2,296,911 visits?

 
It's April 1st and PZ Myers tells us that Pharyngula had 2,296,911 visits last month [What are all you people doing here?].

Problem is, I don't think this is an April Fool's joke.¹

There are already 225 comments to that posting, which is probably what PZ means when he asks what everyone is doing there. Now he knows—they're posting comments!

---

Sandwalk had 107,747 visits or less than 5% of the number that visited Pharyngula.

Read More...

Summary only...

Nobel Laureate: Michael Behe

 

The Nobel Prize in Biochemistry 2009.

"for his contributions to understanding complex biological systems"


Michael Behe (1952 - ) wins the Nobel Prize in Biochemistry for his amazing work on complex biological systems, especially the concept of irreducible complexity.

Beginning with the publication of his first book, Darwin's Black Box, Behe has written numerous articles on the organization of molecular machines such as the snare complex of Mus musculus and the bacterial flagellum. He has shown that these systems exhibit a fundamental property that previous biochemists overlooked—they are so well integrated that their origin cannot be explained by the older naturalistic theory of natural selection.

His later work, The Edge of Evolution, is a seminal contribution to modern evolutionary theory. In that book he explains how previous versions of evolution are incapable of explaining the origin of protein-protein interaction sites.

The presentation speech highlights the importance of this work.
THEME:
Nobel Laureates

The development of protein features, such as protein-protein binding sites, that require the participation of multiple amino acid residues is a profound, fundamental problem that has stumped the evolutionary biology community until the present day (and continues to do so, as I explain below). It is a fundamental problem because all proteins exert their effects by physically binding to something else, such as a small metabolite or DNA or other protein, and require multiple residues to do so. The problem is especially acute for protein-protein interactions, since most proteins in the cell are now known to act as teams of a half-dozen or more, rather than individually. Yet if one can’t explain how specific protein-protein interactions developed, then it is delusional to claim that we can explain how anything that depends on them developed, such as the molecular machinery of the cell. It’s like saying “we understand perfectly well how a car could evolve; we just don’t know how the pieces could get fit together.” If such a basic requirement for putting together complex systems is not understood, nothing is understood. Keep this in mind the next time you hear a blithe Darwinian tale about the undirected evolution of the cilium or bacterial flagellum.

---

Posted on April 1st, 2009.

The images of the Nobel Prize medals are registered trademarks of the Nobel Foundation (© The Nobel Foundation). They are used here, with permission, for educational purposes only.

Read More...

Summary only...