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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David Sloan Wilson on ScienceBlogs

 
David Sloan Wilson has joined ScienceBlogs of the SEED consortium. You can read the new version at: Evolution for Everyone.

This is going to be fun since Wilson is a strong advocate of group selection and, in addition, he is a firm opponent of the co-called "New Atheists."

Here's his opening salvo in Goodbye HuffPost, Hello ScienceBlogs: Science as a Religion that Worships Truth as its God.

Thinking of science as a religion that worships truth as it god enables me to praise its virtues and criticize its shortcomings at the same time. In my previous blogs, I have played the role of scientific reformer for two major issues. The first is the "new atheism" movement spearheaded by the so-called four horsemen: Richard Dawkins, Daniel Dennett, Samuel Harris, and Christopher Hitchens. Isn't it wonderful how scientists and rationalists reflexively adopt religious imagery? I am an atheist in the sense that I regard religion as 100% a human construction, but I'm here to testify that the "new atheists" depart from factual reality in their own way. So did Ayn Rand, the "new atheist" of her day, as we are learning to our sorrow from the collapse of the free market belief system that she helped to create. If we worry about religions for their departures from factual reality, then we should really worry about "stealth religions" that do the same thing without invoking the gods, because they do a better job of masquerading as reality. As someone who is seriously committed to studying religion from a scientific and evolutionary perspective, I'm here to say that the new atheists can't bring themselves to accept the facts about religion as a human construction. Read my six-part series on "Atheism as a Stealth Religion", now archived on my ScienceBlog site, for more. Even better, start acquainting yourself with the emerging field of evolutionary religious studies, whose members are more serious about holding each other accountable for what they say about religion.

Hmmmm ... my sympathies lie with Dawkins et al so I guess this is aimed at me. I was completely unaware of the possibility he mentions; namely, that I don't accept the facts about religion as a human construction. I'll have to think carefully about that one. Is it possible that, as an atheist, I was secretly thinking that religion might actually have been constructed by supernatural beings? Nope, I don't think so.

I was also under the impression that I was "acquainted" with the emerging field of evolutionary religious studies. After all, didn't I just post an article about Michael Persinger [Religion Makes Women Stupid?]? Perhaps David Sloan Wilson is confused about the difference between "getting acquainted" and "recognizing scientific nonsense"?

The second major issue that requires scientific reform is group selection, a theory that explains how groups can become well adapted to their environments in the same sense that individuals do. The theory of group selection began with Darwin and involves a simple set of issues that anyone can understand. Yet, it remains endlessly controversial. Next year marks the 35th anniversary of my first publication on group selection and I'm confident that the controversy will continue for decades more unless something is done. That "something" is a truth and reconciliation process, similar to the resolution of political conflicts that otherwise might continue forever. The idea that a scientific controversy might require a truth and reconciliation process similar to a political controversy speaks volumes about science as a fallible and culturally influenced process.

I don't have a dog in this fight. It will be interesting to watch and learn.

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Evolution Makes Women Stupid

 
I've been a vocal critic of evolutionary psychology and just-so stories but from time to time they might be right.

This article by Lauren Sandler combines all the right scientific arguments for why women are more stupid religious than men [Why Do More Women Than Men Still Believe in God?].

It even quotes that famous Canadian scientist, Michael Persinger, who not only built a cool helmet, but also won an award for being Ontario's best university teacher. Here's what Lauren Sandler writes.

Researchers have offered many theories about why women are religious in greater numbers than men. Most are inconclusive; all are fascinating. Some investigators locate the engine of belief in our very brain chemistry, and find the female brain far more apt to sense the divine. Canadian cognitive neuroscientist Michael Persinger, the reigning cleric of the neurology of belief, has asserted that the “experience” of God, or feeling the presence of the divine, is literally built into the brain, specifically in the limbic system or the temporal lobe. When Persinger applied magnetic fields over the temporal lobe to mimic the reaction he found in electromagnetic studies, the gender difference was “quite impressive”—that women sensed the presence of a “sentient being” in greater numbers than men.

