Charles and Camilla Are in Town

 
Charles and Camilla are visiting Toronto but you wouldn't know it if you didn't read the papers. Unless, of course, you just happen to be caught up in one of the mini traffic jams that are associated with such visits.

I witnessed one last night as several motorcycles and police cars with red and blue lights flashing, and sirens wailing, raced up University Avenue and around Queen's Park. They were escorting a convoy of half a dozen limos. I figure they were exceeding the speed limit by quite a bit.

Today, Charles is accompanying Camilla to Dundurn castle in Hamilton. The great house was built by Sir Allan Napier MacNab who happens to be Camilla's great-great-great grandfather. MacNab was Prime Minister of the Province of Ontario and was a member of the ruling elite that William Lyon Mackenzie opposed in the 1837 "rebellion."

This is Camilla's first visit to Canada. Charles has been here too often.

The couple will be opening the Royal Agricultural Winter's Fair before flying back to England.

For those of you interested in genealogy, here's how Camilla is related to MacNab.

Allen Napier MacNab (1798-1862)
m. Mary Stuart (1812-1846)
      Sophia Mary MacNab (1832-1917)
      m. William Coutts Keppel (1832-1894)
            Honourable George Keppel (1865-1947)
            m. Alice Frederica Edmonstone (1869-1947)
                  Sonia Rosemary Keppel (1900-1986)
                  m. Roland Calvert Cubbitt (1899-1962)
                        Honourable Rosalind Maud Cubbitt (1921-1994)
                        m. Bruce Middleton Hope Shand (1917- )
                              Camilla Rosemary Shand (1947- )
                              m. (1) Andrew Henry Parker-Bowles
                                    (2) Charles, Prince of Wales

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Nobel Laureate: Lee Hartwell

 

The Nobel Prize in Physiology or Medicine 2001

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

Leland H. Hartwell (1939 - ) won the Nobel Prize for his contributions to understanding the cell cycle. His discovery of the regulatory molecule CDC28 led to the idea of "checkpoints"—steps in the cell cycle where specific action is needed to progress to the next stage.

Hartwell shared the 2001 Nobel Prize with Paul Nurse and Tim Hunt.

Some of you may think that elucidation of the cell cycle in yeast isn't such a big deal. You would be wrong. No only did this work stimulate a huge field of study in yeast, but the genes and the pathways uncovered in yeast are similar to those in other eukaryotic cells. This is a case where fundamental basic science has lead to a deep understanding of how life works at the molecular level.

THEME:
Nobel LaureatesI already posted the press release under Nobel Laureate: Sir Paul Nurse. It's a very good description of the work that was done by all three Nobel Laureates.

Here's an excerpt from the Presentation Speech.

This year's Nobel Laureates have discovered the key regulators of the cell cycle, cyclin dependent kinase (CDK) and cyclin. Together these two components form an enzyme, in which CDK is comparable to a "molecular engine" that drives the cell through the cell cycle by altering the structure and function of other proteins in the cell. Cyclin is the main switch that turns the "CDK engine" on and off. This cell cycle engine operates in the same way in such widely disparate organisms as yeast cells, plants, animals and humans.

How were the key regulators CDK and cyclin discovered?

Lee Hartwell realized the great potential of genetic methods for cell cycle studies. He chose baker's yeast as a model organism. In the microscope he could identify genetically altered cells - mutated cells - that stopped in the cell cycle when they were cultured at an elevated temperature. Using this method Hartwell discovered, in the early 1970s, dozens of genes specific to the cell division cycle, which he named CDC genes. One of these genes, CDC28, controls the initiation of each cell cycle, the "start" function. Hartwell also formulated the concept of "checkpoints," which ensure that cell cycle events occur in the correct order. Checkpoints are comparable to the program in a washing machine that checks if one step has been properly completed before the next can start. Checkpoint defects are considered to be one of the reasons behind the transformation of normal cells into cancer cells.

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[Photo Credit: Susie Fitzhugh and the Fred Hutchinson Cancer Research Center]

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.

"Dr." Charlene Werner on Homeopathy

 
This video illustrates the extreme stupidity of those who believe in homeopathy.

The person who posted the video on YouTube recently received the following letter.

