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Monday, January 21, 2008

ReGenesis and Scientific Literacy

 
About a year ago I posted an article about ReGenesis, a TV show based on scientific investigation into fictional events such as pandemics, crimes, etc. One of the main consultants on the show is a colleague of mine, Aled Edwards [ReGenesis].

Eva of easternblot has found an online interview with Aled Edwards about the show [ ReGenesis on LabLit]. You can read the entire interview on the LabLit website [ReGenesis guru Aled Edwards].

I like what Aled has to say. He is trying very hard not to let the TV show get dumbed down.
The scientists on this show are more like real scientists than anything else on screen. They have to publish, they make mistakes. We place caveats into the dialogue, trying to convey that on the edge of science, nothing is certain: we deal in hypotheses and uncertainty. The science in the show has real-life ambiguity – there’s no CSI-like wrap-up at the end in many episodes. And there’s an order of magnitude more science on the show than any other I’ve seen on film or TV.
As many of you know, here's a controversy between many scientists and many journalists about how to communicate science. I think Aled Edwards has the correct attitude here. What do the rest of you think? How many have watched the show?


Sunday, January 20, 2008

Predictions of Intelligent Design Creationism

 
Denyse O'Leary gives us nine "predictions" from the IDiots [ Nine predictions, if intelligent design is true]. I present them here without comment. Notice how almost all of them are predictions of what science will not discover and none of them are predictions of what an intelligent designer creationist is expected to do. That's because the essence of Intelligent Design Creationism is anti-science and not pro-designer. Several of the "predictions" are based on Denyse's latest book The Spiritual Brain.
  1. No good theory will be found for a random origin of the universe, either by the Large Hadron Collider or anything else. The universe will consistently behave more like a great idea than a great machine.

  2. No good theory will be found for a random origin of life, though there will be plenty of huffing and puffing in favour of bad ideas. All theories that exclude purpose and design fail because they leave out the key driver - the purpose that life should come into existence.

  3. Complete series of transitional fossils will not usually be found because most proposed series have never existed. Eventually, researchers will give up on ideologically driven nonsense and address the history that IS there. They will focus on discovering the mechanisms that drive sudden bursts of creativity.

  4. The environment will prove far more resilient than eco-doomsayers believe. People forget that the Permian extinction wiped out 90% of the marine life forms on this planet. Life seems to want to exist on this planet, even at the South Pole (cf March of the Penguins). Note: I have no time for environment destruction, and personally gave up keeping a car, as the simplest and most economical way to reduce my environment footprint. But I am NOT waiting for enviro-apocalypse!! - I don't believe it will happen. There will be changes. That's all. Not the end of the world or anything like it.

  5. No account of human evolution will show a long slow emergence from unconsciousness to semi-consciousness to consciousness, let alone that consciousness is merely the random firing of neurons in the brain. However consciousness got started, it appeared rather suddenly and it permanently separates humans from our genetic kin, however you want to do the gene numbers and however much time researchers spend coaxing monkeys to stop relieving themselves on the keyboard and type something meaningful.

  6. Claims that the human brain is full of "anachronistic junk" will be falsified, just as century old claims that there are hundreds of vestigial organs in the human body were falsified. The human body will be recognized as suitable for the purposes for which we exist. (Not in all cases perfect, to be sure, but in general suitable.)

  7. No useful theory of consciousness will demonstrate that consciousness is merely the outcome of the random firing of neurons in the brain. All useful theories will accept that the mind and the brain exist in a relationship. Research will focus on delineating the relationship more clearly. That will greatly benefit medical research, especially research on difficult mental disorders such as phobias, depression, etc.

  8. No useful theory of free will (human volition) will demonstrate that it does not really exist. Free will (which includes using the mind to help heal bodily injuries) will become an important tool of medicine, especially for helping aging people toward a better quality of life. For example, the fact that a drug only need perform 5% better than a placebo to be licensed for use will encourage the development of mind-based treatments for people who would otherwise be forced to take antagonistic drugs.

  9. No useful theory of human psychology will be founded on claims about what happened in the caves of our ancestors (= evolutionary psychology). That is because there are no genes that simply "cause" behaviour in a clinically normal human being. The mind is real and humans create their social environment by mental effort. Information is passed on from mind to mind, not through genes or physiology.


Gene Genie #24

 
The 24th edition of Gene Genie has been posted at origins genome resources [Gene Genie issue #24: Human genetics (Illumnia conspiracies and Eric Roberts too) provide a light in winter].
Welcome to the 24th edition of Gene Genie!! During these grey winter doldrums, it is all too easy to hunker down and withdraw from the blogosphere into the minutiae of grant writing and lab management (brrr- I haven’t posted in weeks). So it is with true delight that I present and thank our contributors for brightening the season.
The beautiful logo was created by Ricardo at My Biotech Life.

The purpose of this carnival is to highlight the genetics of one particular species, Homo sapiens.


Changing Minds Through Science Communication

 
There are lots of things going on at the North Carolina Science Blogging Conference but the session I'd most like to have attended was on "Changing Minds Through Science Communication." The speakers were Jennifer Jacquet, Sheril Kirshenbaum, and Chris Mooney.1

The next best thing to being there is to watch the videotape of the session (below). I must say I'm somewhat underwhelmed. Most of the presentations seemed to be mouthing the same old unsupported platitudes that we've been seeing for the past year, including a shot at Richard Dawkins.

There's was a great deal of talk about getting US Presidential candidates to engage in a science debate sometime in the next few months [Science Debate 2008]. Chris Mooney and Sheril Kirshenbaum spent a lot of time talking about this. How many people think this is a worthwhile way to spend one's time? What are the chances of it happening? If it does happen, will it advance the goal of effective science communication or is there a chance that it will do the opposite? If it doesn't happen, what message will that send about the importance of science?

The goal of the science debate is to use politics and the media to teach the general public about real science (e.g., evolution, global warming, stem cell research etc.) What if the media and politicians trump the process and use the debate to promote anti-science? Going head-to-head with these groups and trying to beat them at the framing game seems a bit naive to me. Am I the only one who thinks this? Since when have candidate debates stuck to scientific facts?

What if a candidate shows up with a list of ten scientists who think that the effects of global warming have been exaggerated, and has ten scientific papers to prove it? What if a candidate says that opposition to stem cell research is based on morality and not atheistic science? What if several of the candidates advocate teaching the controversy in biology class? Aren't we just begging for trouble? Aren't we just giving the kooks an opportunity to refute science during a "science" debate?

There's a good reason why real scientists avoid public debates with creationists. Perhaps science bloggers and science journalists should think about those reasons before promoting a debate on science. They might not get what they're wishing for.




1. Would it have been impossible to find an active full-time research scientist to participate on this panel? I find it frustrating that scientists are being criticized in a forum like this without being given a chance to present the other side of the case.