“Belief,” Persinger told me, “relates more to how the person relates, interprets, and reconstructs the experience.” In other words, even when men and women had the same response in the brain, women were more apt to attribute it to something divine, “out of body.” Other scientists have found these limbic tendencies particularly pronounced in adolescent girls, concurrent with the final stages of brain development. As Barry Kosmin, a coauthor of the new Trinity College study says, “That's why when anybody sees the Virgin Mary, it's a couple of young girls on a mountainside in Southern Europe.” ....

Some researchers hypothesize that women are hardwired to believe because of evolutionary imperatives. Belief in God—or the Mount Olympus ensemble cast, or a phalanx of wood spirits, and so on—has long been connected with tribal ritual, and formed the center of communities. Women relied on these communities for the survival of their children, while men were off spearing buffalo, pillaging neighboring settlements—or whatever the caveman business trip furnished. The relationship between belonging and belief is an ancient one. It may have resulted in the development of certain alleles connected to a sense of God, or at least a commitment to religion.

It's not their fault that women fall for superstitious nonsense. Their brains are built differently and evolution is to blame.

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[Hat Tip: Friendly Atheist: Science or Sexism?]

Does Evolution Explain Why Some People Are Mean to Strangers?

 
Does Evolution Explain Why Some People Are Mean to Strangers? Yes, according to some researchers in an article published on the Smithsonian website. If it's published by Smithsonian, it must be right? Right?

Rob Dunn writes in: The Culture of Being Rude.

Recently a group of biologists has offered a theory that they say explains, if not tube socks, then nearly everything else. In a series of high-profile papers, Corey Fincher and Randy Thornhill, both at the University of New Mexico, and Mark Schaller and Damian Murray of the University of British Columbia argue that one factor, disease, ultimately determines much of who we are and how we behave.

Their theory is simple. Where diseases are common, individuals are mean to strangers. Strangers may carry new diseases and so one would do best to avoid them. When people avoid strangers—those outside the tribe—communication among tribes breaks down. That breakdown allows peoples, through time, to become more different.

Differences accumulate until in places with more diseases, for example Nigeria or Brazil, there are more cultures and languages. Sweden, for example, has few diseases and only 15 languages; Ghana, which is a similar size, has many diseases and 89 languages. Cultural diversity is, in this view, a consequence of disease.

Then Fincher and colleagues go even further. Where people are more xenophobic and cultures more differentiated from one another, wars are more likely. Democratic governments are less likely because the tribe or group comes first; the nation and individuals in other tribes within the nation come second. And finally, poverty becomes nearly inevitable as a consequence of poor governance, hostility between groups, and the factor that triggered this cascade in the first place—disease.

Dunn expresses some skepticism using appropriate language but he goes on to describe "data" (correlations, actually) that supports the idea. The tone of the article is quite supportive of the idea that evolution is behind this behavior.

Evolution absolutely requires genes and alleles. There no evidence to suggest that we have an allele that encourages us to avoid diseased strangers. It could be entirely cultural based on the fact that we have a large brain that's capable of reasoning.

Keep this in mind next time I'm mean to you. It may not be my genes that are making me do it. It may just be my brain and my life experience telling me that I should behave that way!

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[Hat Tip: a skeptical John Hawks]

Ode to Peter Mitchell

Everyone knows about Watson & Crick and Albert Einstein and a few other famous scientists who have discovered something new.

But few people know Peter Mitchell and why he is more important than most other scientists.

Mitchell is one of a handful of scientists who really have changed the way we think about a subject—in this case how energy is produced in living cells [see PETER MITCHELL
AND CHEMIOSMOTIC THEORY]

Nick Lane has just published an article in New Scientist that highlights Mitchell's contribution to biochemistry. Not only did Peter Mitchell show us how chemical energy is produced in living cells, he also provided tremendous insight into how it must have worked when life first began [Was our oldest ancestor a proton-powered rock? ].