I thought you would like to know that you will be contacted by Dr Werner's Attorney shortly regarding her video. The posting of this video is in violation of copyright laws. We are aware that you have had this video up since March of '08 however I suggest you delete it immediately.

Jayson Patrick

This immediately triggers the Streisand Effect. Won't these people ever learn? No, of course not, that's because they are stupid.

Watch if you dare.

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Monday's Molecule #142: Winner

 
The diagram should remind you of the cell cycle and the 2001 Nobel Prize in Physiology and Medicine. Since I already covered Tim Hunt and Paul Nurse, this must be about Lee Hartwell. That means the molecule must be "start" or CDC28.

The winner is Bill Chaney of the University of Nebraska. He has agreed to donate his free lunch to an undergraduate. Unfortunately, there weren't any undergraduate who got the right answer this week so I still have three free lunches to give away.

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Sometimes it's almost impossible to find an image of a specific molecule that honors a Nobel Laureate. This is one of those times.

The diagram provides all the clues necessary to identify an important process and then to identify a particular molecule associated with this week's Nobel Laureate.

You must name the molecule and the Nobel Laureate. Be careful 'cause it's easy to make a mistake and name someone who has already been the subject of a Monday's Molecule.

The first person to identify the molecule and name the Nobel Laureate(s) wins a free lunch. Previous winners are ineligible for six weeks from the time they first won the prize.

There are only six ineligible candidates for this week's reward: Frank Schmidt of the University of Missouri, Joshua Johnson of Victoria University in Australia, Markus-Frederik Bohn of the Lehrstuhl für Biotechnik in Erlangen, Germany, Jason Oakley a biochemistry student at the University of Toronto, Dima Klenchin of the University of Wisconsin, Madison and Alex Ling of the University of Toronto.

Joshua and Dima have agreed to donate their free lunch to an undergraduate. Consequently, I have two extra free lunches for deserving undergraduates so I'm going to award an additional prize 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. If you can't make it for lunch then please consider donating it to someone who can in the next round.

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(s) 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.

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Nobel Laureates: Archer Martin and Richard Synge

 

The Nobel Prize in Chemistry 1952.

"for their invention of partition chromatography"




Archer John Porter Martin (1910 - 2002) and Richard Laurence Millington Synge (1914 - 1994) won the Nobel Prize in Chemistry for their work on separating substances by partition chromatography.

The technique they developed was called paper chromatography but today there are many other, more effective, versions of partition chromatography. The example shown below is from Monday's Molecule #134 and it's taken from an article on paper chromatography.

In this example, a soluble extract of pigments from plant leaves is spotted at the bottom of a piece of paper and the end with the sample is placed in a suitable solvent such as a mixture of acetone and ether. The solvent rises up the paper by capillary action taking the dissolved pigments with it. The trick is to choose a solvent mixture where the pigments (or other compounds) are differentially soluble so they migrate at different rates and separate on the paper.

The theory behind partition chromatography is complex. It used to be part of graduate courses in biochemistry.

I still remember taking Chemistry 542 back in 1969 and learning about Craig's ideas of counter-current distribution. We even covered the Martin & Synge 1941 paper in the Biochemical Journal (Biochem J. 35:1358). I still have my notes.

And I still get anxious whenever I hear the words "theoretical plates."

Martin & Synge, and others, developed techniques for separating amino acids and this was the basis of the sequencing technology employed by Fred Sanger for determining the amino acid sequence of insulin.

Back in 1952 it must have seemed unusual to be awarding a Nobel prize for chromatography. That's why the first part of the Presentation Speech explains why the discovery is important.

THEME:
Nobel Laureates

Your Majesties, Your Royal Highnesses, Ladies and Gentlemen.

This year's Nobel Prize in Chemistry is awarded for the discovery of a method for the separation of substances from complicated mixtures.

How can it happen, one may ask, that something apparently so commonplace as a separation method should be rewarded by a Nobel Prize? The answer is that from the very beginnings of chemistry until our own time, methods for separating substances have occupied a key position in this science. Even today, in Holland, chemistry is called "Scheikunde", or "the art of separation", and even today some of chemistry's most important advances are linked to the invention of new methods for separating various substances.