Eating Clones

 
We eat cloned organisms every day, but they're plants (e.g., bananas).

Apparently, some people have a great fear of eating cloned animals. Is this irrational fear an "ethical" problem? The underlying question is how do we define an ethical problem? Just because some people incorrectly see a problem where none exists, are we obliged to bow to their definition of "ethics."

Join the discussion on Balblab [Clonal Discrimination].


The Cloning of Steve Steve

 
Many of our science blogger friends are having a good time in North Carolina at the second North Carolina Science Blogging Conference. I was at the last one and it was lots of fun.

Joshua Rosenau is there and he breaks the news that Steve Steve has been cloned [Scienceblogging]. It has long been suspected that Reed Cartwright had succeeded in cloning Steve Steve but this is the first photographic proof that I'm aware of. As you can see from the photo, some of the cloning attempts were not successful.

I'm waiting to hear the response from the Vatican.


This ranks among the most morally illicit acts, ethically speaking ...

 
Researchers from Stemagen a private stem-cell research company in California, have created human clones by the same techniques used to clone other mammals. The clones only went through a few cell divisions before being discarded [Ethical storm as scientist becomes first man to clone HIMSELF].

There's nothing remarkable about the science. It's one step toward cloning humans using standard procedures that have been worked out over the past three decades. What's remarkable is the reaction to this announcement. I'm still having trouble figuring out what is the ethical problem here.

I think it's all related to abortion. If you are opposed to allowing a woman to decide what to do with her own body then you're also against stem cell research. The "ethical issue" is mostly confined to religious people (men?) who oppose abortion. At least that's how it appears to me.

Stemagen isn't doing anything wrong; they make this clear on their webpage.
All research at Stemagen is performed in strict accordance with US Federal Regulations for the ethical treatment and protection of human subjects covered in the 45 CFR Part 46 policy issued by the Office of Human Research Protection (OHRP). More specifically, this requires that all research involving human eggs, embryos or human subjects be approved and carefully monitored by an independent Institutional Review Board (IRB) composed of members of the medical and general community, with additional ethical and legal expertise sought when required.

Those who choose to donate oocytes (eggs) and embryos for this type of research do so through informed consents that follow the guidelines for Human Embryonic Stem Cell Research from the National Academy of Sciences (www.nationalacademies.org).

Stemagen's mission is to maintain exemplary standards in human embryonic stem cell research in accordance with the highest ethical and research principles.
This is an important point in so-called "ethical" debates. The scientists are not being unethical and many observers, like me, don't see any ethical problem. Others see an ethical problem as described in the newspaper article.
John Smeaton, of the Society for the Protection of Unborn Children, said: "We have got scientists wandering around in an ethical wilderness, forgetting about matters of justice relating to our fellow human beings.

"We have people creating human beings with the intention of destroying them. That's appalling."

And the Vatican condemned the cloning of human embryos, calling it the "worst type of exploitation of the human being".

"This ranks among the most morally illicit acts, ethically speaking," said Monsignor Elio Sgreccia, president of the Pontifical Academy for Life, the Vatican department that helps oversee the Church's position on bioethics issues.
Here's the issue. At what point does something become an "ethical" issue for society? How many people have to be against something on "ethical" grounds" in order for it to become an ethical problem?

What if their objections are irrational? For example I imagine that US Presidential candidate Mike Huckabee is against stem cell research but his reasons are likely to be as ridiculous as his reasons for opposing same-sex marriage. Does that still count as an ethical problem? It seems to me that elevating stupidity to the level of "ethics" is not the way we want to go.

Why couldn't the headline have been "No Ethical Problem, According to Most Atheists?" Why do we let religious groups define ethics for us? I don't subscribe to their version of ethics, do you?


Saturday, January 19, 2008

Teaching IDiots About Evolution

 
The National Academies (Science, Engineering, Medicine) (USA) have just published their latest book on the evolution/creationism controversy. You can download it for free on their website [Science, Evolution, and Creationism].

The book attempts to define evolution and it doesn't do a bad job of describing a minimal definition that would be acceptable—that is if you only look at the actual definition. Here it is from page 5.
Evolution consists of changes in the heritable traits of a population of organisms as successive generations replace one another. It is populations of organisms that evolve, not individual organisms.
Sandwalk readers will know that this is the kind of definition that I prefer as well [What Is Evolution?]. This sort of definition is neutral with respect to mechanisms. It doesn't matter whether evolution occurs by natural selection, random genetic drift, of something else entirely. That's just as it should be because the explanation of how evolution occurs lies properly in the domain of evolutionary theory. Thus, we can say that evolution is a fact because we see it happening and we have overwhelming evidence that has happened in the past. We can be confident that it is a fact even though we may not be as certain about how it happened.

Once we start committing to an explanation we can no longer talk about facts, in many cases, since the exact mechanism of evolution is often disputed. The National Academies book begins with a wonderful description of Tiktaalik, a fossil animal that shares characteristics of both fish and primitive tetrapods. It is strong evidence in support of the evolution of tetrapods from fish and that lineage is now considered to be a well established fact.

However, it would be wrong to use Tiktaalik as support for a particular mechanism of evolution. The fossil suggests that natural selection is playing a role but random genetic drift is not ruled out. We know from other sorts of data that natural selection and random genetic drift are facts, as well as being part of evolutionary theory, but it's a good idea to draw a distinction between evolution, the process, and theories about how it occurs. This is especially true when trying to explain things to IDiots.

Unfortunately, the authors of Science, Evolution, and Creationism don't do as good a job in this regard as they should have. For example, the (reasonably correct) definition that I quoted above is found at the end of a paragraph that weakens it considerably. Here's the entire paragraph ...
If a mutation increases the survivability of an organism, that organism is likely to have more offspring than other members of the population. If the offspring inherit the mutation, the number of organisms with the advantageous trait will increase from one generation to the next. In this way, the trait — and the genetic material (DNA) responsible for the trait — will tend to become more common in a population of organisms over time. In contrast, organisms possessing a harmful or deleterious mutation are less likely to contribute their DNA to future generations, and the trait resulting from the mutation will tend to become less frequent or will be eliminated in a population. Evolution consists of changes in the heritable traits of a population of organisms as successive generations replace one another. It is populations of organisms that evolve, not individual organisms.
The next paragraph then goes on to describe natural selection. There is no mention of random genetic drift anywhere in the book, although there is a passing reference to the fact that neutral mutations can be fixed. This reference is found on page 29 near the end of the book.

The net result is that evolution the process, is intimately connected to the mechanism of natural selection in this book. Readers will assume that scientists equate evolution with natural selection and use the terms interchangeably.