Here's the opening paragraphs of Nick Lane's excellent article. You really should read the whole thing—buy the magazine if you have to.

PETER MITCHELL was an eccentric figure. For much of his career he worked in his own lab in a restored manor house in Cornwall in the UK, his research funded in part by a herd of dairy cows. His ideas about the most basic process of life - how it gets energy - seemed ridiculous to his fellow biologists.

"I remember thinking to myself that I would bet anything that [it] didn't work that way," biochemist Leslie Orgel wrote of his meeting with Mitchell half a century ago. "Not since Darwin and Wallace has biology come up with an idea as counter-intuitive as those of, say, Einstein, Heisenberg and Schrödinger."

Over the following decades, however, it became clear that Mitchell was right. His vindication was complete when he won a Nobel prize in 1978. Even today, though, most biologists have yet to grasp the full implications of his revolutionary ideas - especially for the origin of life.

I wish this weren't so but I'm afraid the last statement is correct. It's not only biologists who fail to grasp the implications, there are even biochemists who don't understand chemiosmotic theory and don't teach it correctly in undergraduate courses.

Some of the most popular biochemistry textbooks didn't explain it properly until their most recent editions in 2006 and 2007. That's shocking.

Peter Mitchell deserves a lot more credit than he gets.

The molecule shown above is ubiquinone:cytochrome c oxidoreductase, also known as complex III [PDB 1PP9]. It is one of the most important enzymes in all of biology. It's structure provided the ultimate proof of chemiosmotic theory since it catalyzes the Q cycle, the key step in creating a proton gradient across a membrane [see Ubiquinone and the Proton Pump].

Every student who takes an introductory biochemistry course should be intimately familiar with this enzyme and how it works. In fact, if they're not, you can be sure that the biochemistry course was not taught properly.

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Monday's Molecule #141: Winner

 
The molecule is cholic acid, which usually exists as sodium cholate. It's one of the major bile acids in mammals. The bile acids help solubilize lipids during digestion.

The Nobel Laureate is Heinrich Otto Wieland who received the prize for his work on the structure and function of bile acids.

This week's winner is Alex Ling of the University of Toronto. There were quite a few people who got the right answer and this was a surprise to me. Lipids are not the kind of molecules that excite me and I was not expecting that so many of you would recognize cholic acid.

There were winners from four continents. I think that's a first. Readers in Africa and South America are going to have to get try harder if we're ever going to set a six continent record. (As far as I know, there are no Sandwalk readers in Antarctica.

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Identify this molecule. Be as specific as possible. Briefly describe what it does.

There's a Nobel Prize connected to this molecule. The prize was for identifying it and working out its structure, and the structure of many derivatives.

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: Ben Morgan of the University of North Carolina at Chapel Hill, 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, and Dima Klenchin of the University of Wisconsin, Madison.

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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Monday's Molecule #141

 
Identify this molecule. Be as specific as possible. Briefly describe what it does.

There's a Nobel Prize connected to this molecule. The prize was for identifying it and working out its structure, and the structure of many derivatives.

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: Ben Morgan of the University of North Carolina at Chapel Hill, 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, and Dima Klenchin of the University of Wisconsin, Madison.

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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What's the Connection between Hpa II and CpG Islands?

 
Epigenetics is all the rage today but the idea that gene expression could be regulated by modifying DNA and/or chromatin has been around for three decades.

Methylation is one of the ways that DNA can be modified and methylation at specific sites can be heritable. This observation grew out of studies on restriction/modification systems where DNA is protected from the action of restriction endonucleases by methylating the bases.

I didn't realize that the study of restriction enzymes led to the discovery of methylated regions of eukaryotic DNA. Find out how by reading an interview with Adrian Bird in PLoS Genetics: On the Track of DNA Methylation: An Interview with Adrian Bird.

This is also a good example of chance and serendipity in science. You can't plan for this stuff to happen—but that doesn't prevent politicians and administrators from trying.

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