Chemistry today is to a large extent concentrated upon the study of natural products, which are obtained from animals, plants, or even bacteria and other microorganisms. A starting material of this type contains a great number of widely varied substances, some simple, others more complicated. The first thing the chemist must do is to isolate the substances he is interested in from the material and prepare them in a pure state. The next step is, if possible, to identify these substances and find out what they consist of and how they are built up from simple constituents.

The first problem, the isolation, can indeed be difficult, as it is often a matter of preparing in a pure state substances which constitute only an extremely small fraction of the starting material and which have the disagreeable tendency of, so to speak, disappearing between one's fingers when one tries to get hold of them. It is here that Martin and Synge's method has enjoyed great success, especially in what is perhaps its most important form, and is called filter-paper chromatography.

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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.

Monday's Molecule #142

 
Sometimes it's almost impossible to find an image of a specific molecule that honors a Nobel Laureate. This is one of those times.

The diagram provides all the clues necessary to identify an important process and then to identify a particular molecule associated with this week's Nobel Laureate.

You must name the molecule and the Nobel Laureate. Be careful 'cause it's easy to make a mistake and name someone who has already been the subject of a Monday's Molecule.

The first person to identify the molecule and name the Nobel Laureate(s) wins a free lunch. Previous winners are ineligible for six weeks from the time they first won the prize.

There are only six ineligible candidates for this week's reward: Frank Schmidt of the University of Missouri, Joshua Johnson of Victoria University in Australia, Markus-Frederik Bohn of the Lehrstuhl für Biotechnik in Erlangen, Germany, Jason Oakley a biochemistry student at the University of Toronto, Dima Klenchin of the University of Wisconsin, Madison and Alex Ling of the University of Toronto.

Joshua and Dima have agreed to donate their free lunch to an undergraduate. Consequently, I have two extra free lunches for deserving undergraduates so I'm going to award an additional prize 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. If you can't make it for lunch then please consider donating it to someone who can in the next round.

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(s) 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.

---

A Confused Philosopher (Part II)

I've written a lot about Michael Ruse over the past few years. Mostly I'm upset by his lack of understanding of modern evolutionary theory [A Confused Philosopher, Down with Darwinism!, Darwinism at the ROM].

I'm also annoyed at the accommodationist position that Ruse takes from time to time and his support for the Courtier's Reply. He's one of those people who think that there are very sophisticated arguments for the existence of God—arguments that most atheists can't refute.

Ruse's latest foray into this philosophical mine field was just published in The Guardian: Dawkins et al bring us into disrepute.

It's a pile of crap but Jerry Coyne [Ruse gibbers on. . . .] and PZ Myers [Schisms, rifts, and apologia for insanity] have already proven that beyond a shadow of a doubt.

Ruse moved from the University of Guelph to a university in Florida so he could avoid mandatory retirement. Perhaps he should consider voluntary retirement?

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[Image Credit: The photo is from Paul Nelson on the Intelligent Design website. It refers to Ruse's idea that evolution is a form of religion.]

Charles Darwin's Brave New World: A Dangerous Idea

 
I watched the first part last night on The Nature of Things with David Suzuki. It was pretty good, although the emphasis on how Darwin was afraid to discuss his ideas got a bit tedious.

I'm also skeptical about the film's claim that evolution caused Darwin to abandon religion. It's worth remembering that his father (Robert) and his grandfather (Erasmus) were well-known skeptics about religion and Darwin's brother, Erasmus, was not religious. Darwin hung out with a lot of people who were questioning religion even though they knew nothing about evolution.

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Falling Back

 
Last night was the night we turned our clocks back one hour in Canada and the USA. It's easy to remember whether we lose an hour or gain an hour because even school children learn the phrase "Spring forward, Fall back." ("Fall" is the local jargon for "Autumn.")

For most people, this concept of adjusting your clocks twice a year is terribly confusing. Do you understand it?

Here's a short quiz to test your knowledge of time.

What do Australians do at this time of the year?

1. turn their clocks back one hour
2. turn their clocks forward one hour
3. don't adjust their clocks
4. who cares what happens in Vienna?

What is the astronomical reason for turning our clocks back one hour?

1. there is no astronomical reason for adjusting our clocks
2. the rotation of the Earth slows down when it nears apogee
3. there aren't exactly 24 hours in a day
4. clocks run slower when the Earth is farther from the sun

What happened last night in Saskatchewan?