Why is this a problem? Well, for one thing, it's wrong. Normally that should be a good enough reason to avoid such errors, but these days there's a movement afoot to frame evolution in a way that resonates with the general public. Perhaps it's okay to define evolution as natural selection if it helps educate the average person? I object to such reasoning in the strongest possible terms. The essence of science is being honest and accurate and those goals should never be sacrificed for political gain. It may be easier to avoid confusion by not mentioning other mechanisms of evolution but the end result is that the public is not being educated correctly about evolution. You can't then turn around and complain that the public doesn't understand evolution.

The IDiots are upset about this book. They have found many ingenious ways of criticizing the contents. Here's a perfect example from Casey Luskin [The Facts about Intelligent Design: A Response to the National Academy of Sciences’ Science, Evolution, and Creationism].

I don't have the time, or the patience, to correct everything that's wrong with this article but there's one point I'd like to address. Here's what Casey Luskin says about evolution.
The NAS unscientifically elevates evolution to the status of unquestionable dogma.

The NAS defines evolution as evolution by natural selection and claims that “[t]here is no scientific controversy about the basic facts of evolution,” asserting that evolution is “so well established that no new evidence is likely to alter” it. In doing so, the NAS treats Neo-Darwinian evolution like an unquestionable dogma, not like a science. Such proclamations from the NAS are dangerous because they threaten the prestige of the NAS as an objective and trustworthy voice advising society.

Moreover, the NAS’s claim that there is no controversy over evolution is a bluff, for there is significant scientific dissent from the view of evolution by natural selection. Leading biologist Lynn Margulis, who opposes ID, criticizes the standard Darwinian mechanism by stating that the “Darwinian claim to explain all of evolution is a popular half-truth whose lack of explicative power is compensated for only by the religious ferocity of its rhetoric.”[7] She further observes that “new mutations don’t create new species; they create offspring that are impaired.”[8] In 2001, biochemist Franklin Harold admitted in an Oxford University Press monograph that "there are presently no detailed Darwinian accounts of the evolution of any biochemical or cellular system, only a variety of wishful speculations.”[9] Other scientists have gone much further.

Over 700 doctoral scientists have signed a public statement asserting their agreement that they "are skeptical of claims for the ability of random mutation and natural selection to account for the complexity of life."[10] But what are these scientists to do when the top scientific organization in the U.S. proclaims that evolution is as unquestionable as the existence of atoms or the heliocentric model of the solar system? Clearly the NAS’s statements threaten the academic freedom of scientists to dissent from Neo-Darwinian evolution.
In the past it has been easy to show that the IDiots are either mistaken or lying when they make comments like this. I've said many times that they deliberately try to confuse people by making it seem as though evolution, the fact, is the same as natural selection, the mechanism. They know full well that there's a difference between controversies over the sufficiency of natural selection and whether evolution, per se, is overwhelmingly support by hard evidence. They know that evolution is not the same as Darwinism and attacks on Darwinism are not the same thing as attacks on evolution.

This rebuttal is now a bit more difficult with the publication of Science, Evolution, and Creationism. Nowhere in the book do the authors deliberately make the distinction between natural selection and evolution and nowhere do they mention any other mechanism of evolution (e.g., random genetic drift). When reading the book, most of us recognize that there are abundant, oblique, references to the fact that the authors are not stupid, but that is only apparent to scientists who know about evolution.

Casey Luskin has taken advantage of this lost opportunity on the part of the National Academies to make it look like they are being dogmatic and forcing everyone to accept Darwinism. When I decided to write about Luskin's silly article, I thought it would be easy to refute what he was saying by referring back to the book. I thought the book would make it clear that evolution is not the same as natural selection. Unfortunately, there's nothing I can quote from the book that explicitly makes that point even though it's there implicitly. That's a missed opportunity that I hope can be remedied in future printings.


Friday, January 18, 2008

Map That Campus XLII

 
This is one of my favorite challenges in the blogosphere. Can you identify the campus on The Daily Transcript?


Backwards Bush Countdown Clock

 
Trust me, it's not just Americans who are counting the days.




Science in an Age of Endarkment

 
Be sure to come to this special event sponsored by the Centre for Inquiry, Toronto. The talk will be given in the auditorium just beside my building. I'll be going to the reception beforehand at CFI—join CFI and you can come too!!!



SCIENCE IN AN AGE OF ENDARKENMENT: scientific fraud, quackery, religion and university politics


Friday, January 25th, 2008: 7:00 pm - 9:00 pm, MacLeod Auditorium, Medical Sciences Building, University of Toronto (1 King's College Circle, Toronto)

When alternative medicine and academia collide... Featuring a major public symposium with David Colquhoun

Eminent UK scientist and noted skeptic David Colquhoun was recently at the centre of controversy after critiquing the pseudoscientific claims of a homeopathic practitioner. Prof. Colquhoun was asked to remove his site from the UCL server, but after a backlash from the scientific community, his website was revived. He will be speaking about alternative medicine, academia, and the conflicts that arise when the two intersect.

David Colquhoun is professor of pharmacology at University College London and fellow of the Royal Society. He runs a blog called "Improbable Science" (http://www.dcscience.net) dedicated to exposing and debunking pseudoscientific claims.

Dr. Colquhoun will appear at a special reception with food and drinks exclusively for Friends of the Centre from 5:00-6:30pm at CFI Ontario preceding his talk. Contact us at toronto@centerforinquiry.net to find out how you can join.


[Image Credit: Homeopathy wars in the UK]


[For a short summary of the blogging ban see University College London Restores Professor Colquhoun's Website]

Soybean Genome

 
A preliminary draft of the soybean (Glycine max) genome has been released on the Phytozome website [Glycine max Genome].

The reported size of the genome is 950 Mb (950 × 106 base pairs). This is considerably larger that the genomes of grape (505 Mb), Arabidopsis (157 Mb), rice (389 Mb), and polar (485 Mb).

The larger size suggests a recent polyploidization event in the lineage leading to soybean. The number of genes in the draft sequence is 51,320. This also suggests that many genes are duplicated. (Grape has about 30,000 genes, poplar has about 45,000, rice has 38,000 and Arabidopsis has only 27,029.) Keep in mind that the total number of genes is likely to drop by a considerable amount once detailed annotation gets underway. Nevertheless, it looks like the soybean has a lot more genes than the other flowering plants.


[Photo Credit: [Photograph]. Retrieved January 18, 2008, from Encyclopædia Britannica Online: bean: soybean]

Brampton Prude

 
Brampton is a city west of Toronto and north of Mississauga, where I live. Heart Lake United Church is trying to attract customers so they put up the sign shown here. I think it's funny.

Nicole Cedrone doesn't agree. She thought it was offensive when she drove by on her way home from the doctor [Church Strips Saucy Sign]. She complained and the sign was removed.
"I have to admit, it is funny, but it's not appropriate for where it is," Cedrone said. "I just think it's offensive."