1. people turned their clocks back one hour
2. people turned their clocks forward one hour
3. nobody adjusted their clocks
4. who cares what happens in Saskatchewan? (and where is it?)

If you normally catch the 7:33 commuter train, what will you do tomorrow?

1. take the 6:33 train
2. take the 8:33 train
3. get on the 7:33 train as usual
4. call in sick

What happens to the international date line at this time of year?

1. it moves 15° east
2. it moves 15° west
3. it stays right where it is but "midnight" becomes 1 AM during the winter months
4. nothing happens to the international date line

Did you ....

1. get one hour less sleep last night?
2. get one hour more sleep last night?
3. slept exactly the same amount as the night before
4. stayed up all night celebrating?

Mr. Big has an appointment to meet his accountant tomorrow at 12 noon. His secretary sent him an email message on Friday telling him that the appointment would have to be delayed by two hours. Mr. Big forgot to adjust his watch, so on Monday morning it was out of sync with the rest of the world. Assuming he got the email message, what time will he show up for the appointment according the adjusted clock in the accountant's office?

1. 11 AM
2. 12 noon
3. 1 PM
4. 2 PM
5. 3 PM

Which, if any, of the following count as valid and rational objections to daylight saving time, assuming it is properly implemented?

1. farmers will have to feed their animals in the dark
2. children will have to go to school before the sun rises
3. it wastes electricity
4. you lose an hour's sleep in the summer
5. it reduces crime
6. it disrupts international flight schedules
7. it's unnatural to adjust time
8. it causes health problems by messing with your circadian rhythm

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Chicago

 
I'm in Chicago with Ms. Sandwalk and another couple who we hang out with. We have a wonderful time at the art gallery, took the architectural boat tour and ate delicious deep dish pizza.

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Are You Sexually Attracted to Male Musk Deer?

 
The other day I had to get up and move to new seat on the subway. The cause of my discomfort was a young woman who reeked of musk—the scent that male musk deer (Moschus moschiferus) use to attract females. I don't know why this woman wanted attention from female musk deer but I was pretty sure she wasn't going to find any on the subway.

The main scent is due to muscone [see Monday's Molecule #127] and nowadays the muscone used in perfumes is completely artificial. But that wasn't always the case. Musk originally came from the scent glands of Asian musk deer [MUSK An Essay].

Only the mature male Moschus produces musk. The substance occurs in only one location on the deer's body: on its abdomen, just in front of its penis, is a hairy pouch known as the musk gland. This sac is about the size of a golf ball. It is composed of several layers of skin, with two openings immediately above the animal's urethra.

In the early summer, unripe liquid musk drains into the gland from the surrounding tissues, and is stored there for some weeks or months. During the course of this time, the musk - 30 grams of it or so - "matures" into a granular, waxy, reddish-brown substance with an extremely potent and familiar smell.

When the musk has ripened - shortly before the autumn rutting season - the deer begin to discharge it mixed with their urine, apparently to mark their territory and attract females. (This behavior is familiar to anyone who has come in contact with a tomcat that "sprays.") Even in winter, male musk deer have been reported to leave behind fragrant red snow, rather than yellow.

I'm told that humans of both sexes get turned on by this smell. If so, the woman on the subway is not only going to attract female musk deer but she's also going to get a lot of attention from both men and women of a different species. I guess it's a good thing that I freed up the seat next to her.

There ought to be rules about perfume, When a man or a woman is wearing too much, they should be told to go home and take a shower—with lots of unscented soap.

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Picking a Religion

 
What if you are truly confused about what you believe and which group you should belong to? Here's a handy-dandy algorithm to help you decide. I got it from Friendly Atheist.

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Richard Dawkins' View of Random Genetic Drift

The Greatest Show on Earth is Richard Dawkins' latest book. It's his eighth book on evolution: the others are The Selfish Gene (1976), The Extended Phenotype (1982), The Blind Watchmaker (1986), River Out of Eden (1995), Climbing Mount Improbable (1996), Unweaving the Rainbow (1998) and The Ancestors Tale (2004).

I'm interested in the evolution of Richard Dawkins' ideas about evolution; in particular, his ideas about random genetic drift and mechanisms of evolution other than natural selection.

In Chapter 1 Dawkins says, "All reputable biologists go on to agree that natural selection is one of its most important driving forces, although—as some biologists insist more than others—not the only one."