She said she is glad her 11-year-old wasn't in the car with her to ask, `Mom, what does that mean?'"
Well, the photograph of the "offensive" sign is now prominently featured in The Toronto Star where, hopefully, her 11-year-old son will read it and ask questions like, "Mom, what does 'saucy' mean?" By being such a prude, Nicole Cedrone has ensured that the sign will be viewed by millions and not just a small number of people driving along Sandalwood Parkway. Way to go, Nicole.


Bobby Fischer

 
Bobby Fischer died yesterday in Reykjavik, Iceland, where he had been living for the past several years [Bobby Fischer, 64: Former chess champion].

Back in 1972, Fischer beat Boris Spassky of the USSR to become world chess champion. The event has been glorified as part of the cold war competition between the USA and the USSR but this was only part of the story. Some of us were just interested in it as a major sporting event featuring a radical new hero who didn't always play by the rules.

I remember following the games live on television—yes, that's right, the moves in each game were broadcast live on a large chessborad, with plenty of color commentary. As an amateur chess player, it was a real insight into the world of high level play.

Go to World Chess Championship 1972 for a brief summary of this extraordinary event. We'll never see anything like it again.

Here's the position at adjournment in the final (21st) game [Spassky vs Fischer Game #21]. Fischer (black) has just played h5. After thinking about the position all night Spassky phoned in the next morning to resign and concede the championship. Can you see why he gave up?



Why I Like Richard Dawkins

 
Richard Dawkins doesn't pull punches and he doesn't beat around the bush. You always know where he stands on any given issue. This is what I admire about Richard Dawkins.

I don't agree with him on lots of things but whenever you engage him you know you've got a fight on your hands. It's the combination of intelligence and forthrightness that make him such a powerful voice in science. We need more scientists who are both smart, and willing to stand up for their ideas. We need more open controversy in science these days. Scientists need to speak up when they encounter silly ideas in the scientific literature. It is not a scientific virtue to be polite in such cases; in fact, it can be detrimental to science to clog up the scientific literature with scientific nonsense on the grounds that one shouldn't criticize fellow scientists in public. Richard Dawkins does not make that mistake.

Dawkins does not like group selection because it conflicts with his adaptationist, gene-centric, worldview. He's been very clear about this over the years. I admire him for sticking to his guns and standing by the original dismissal of group selection by George Williams.1

David Sloan and E.O. Wilson have recently been pushing for a revival of group selection. They published a short summary of their new book in the Nov. 3 edition of New Scientist [Evolution: Survival of the selfless] where they said,
The concept of genes as "replicators" and "the fundamental unit of selection" averages the fitness of genes across all contexts to predict what evolves in the total population. The whole point of multilevel selection theory, however, is to ask whether genes can evolve on the strength of between-group selection, despite a selective disadvantage within each group. When this happens, the gene favoured by between-group selection is more fit overall than the gene favoured by within-group selection in the total population.

It is bizarre (in retrospect) to interpret this as an argument against group selection. Both Williams and Dawkins eventually acknowledged their error, but it is still common to find the "gene's-eye view" of evolution presented as a drop-dead argument against group selection.

The old arguments against group selection have all failed. It is theoretically plausible, it happens in reality, and the so-called alternatives actually include the logic of multilevel selection. Had this been known in the 1960s, sociobiology would have taken a very different direction. It is this branch point that must be revisited to put sociobiology back on a firm theoretical foundation.
Dawkins responds to this in a letter published in the Dec. 15 issue [Genes Still Central].
Genes still central

David Sloan Wilson's lifelong quest to redefine "group selection" in such a way as to sow maximum confusion - and even to confuse the normally wise and sensible Edward O. Wilson into joining him - is of no more scientific interest than semantic doubletalk ever is. What goes beyond semantics, however, is his statement (it is safe to assume that E. O. Wilson is blameless) that "Both Williams and Dawkins eventually acknowledged their error..." (3 November, p 42).

I cannot speak for George Williams but, as far as I am concerned, the statement is false: not a semantic confusion; not an exaggeration of a half-truth; not a distortion of a quarter-truth; but a total, unmitigated, barefaced lie. Like many scientists, I am delighted to acknowledge occasions when I have changed my mind, but this is not one of them.

D. S. Wilson should apologise. E. O. Wilson, being the gentleman he is, probably will.

* Richard Dawkins, Oxford UK
Does anyone have any doubts about where Dawkins stands on the issue of group selection?

David Sloan Wilson and E.O. Wilson responed to Dawkins' letter by claiming that they were only referring to one minor aspect of the argument against group selection but I don't think anyone is going to be fooled by that. In their article, they clearly imply that Dawkins has acknowledged his "error" in opposing group selection. This is a case where a simple apology would have worked better.


1. Ironically, Dawkins is a huge fan of kin selection, which, in my opinion is just about as weak as group selection.

Thursday, January 17, 2008

Gerty Cori Biochemist on USA Stamp

Biochemist Gerty Cori is going to be on a new USA stamp to be issued in March. Cori and her husband won the Nobel Prize in 1947 for their work on glycogen metabolism [Nobel Laureates: Carl Ferdinand Cori and Gerty Theresa Cori].

One of the key intermediates in this pathway is the Cori ester [Monday's Molecule #25]. That's the molecule pictured on the stamp. Unfortunately, there's a mistake in the structure. How many can spot it? Why didn't they ask a biochemist to check the design?

UPDATE: Here's the correct structure.
The error was first discovered by a reader of Chemical & Engineering News [Going postal over structural errors]. Here's how C&EN describes the mistake ...
It is a sad state of affairs, because it was precisely the isolation of glucose-1-phosphate, and discovery of the so-called Cori ester, that garnered Cori the Nobel Prize. "Long-dead carbohydrate chemists would roll over in their graves to see this structure after all the effort they made to get it right," one sugar chemist wrote in an e-mail to Newscripts.

The glitch made us rather glum, despondent even, as we considered the squandered opportunity to serve some first-class carbohydrates to the American public. For alas, the suboptimal stamps have already been printed and are still scheduled for release in early March, despite the error.


[Hat Tip: Living the Scientific Life]

A Junk DNA Quiz

 
Take the junk DNA quiz in the left sidebar to let me know what you think of your genome. How much of it could be removed without affecting our species in any significant1 way in terms of viability and reproduction? Or even in terms of significant ability to evolve in the future? In other words, how much is junk?


1. I did not choose the word "significant" in order to be obtuse. I picked it in order to eliminate some trivial possibilities that really don't make any difference. For example, no matter how little DNA you delete you would be able to detect some change, even if it's just a reduction in the time to replicate the genome of the amount of energy used. If you think that such changes are "significant" then you should answer "none" to the question in the quiz.