This looks promising. Dawkins is saying— in chapter 1—that there are two mechanisms (driving forces) of evolution. He implies that he accepts random genetic drift as a "driving force" of evolution. (Assuming that random genetic drift is what he has in mind.) It's clear that "some biologists" have influenced him, although it's not clear from the sentence whether those biologists are "reputable"!

Since this is a book about the evidence for evolution, I eagerly anticipated his explanation of random genetic drift. Would it be as good as Jerry Coyne's?¹ In fact, I was so eager that I couldn't wait. I jumped to the index to look under "random."

Nothing. Not to worry. The other important mechanism must be here somewhere. Is it indexed under "genetic"? No. What about "drift"? No, not there either.

What gives? How can you write a book about evolution in the 21st century without mentioning random genetic drift as an important mechanism of evolution? Even the other adaptationist, Jerry Coyne, has it in the index to Why Evolution Is True.

Maybe Dawkins uses another term for the second mechanism of evolution. I recalled that he often gets mixed up about the difference between neutral theory and random genetic drift. Let's see if "Neutral Theory" is in the index. Nope.

What about "Kimura"? Success at last! Check out page 332.

Page 332 is in the middle of a section on The Molecular Clock in Chapter 10. It seems a bit late to begin discussing the second mechanism of evolution, but, as I said before, it's promising that Dawkins even concedes that there is one.

Dawkins explains that the reason why there's a molecular clock is because the majority of changes at the genetic level are neutral and these changes are fixed in a regular, clock-like, albeit stochastic, process. He then goes on to say...

When the neutral theory of molecular evolution was first proposed by, among others, the great Japanese geneticist Motoo Kimura, it was controversial. Some version of it is now widely accepted and, without going into the detailed evidence here, I am going to accept it in this book. Since I have a reputation as an arch-"adaptationist" (allegedly obsessed with natural selection as the major or even only driving force of evolution) you can have some confidence that if even I support the neutral theory it is unlikely that many other biologists will oppose it!

I can't think of any serious biologists who would deny that neutral mutations exist. The essence of Neutral Theory, or Nearly Neutral Theory as it is currently called, is undoubtedly correct. The fact that Richard Dawkins accepts it in this book is not remarkable. What's remarkable is that he has to tell us that he accepts it, especially in a book about the evidence for evolution.

Meanwhile, we are still waiting for the explanation of the "other" mechanism of evolution. The one that was mentioned in Chapter 1 when he said that natural selection does not account for all of evolution. He can't have been thinking about "Neutral Theory" since that's not a mechanism of evolution. And he can't just have been thinking about a mechanism for fixing neutral mutations since he surely knows that the "other" mechanism can result in the loss of beneficial alleles and the fixation of detrimental ones.

Still waiting. What we see in Chapter 10 is an explanation of neutral mutations but no mention of random genetic drift—the mechanism responsible for fixing neutral mutations in a population. He does briefly mention on page 335 that neutral mutations can "go to fixation by chance." I get the impression that he goes out of his way to not name the other mechanism of evolution. You know what I'm referring to, it's the mechanism that gets a whole chapter to itself in all the evolutionary biology textbooks [Evolution: Table of Contents].

Dawkins concedes that the vast majority of the human genome consists of sequences that aren't genes. Here's how he puts it ...

It is a remarkable fact that the greater part (95% in the case of humans) of the genome might as well not be there, for all the difference it makes. The neutral theory applies even to many of the genes in the remaining 5%—the genes that are read and used. It applies even to genes that are totally vital for survival. I must be clear here. We are not saying that a gene to which the neutral theory applies has no effect on the body. What we are saying is that a mutant version of the gene has exactly the same effect as the unmutated version.

In other words, the vast majority of the DNA in our genome is junk. Mutations that occur in junk DNA will become fixed in spite of the fact that they are not seen by natural selection. This is what he means when he says that most mutations are neutral and it's equivalent to saying that the dominant mechanism of evolution, in terms of overall frequency, is random genetic drift and not natural selection. I just wish he'd come right out and say it.

It's a shame that Dawkins does not actually mention the mechanism by which those neutral mutations become fixed but instead continuously refers to neutral theory as the alternate mode of evolution. The general public needs to hear about random genetic drift and Dawkins is—like it or not—the most prominent evolutionist on the planet.