The Plausibility of Life

The Plausibility of Life is an evo-devo book by Mark Kirschner and John Gerhart. I read it a long time ago and had pretty much put it out of my mind except for the occasional potshot [Evo-Devo: Innovation and Robustness in Evolution] [Animal Chauvinism].

A couple of days ago I was shocked into taking another look at the book. The shocker was Alex Palazzo of The Daily Transcript who wrote [Today's rant - the biggest story never covered].
The most insightful book on biology written in the past decade was Gerhart & Kirschner's book, The Plausibility of Life.
That's so far out of line with my opinion that I began to wonder if I had missed something important. Alex is a smart guy and he's not likely to be way off base.

Alas, in this case Alex got it wrong. This is certainly not one of the most insightful books on biology in this decade, or any other decade. It's pretty much adaptationist, animal chauvinistic, evo-devo-centric gobbledygook from a pair of scientists who don't understand evolution.

The central question of the book is, "... how can small, random genetic changes be converted into complex and useful innovations?" (p. ix). Apparently this is a puzzlement to evolutionary developmental biologists. One that has eluded them until the last decade of the twentieth century.

Kirschner and Gerhart's effort is a valuable update of some of these ideas, but it hardly constitutes "a new theory" to complement the Modern Synthesis.

Massimo Pigliucci
Have We Solved Darwin's Dilemma?
Kirschner and Gerhart have the solution.
In this book we propose a major new scientific theory: facilitated variation that deals with the means of producing useful variation.
Since the essence of their theory is "facilitated variation" you would think that this concept would be clearly explained in the book. It isn't. There's a lot of beating around the bush and hand waving about a fundamental new process of evolution but little in the way of concrete facts and evidence.

When I read the book for the very first time I was astonished to realize that by the end of the book I still didn't know what the authors meant by "facilitated variation." So, I looked it up in the glossary ....
Facilitated Variation: An explanation of the organism's generation of complex phenotypic change from a small number of random changes of the genotype. We posit that the conserved components greatly facilitate evolutionary change by reducing the amount of genetic change required to generate phenotypic novelty, principally through their reuse in new combinations and in different parts of their adaptive ranges of performance.
Is that clear? Of course it isn't. You have to go back and read very carefully to even begin to understand what they're talking about.

... Kirschner and Gerhart do not present any detailed examples of how the properties of developmental systems have actually contributed to the evolution of a major evolutionary novelty. Nor have they shown that alternative properties would have prevented such evolution. Although The Plausibility of Life contains many interesting facts and arguments, its major thesis is only weakly supported by the evidence.

Brian Charlesworth
On the Origins of Novelty and Variation
Here's how I see it. Animals have a number of conserved core processes like transcription, membrane trafficking, formation of eyes, compartments, etc. that contribute to the success of the organism. You can't mess with these core processes because that would be lethal. However, new phenotypes can arise when existing core processes are expressed in new combinations or at different times during development. The core processes have been selected for adaptability. In particular, they have evolved in a way that facilitates phenotypic variation by encouraging the evolution of new combinations and new timing while, at the same time discouraging evolution of the core processes themselves.

Over time, animal species have been selected for the ability to evolve by taking advantage of facilitated variation without threatening the core processes. This one of the definitions of evolvability.
In summary, we believe that evolvability—the capacity for organisms to evolve—is a real phenomenon. We believe that facilitated variation explains the variation side of evolvability, through the reuse of a limited set of conserved processes in new combinations and in different parts of their adaptive ranges due to genetic modifications of nonconserved regulatory components ....

Facilitated variation has arisen and increased by selection, we say. Since it facilitates the generation of innumerable complex, selectable heritable traits with only a small investment of random genetic variation, it is indeed the greatest adaptation of all, at least for animals since the Cambrian.
I'm not buying any of this. I'd like to see real evidence that the process of evolution in animals is different than evolution in prokaryotes. Whether you're dealing with the genetic switch in bacteriophage λ, sporulation in Bacillus subtilis, or the formation of heterocysts in cyanobacteria, it is always the case that the processes are controlled by a cascade of regulatory factors and drastic changes in the timing and extent of these regulatory genes can lead to significant phenotypic effects.

What's so special about animals that we have to develop a "major new scientific theory" to explain similar observations?


Wednesday, January 16, 2008

Nobel Laureate: Sidney Altman

 

The Nobel Prize in Chemistry 1989.

"for their discovery of catalytic properties of RNA"



In 1989, Sidney Altman (1939 - ) was awarded the Nobel Prize in Chemistry for discovering that the RNA component of RNase P was the catalytic component of the enzyme [Transfer RNA Processing: RNase P]. He shared the prize with Thomas Cech who worked on self-splicing ribosomal RNA precursors.

The presentation speech was delivered by Professor Bertil Andersson of the Royal Swedish Academy of Sciences.
THEME:

Nobel Laureates
Your Majesties, Your Royal Highnesses, Ladies and Gentlemen,

The cells making up such living organisms as bacteria, plants, animals and human beings can be looked upon as chemical miracles. Simultaneously occurring in each and every one of these units of life, invisible to the naked eye, are thousands of different chemical reactions, necessary to the maintenance of biological processes. Among the large number of components responsible for cell functions, two groups of molecules are outstandingly important. They are the nucleic acids - carriers of genetic information - and the proteins, which catalyze the metabolism of cells through their ability to act as enzymes.

Genetic information is programmed like a chemical code in deoxyribonucleic acid, better known by its abbreviated name of DNA. The cell, however, cannot decipher the genetic code of the DNA molecule directly. Only when the code has been transferred, with the aid of enzymes, to another type of nucleic acid, ribonucleic acid or RNA, can it be interpreted by the cell and used as a template for producing protein. Genetic information, in other words, flows from the genetic code of DNA to RNA and finally to the proteins, which in turn build up cells and organisms having various functions. This is the molecular reason for a frog looking different from a chaffinch and a hare being able to run faster than a hedgehog.

Life would be impossible without enzymes, the task of which is to catalyze the diversity of chemical reactions which take place in biological cells. What is a catalyst and what makes catalysis such a pivotal concept in chemistry? The actual concept is not new. It was minted as early as 1835 by the famous Swedish scientist Jöns Jacob Berzelius, who described a catalyst as a molecule capable of putting life into dormant chemical reactions. Berzelius had observed that chemical processes, in addition to the reagents, often needed an auxiliary substance - a catalyst - to occur. Let us consider ordinary water, which consists of oxygen and hydrogen. These two substances do not react very easily with one another. Instead, small quantities of the metal platinum are needed to accelerate or catalyze the formation of water. Today, perhaps, the term catalyst is most often heard in connection with purification of vehicle exhausts, a process in which the metals platinum and rhodium catalyze the degradation of the contaminant nitrous oxides.

As I said earlier, living cells also require catalysis. A certain enzyme, for example, is needed to catalyze the breakdown of starch into glucose and then other enzymes are needed to burn the glucose and supply the cell with necessary energy. In green plants, enzymes are needed which can convert atmospheric carbon dioxide into complicated carbon compounds such as starch and cellulose.

As recently as the early 1980s, the generally accepted view among scientists was that enzymes were proteins. The idea of proteins having a monopole of biocatalytic capacity has been deeply rooted, and created a fundamental dogma of biochemistry. This is the very basic perspective in which we have to regard the discovery today being rewarded with the Nobel Prize for Chemistry. When Sidney Altman showed that the enzyme denoted RNaseP only needed RNA in order to function, and when Thomas Cech discovered self-catalytic splicing of a nucleic acid fragment from an immature RNA molecule, this dogma was well and truly holed below the waterline. They had shown that RNA can have catalytic capacity and can function as an enzyme. The discovery of catalytic RNA came as a great surprise and was indeed met with a certain amount of scepticism. Who could ever have suspected that scientists, as recently as in our own decade, were missing such a fundamental component in their understanding of the molecular prerequisites of life? Altman's and Cech's discoveries not only mean that the introductory chapters of our chemistry and biology textbooks will have to be rewritten, they also herald a new way of thinking and are a call to new biochemical research.

The discovery of catalytic properties in RNA also gives us a new insight into the way in which biological processes once began on this earth, billions of years ago. Researchers have wondered which were the first biological molecules. How could life begin if the DNA molecules of the genetic code can only be reproduced and deciphered with the aid of protein enzymes, and proteins can only be produced by means of genetic information from DNA? Which came first, the chicken or the egg? Altman and Cech have now found the missing link. Probably it was the RNA molecule that came first. This molecule has the properties needed by an original biomolecule, because it is capable of being both genetic code and enzyme at one and the same time.

Professor Altman, Professor Cech, you have made the unexpected discovery that RNA is not only a molecule of heredity in living cells, but also can serve as a biocatalyst. This finding, which went against the most basic dogma in biochemistry, was initially met with scepticism by the scientific community. However, your personal determination and experimental skills have overcome all resistance, and today your discovery of catalytic RNA opens up new and exciting possibilities for future basic and applied chemical research.

In recognition of your important contributions to chemistry, the Royal Swedish Academy of Sciences has decided to confer upon you this year's Nobel Prize for Chemistry. It is a privilege and pleasure for me to convey to you the warmest congratulations of the Academy and to ask you to receive your prizes from the hands of His Majesty the King.


Transfer RNA Processing: RNase P

 

RNase P is one of the key enzymes in the processing of tRNA primary transcripts [Transfer RNA: Synthesis].

RNase P is a ribozyme. Most of the enzyme consists of an RNA molecule called RNA P and the rest is composed of small proteins. In bacteria there is a single protein subunit while in eukaryotes there are up to eight small proteins bound to the RNA component.

RNA P, by itself, can catalyze the cleavage reaction [Monday's Molecule #58]. The role of the protein is simply to facilitate the reaction.1

The structure of the RNA component from two different species has recently been published. The one shown here is RNA P from Thermophilus maritima (reviewed in Baird et al. 2007). This catalytic RNA is found in all species and it's the classic example of an RNA that can catalyze a reaction in the absence of protein. Sidney Altman received the Nobel Prize in 1989 for demonstrating that the activity was confined to the RNA part of the holoenzyme.

The exact structure of the complete holoenzyme (RNA + protein) is not known but the evidence suggest a model such as the one shown on the left (Smith et al. 2007). The RNA is blue, the protein subunit is red, and the bound tRNA precursor is brown. Note that the protein subunit is positioned at the site of the cleavage near the 5′ end of the mature tRNA.

Part of the RNA ribozome is interacting with the TΨC loop of the tRNA molecule. This loop is present in all tRNAs which explains why the RNase P enzyme can cleave all tRNA precusors no matter which particular tRNA going to be produced.

There are two different types of RNase P depending on the species. Although both of them have similar catalytic RNAs they differ in size of the RNA and in the proteins that are bound to it.


1 When the reaction is carried out under in vivo concentrations of ionic strength, temperature etc., the protein component is absolutely required in order to get significant activity.

Baird, N.J., Fang, X.W., Srividya, N., Pan, T. and Sosnick, T.R. (2007) Folding of a universal ribozyme: the ribonuclease P RNA. Quarterly Rev. Biophys. 40:113-161. [doi:10.1017/S0033583507004623] [PubMed]

Smith, J.K., Hsieh, J. and Fierke, C.A. (2007) Importance of RNA-protein interactions in bacterial ribonuclease P structure and catalysis. Biopolymers 87:329-38. [PubMed]

Transfer RNA: Synthesis

 
Transfer RNA's are produced by transcribing a tRNA gene to produce a single-stranded tRNA precursor molecule. tRNA genes are just one of the many examples of genes that don't encode proteins. It's worth keeping this in mind when you read discussions about how genes are defined and the role of "noncoding" DNA in the genome.

tRNA genes can be individual isolated genes or they can be linked to other genes in a larger transcriptional unit. A common example of the latter situation occurs in ribosomal RNA operons where tRNA genes are located in the regions between the large and small ribosomal RNA genes. In bacteria, the tRNA genes can be part of a co-transcribed operon containing protein-encoding genes. In eukaryotes the tRNA genes are transcribed by RNA polymerase III [Eukaryotic RNA Polymerases].

No matter how the tRNA genes are arranged, the primary transcriptional product is larger than the functional tRNA and it contains no modified bases. This primary transcript has to be processed to: (a) reduce it to the proper length, (b) remove any introns and (c) convert the standard nulceotides into modified nucleotides like dihydrouridylate (D) or pseudouridylate (Ψ) [Transfer RNA: Structure].

The trimming steps involve a number of specific RNA cleavage enzymes. RNase P specifically cuts the precursor at the 5′ end of the mature tRNA. Other endonucleases cut the precursor near the 3′ end of the mature molecule.

The 3′ end must then be trimmed back to the proper position. This step is carried out by an exonuclease called RNase D in bacteria. Finally, the nucleotides CCA are added to the 3′ end by tRNA nucleotidyl transferase. (All tRNA's have the same 3′ nulceotides—this is where the amino acid is attached later on.) Some tRNA genes have already have the sequence CCA at the 3′ end of the mature molecular so the last step isn't always required.


Transfer RNA: Structure

 
Transfer RNA (tRNA) is an essential component of the protein synthesis reaction. There are at least twenty different kinds of tRNA in the cell1 and each one serves as the carrier of a specific amino acid to the site of translation.

tRNA's are L-shaped molecules. The amino acid is attached to one end and the other end consists of three anticodon nucleotides. The anticodon pairs with a codon in messenger RNA (mRNA) ensuring that the correct amino acid is incorporated into the growing polypeptide chain.