Dawkins has not changed his mind about the existence of these neutral mutations and he has not changed his mind about their importance. While they may exist, they are not important as far as evolution is concerned. He makes this very clear—once again—in this book.

As it happens, it is probably true to say that most mutations are neutral. They are undetectable by natural selection, but detectable by molecular geneticists; and that is an ideal combination for an evolutionary clock.

None of this is to downgrade the all-important tip of the iceberg—the minority of mutations that are not neutral. It is they that are selected, positively or negatively, in the evolution of improvements. They are the ones whose effects we actually see—and natural selection "sees" too. They are the ones whose selection gives living things their breathtaking illusion of design. But it is the rest of the iceberg—the neutral mutations which are in the majority—that concerns us when we are talking about the molecular clock.

As geological time goes by, the genome is subjected to a rain of attrition in the form of mutations. In that small portion of the genome where the mutations really matter for survival, natural selection soon gets rid of the bad ones and favors the good ones. The neutral mutations, on the other hand, simply pile up, unpunished and unnoticed—except by molecular geneticists.

This is the way the adaptationist dismisses non-adaptive evolution. It's not really of interest to real biologists. It's only interesting to molecular geneticists. And we all know that those people are not real evolutionary biologists!

Now we come to one of the most interesting sentences in the entire book; at least as far as I'm concerned. As most Sandwalk readers know, we have long debated whether or not visible mutations can be neutral. Once you have an observed phenotype, can you ever attribute it to neutrality? Many adaptationists argue that you can't.

Here's what Richard Dawkins says in his latest book.

It is also possible (although "ultra-Darwinists" like me incline against the idea) that some mutations really do change the body, but in such a way as to have no effect on survival, one way or the other.

This is progress. Back when he wrote The Extended Phenotype, in 1982, Richard Dawkins said.

The adaptationism controversy is quite different. It is concerned with whether, given that we're dealing with a phenotypic effect big enough to see and ask questions about, we should assume that it is the product of natural selection. The biochemist's "neutral mutations" are more than neutral. As far as those of us who look at gross morphology, physiology and behavior are concerned, they are not mutations at all. It was in this spirit that Maynard Smith (1976) wrote: "I interpret 'rate of evolution' as a rate of adaptive change. In this sense, the substitution of a neutral allele would not constitute evolution ..." If a whole organism biologist sees a genetically determined differences among phenotypes, he already knows he cannot be dealing with neutrality in the sense of the modern controversy among biochemical geneticists.

Finally, in 2009, Richard Dawkins admits that it is "possible" that visible mutations could be neutral. Hallelujah!

I'm looking forward to book #9.

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1. Jerry Coyne's View of Random Genetic Drift

Evolution in Action and Michael Behe's Reaction

Of the many scientists who are trying to understand evolution, Richard Lenski stands out for his experimental approach. He has maintained stocks of E. coli growing under stressful conditions for over 40,000 generations.

During that time, the cells have been forced to adapt to conditions of low carbon source (glucose) and Lenski's group has been tracking the mutations that arise. In the past, they have done a heroic job of identifying new mutations but that job has become much easier with new technology. Now that rapid genome sequencing is possible it becomes feasible to sequence the genomes of bacteria that were preserved from earlier generations and determine every single mutation that arose.

Barrick et al. (2009) have published the result from just such an experiment. They sequenced the genomes of the original, ancestral, strain and samples of a single lineage from 2,000, 5,000, 10,000, 15,000 20,000 and 40,000 generations.

This information can address a number if issues as they explain in the introduction to their paper.

Genomic changes underlie evolutionary adaptation, but mutations—even those substituted (fixed) in evolving populations—are not necessarily beneficial.Variation in the rate of genomic evolution is also subject to many influences and complications.On the one hand, theory predicts that neutral mutations should accumulate by drift at a uniform rate, albeit stochastically, provided the mutation rate is constant. On the other hand, rates of substitution of beneficial and deleterious mutations depend on selection, and hence the environment, as well as on population size and structure. Moreover, the relative proportions of substitutions that are neutral, deleterious and beneficial are usually difficult to infer given imperfect knowledge of any organism’s genetics and ecology, in the past as well as in the present.