The L-shaped tRNA is formed from a small single-stranded RNA molecule that folds into the proper conformation. Four different regions of double-stranded RNA are formed during the folding process.

The two ends of the molecule form the acceptor stem region where the amino acid is attached. The anticodon is an exposed single-stranded region in a loop at the end of the anticodon arm.

The two other stem/loop structures are named after the modified nucleotides that are found in those parts of the molecule. The D arm contains dihydrouridylate residues while the TΨC arm contains a ribothymidylate residue (T), a pseudouridylate residue (Ψ) and a cytidylate (C) residue in that order. All tRNA's have a similar TΨC sequence. The variable arm is variable, just as you would expect. In some tRNA's it is barely noticable while in others it is the largest arm.

tRNA's are usually drawn in the "cloverleaf" form (below) to emphasize the base-pairs in the secondary structure.


1. Most genomes contain 40-80 different tRNA genes. While there are only 20 common amino acids, there are 61 different codons. Many codons are recognized by more than one different tRNA—the classic example is the codon AUG that can be recognized by methionyl-tRNA and initiator tRNA.

First Rule of Holes

 
Greg Laden has responded to criticism of his views on junk DNA [Moran, Gregory, Give me a Break!].

In the comments to Greg's post, Steve LaBonne brings up the First Rule of Holes. This is an excellent example. In case there are some people who are not familiar with the First Rule of Holes, here it is ....
FIRST RULE OF HOLES

If you're in one, stop digging.


Tuesday, January 15, 2008

Greg Laden Gets Suckered by John Mattick

 
Oh dear. Greg Laden reviews a paper from John Mattick's group and he falls for the hype, hook line and sinker. Here's what Greg says [Genes are only part of the story: ncRNA does stuff].
The "Junk DNA" story is largely a myth, as you probably already know. DNA does not have to code for one of the few tens of thousands of proteins or enzymes known for any given animal, for example, to have a function. We know that. But we actually don't know a lot more than that, or more exactly, there is not a widely accepted dogma for the role of "non-coding DNA." It does really seem that scientists assumed for too long that there was no function in the DNA.
I hate to break it to you Greg, but junk DNA is not a myth. It really is true that a huge amount of our genome is junk. It's mostly defective transposons like SINES and LINES [Junk in your Genome: LINEs]. It's a lie that we don't know what most non-coding DNA is doing. We do know. It's not doing anything because it's mostly screwed up transposons and pseudogenes like Alu's.

Mattick may have found a few bits of DNA that encode regulatory RNAs but that's only a small part of the total genome. He, and you, have fallen for excuse #5 of The Deflated Ego Problem.

Ryan Gregory has already tried to teach Greg some real science about junk DNA so I won't pile on any more than I have [Signs of function in non-coding RNAs in mouse brain.].

UPDATE: RPM chimes in to expose the flawed thinking of Greg Laden [How Easy is it to Write About Junk DNA?]


Humans Have Only 20,500 Protein-Encoding Genes

The first drafts of the human genome indicated about 30,000 genes, a number that was very much in line with many predictions that had been made over the years by scientists who were studying the topic. (Other scientists, and most science writers, thought there were about 100,000 genes [Facts and Myths Concerning the Historical Estimates of the Number of Genes in the Human Genome]).

Since the publication of the first draft, the number of genes has been dropping as annotators eliminate sequences that were falsely attributed to protein-encoding genes. Current estimates suggest there are about 28,000 different genes all together with about 4,000 of them encoding RNA products such as ribosomal RNA, tRNA, and the small RNAs involved in a numer of metabolic processes [Ensembl: Homo sapiens].

A gene encoding a protein will have an open reading frame (ORF) consisting of multiple codons— usually more than 100. Some of these potential protein-encoding genes appear to be unique to humans. They weren't found in the other mammalian genomes that had been sequenced (e.g., mouse, dog). Quite a few scientists took this as evidence for genes that distinguish humans from other mammals. According to them, these unique genes arose during the recent evolution of Homo sapiens and that's why there are no homologues in the other mammalian genomes.

Other scientists looked at the data in a different light. They suspected that these "unique" or "orphan" genes were more likely to be artifacts because they were not conserved. In other words, they reached exactly the opposite conclusion based on their understanding of evolution. Their prediction was that these orphan genes resulted from spurious ORF's and not real genes.

Blogging on Peer-Reviewed ResearchThis problem has been examined by Eric Lander's group in Boston, MA (USA) and the results were published in PNAS (Clamp et al., 2007). Their careful analysis has eliminated most of the orphan genes and the new gene count for protein-encoding genes is now 20,488.

Here's how the authors describe the purpose of their study,

The purpose of this article is to test whether the nonconserved human ORFs represent bona fide human protein-coding genes or whether they are simply spurious occurrences in cDNAs. Although it is broadly accepted that ORFs with strong cross-species conservation to mouse or dog are valid protein-coding genes (7), no work has addressed the crucial issue of whether nonconserved human ORFs are invalid. Specifically, one must reject the alternative hypothesis that the nonconserved ORFs represent (i) ancestral genes that are present in our common mammalian ancestor but were lost in mouse and dog or (ii) novel genes that arose in the human lineage after divergence from mouse and dog.
To begin the study they choose to analyze the 21,895 protein-encoding genes in the Ensembl database. They looked for genes that were related to similar sequences in the mouse and dog genomes. (These are the only two well-characterized non-human, mammalian genomes.) After visual inspection of low scoring sequences they were able to eliminate about 1600 potential genes because they were pseudogenes, transposons, or artifacts of various sorts.

They were left with 19,108 verified genes and 1177 orphan "genes"—human ORF's that were not similar to any gene in the mouse and dog genomes. These genes could be newly evolved genes in the human/primate lineage or ancient genes that had been lost in mice and dogs.

The next step was to categorize the orphan "genes" to see if they looked like real protein-encoding genes. The results indicated that in terms of sequence similarity to the same regions in the mouse and dog genomes, the orphan ORF's were indistinguishable from random sequences. Similarly, the characteristics of the presumed codons of these genes were very different from conserved genes and very similar to random sequences with short accidental reading frames. Thus, the orphan sequences look like artifacts.