Experiments with tractable model organisms evolving in controlled laboratory environments minimize many of these complications and uncertainties15,16. Moreover, new methods have made it feasible to sequence complete genomes from evolution experiments with bacteria. To date, such analyses have focused on finding the mutations responsible for particular adaptations. However, the application of comparative genome sequencing to experimental evolution studies also offers the opportunity to address major conceptual issues, including whether the dynamics of genomic and adaptive evolution are coupled very tightly or only loosely.

At 20K generations, there were 29 single nucleotide polymorphisms (SNP) and 16 deletions, insertions, and chromosomal rearrangements (DIP) for a total of 45 different events (see figure). Not all of these contributed to adaptation and the rapid growth phenotype but many of them did. Some were mutations that inactivated a gene and some were amino acid substitutions that change activity of an enzyme.

The authors do not report the distribution of beneficial vs neutral mutations but the data suggests that most of the 45 mutations were beneficial. The authors do not tell us how many of these beneficial mutations destroyed the activity of a gene and how many just changed the activity of a gene product but it looks like there were about equal numbers of both kinds of mutations.

Much of the paper is about adaptive vs. non-adaptive mutations. At 40,000 generations there were 627 SNP and 26 DIP mutations. The increase was due, in part, to an increase in mutation rate because of a mutation in the mutT gene. One might expect that the initial adaptation would result in selection for beneficial alleles and that neutral alleles would accumulate by random genetic drift in subsequent generations (i.e. from 20K generations to 40K generations). This is probably what happened from 20K generations to 40K generations

In the first 20K generations the strain adapted rapidly to the low glucose concentration and from then on its rate of growth under these conditions increased more slowly. This could also be explained by the initial fixation of adaptive mutations followed by fixation of non-adaptive, neutral, alleles. The authors argue convincingly that this didn't happen. Instead, almost all of the first 45 mutations were probably adaptive. Presumably, the mutations that arose later on (between 10K and 20K generations) were much less beneficial (lower selection coefficient) than the ones that first appeared in the population. This is the interesting, and controversial, part of the paper.

This is a paper that the IDiots can't ignore because it's all about evidence for evolution. It doesn't come as a big surprise that Michael Behe already has a poting on the DISCO website: New Work by Richard Lenski.

There was a time a few years ago when you could predict that the IDiots would try to discredit such a paper. The new strategy seems to be the opposite. They agree with the conclusions and offer them as support for Intelligent Design Creationism.

Here's the latest example from Behe's posting.

Despite his understandable desire to spin the results his way, Lenski’s decades-long work lines up wonderfully with what an ID person would expect — in a huge number of tries, one sees minor changes, mostly degradative, and no new complex systems. So much for the power of random mutation and natural selection. For his work in this area we should be very grateful. It gives us solid results to point to, rather than having to debate speculative scenarios.

I don't think I need to comment on such stupidity.

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Barrick, J.E., Yu, D.S., Yoon, S.H., Jeong, H., Oh, T,K., Schneider, D., Lenski, R.E., and Kim, J.F. (2009) Genome evolution and adaptation in a long-term experiment with Escherichia coli. Nature Oct 18. [Epub ahead of print] [PubMed] [doi: 10.1038/nature08480]

What Does a Skeptic Believe?

 
Jim Lippard has posted some controversial opinions about skepticism: Skepticism, belief revision, and science.

I don't have time to debate him but I know there are skeptics out there who will want to take him on. They may read Sandwalk but may not be aware of The Lippard Blog. I'm quoting part of Jim's beliefs here but I'm going to shut off comments in order to encourage you to comment on Jim's blog.

Is everything a skeptic believes something which is a conclusion reached by scientific methods?

No. Much of what we believe, we believe on the basis of testimony from other people who we trust, including our knowledge of our own names and date and place of birth, parts of our childhood history, the history of our communities and culture, and knowledge of places we haven't visited. We also have various beliefs that are not scientifically testable, such as that there is an external world that persists independently of our experience of it, that there are other minds having experiences, that certain experiences and outcomes are intrinsically or instrumentally valuable, that the future will continue to resemble the past in various predictable ways, etc. If you did believe that skeptics should only believe conclusions which are reached by scientific methods, that would be a belief that is not reached by scientific methods.

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