To confirm this conclusion, the authors compared the sequences to the macaque and chimpanzee genomes. They were not found in those genomes either.
If the orphans represent valid human protein-coding genes, we would have to conclude that the vast majority of the orphans were born after the divergence from chimpanzee. Such a model would require a prodigious rate of gene birth in mammalian lineages and a ferocious rate of gene death erasing the huge number of genes born before the divergence from chimpanzee. We reject such a model as wholly implausible. We thus conclude that the vast majority of orphans are simply randomly occurring ORFs that do not represent protein-coding genes.
This analysis was extended to the other gene catalogs (Vega, and RefSeq) as well as an updated version of the Ensembl catalog (v38). This resulted identification of an additional 1271 valid genes. Adding in the genes in the mitochondrial genome (13) and the Y chromosome (78) gives a total of 20,470 genes.

Finally, reanalysis of the transposons and pseudogenes revealed 18 cases where a real gene had evolved from an inactive pseudogene. This gives a grand total of 20,488 protein-encoding genes in the human genome.

There are several conclusions that can be drawn from this excellent study.
We show that the vast majority of ORFs without cross-species counterparts are simply random occurrences. The exceptions appear to represent a sufficiently small fraction that the best course is would be consider such ORFs as noncoding in the absence of direct experimental evidence.
This is going to be a major challenge for many workers who prefer to see evolution in a different manner. There are a number of papers that view these orphans sequences as direct evidence that human specific genes had arisen in the recent past. Clamp et al. (2007) are saying that if the sequences aren't present in the macaque and chimpanzee then one should conclude that they are artifacts.

Remember, many of the artifactual genes are supported by EST/cDNA data suggesting that they are transcribed. This study calls that evidence into question—correctly in my opinion—indicating that we should be skeptical of the EST data.
One important biological implication of our results is that truly novel protein-coding genes (encoding at least 100 amino acids) arise only rarely in mammalian lineages. With the current gene catalogs, there are only 168 "human-specific" genes (<1% of the total; only 11 are manually reviewed entries in RefSeq; see SI Table 4). These genes lack clear orthologs or paralogs in mouse and dog, but are recognizable because they belong to small paralogous families within the human genome (2 to 9 members) or contain Pfam domains homologous to other proteins. These paralogous families shows a range of nucleotide identities, consistent with their having arisen over the course of ~75 million years since the divergence from the mouse lineage.
This is an important conclusion and I think it is accurate. There are very few "new" genes in the human genome, and, by implication, in other mammalian genomes. This conclusion is consistent with what we know about evolution but it contradicts studies that purport to show rapid evolution of novel genes and novel regulatory mechanisms in humans.


[Image Credit: The human karyotype is from the Ensembl website.]

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]

Digital Object Identifier (DOI)

 
The digital object identifier, or DOI, is a unique identifier that's given to electronic documents. The idea is that it serves as a permalink to the item. An item can be moved to a different webpage but the DOI will always point to it as long as the DOI is undated when the item is moved.

We often encounter these DOI identifiers in online journal articles. For example, a recently published PNAS article has the following DOI 10.1073/pnas.0709013104. I usually forget how to resolve those DOI's. In case I'm not the only one, I thought I'd post the information.

The resolver is locatad at http://dx.doi.org/. So if you want to see the PNAS article you type in the following URL: http://dx.doi.org/10.1073/pnas.0709013104. Try it.


Best Canadian Sci/Tech Blog 2007

 
Nominations have closed and the voting has begun for the best Sci/Tech blog in Canada. Here's the ballot.

The nominees are ....
The only blogs that I've read before today are Eastern Blot and The World's Fair. Should I be reading the others? Please let me know if you think any of these are science blogs worth reading. Several of the Canadian science blogs that I read every day are not on the list.

Is there an easy way of finding out how popular those blogs are? There must be some tool out there that will tell me the average number of visits per day/week/month for each of the nominees.


Monday, January 14, 2008

What Is this Dog Thinking?

 
If you think you know what's going on in the mind of this dog, get over to Friendly Atheist and enter the contest [Friendly Atheist Contest #14: Dog Prays to God].

Remember the rules. According to Hemant Mehta, "Funny and creative answers will have a shot at winning."

You can enter as often as you like.

Here's what the boy is thinking, "This is so embarrassing. I'm soon gonna have to break it to him that I'm an atheist."


Insurance Against Alien Abductions

 
According to some studies, up to four million Americans may have been abducted by aliens [Abduction by Aliens or Sleep Paralysis?]. I often use this information when questioning religious people about the rationality of their inner convictions. As it turns out, most theists reject the silly beliefs of alien abductees without seeing any connection between this and their own proof of God by religious experience.

A group of people have banded together to exploit help those who fear being abducted by aliens. They have prepared special dog tags [www.earthbounddog.com].
Picture yourself lost in the galaxy...UFO sightings and Alien Abductions are on the rise...Will you return to tell the story?

In case of alien abduction these dog tags may save your life. The crucial data an alien will need to get you back to Earth is die stamped into these dog tags.

The design is based on NASA research for the Pioneer 10 Space Mission that used a gold plaque attached to the craft to inform any Extraterrestrials of it's Earthly origin.
You can buy them for only $12.99 (US). I suggest you buy several sets of dog tags for all your close friends. Do not buy them for other people.


[Hat Tip: Bad Astronomy]

Convocation 2007

 
A few months ago I told you about my first convocation as a Professor [Bruce Alberts in Toronto]. Here's the formal photograph of the main participants. Don't we look pretty?




Monday's Molecule #58

 
This is one example of a very common molecule found in every cell. You have to give us the common name of this molecule and identify the species. You'll be pleased to know that I don't need the systematic IUPAC name for this one.

There's a direct connection between this molecule and Wednesday's Nobel Laureate. Your task is to figure out the significance of today's molecule and identify the Nobel Laureate who studied its function. (Hint: The Nobel Laureate is a Canadian—there aren't very many Canadian Nobel Laureates so this is a very big hint.)

The reward goes to the person who correctly identifies the molecule and the Nobel Laureate. Previous winners are ineligible for one month from the time they first collected the prize. There is one ineligible candidates for this week's reward because Sandwalk readers were not very successful in December. The prize is a free lunch at the Faculty Club.

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 the Nobel Laureate. Note that I'm not going to repeat Nobel Laureates so you might want to check the list of previous Sandwalk postings.

Correct responses will be posted tomorrow along with the time that the message was received on my server. I may select multiple winners if several people get it right.

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

UPDATE: We have a winner! This one proved to be far more difficult than I imagined. Everyone got the Nobel Laureate (Sidney Altman) but very few people got the molecule correct. Some people failed to identify the species correctly even though I specifically asked for the species. Most people said that the molecule is RNase P but that isn't quite correct.

The molecule is the M1 RNA subunit of RNase P from E. coli. The other subunit is a small protein called the C5 protein cofactor. This RNA is sometimes called RNA P and that would have been an acceptable answer.

Only one person got everything right and that response just arrived a few minutes ago. Congratulations to PonderingFool for knowing that the molecule was the M1 RNA component of E, coli RNase P and the Nobel Laureate is Sidney Altman.