Methodological Naturalism - How Not to Attack Intelligent Design Creationism

My philosopher friends from Ghent have published their paper ...

Boudry, M., Blancke, S., and Braeckman, J. (2010) How Not to Attack Intelligent Design Creationism: Philosophical Misconceptions About Methodological Naturalism. Foundations of Science doi:10.1007/s10699-010-9178-7.

Abstract
In recent controversies about Intelligent Design Creationism (IDC), the principle of methodological naturalism (MN) has played an important role. In this paper, an often neglected distinction is made between two different conceptions of MN, each with its respective rationale and with a different view on the proper role of MN in science. According to one popular conception, MN is a self-imposed or intrinsic limitation of science, which means that science is simply not equipped to deal with claims of the supernatural (Intrinsic MN or IMN). Alternatively, we will defend MN as a provisory and empirically grounded attitude of scientists, which is justified in virtue of the consistent success of naturalistic explanations and the lack of success of supernatural explanations in the history of science (Provisory MN or PMN). Science does have a bearing on supernatural hypotheses, and its verdict is uniformly negative. We will discuss five arguments that have been proposed in support of IMN: the argument from the definition of science, the argument from lawful regularity, the science stopper argument, the argument from procedural necessity, and the testability argument. We conclude that IMN, because of its philosophical flaws, proves to be an ill-advised strategy to counter the claims of IDC. Evolutionary scientists are on firmer ground if they discard supernatural explanations on purely evidential grounds, instead of ruling them out by philosophical fiat.

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If I Had a Billion Dollars: the Video

 
Go to Jennifer's blog and see the video. It's fantastic.

If I Had a Billion Dollars - The Video!

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If I Had a Billion Dollars

 
Stephen Harper and his cronies have spent over one billion dollars preparing for the G8 and G20 meetings in Canada this month. That's a lot of money. The city of Toronto will be pretty much shut down from June 24 to June 27. The University of Toronto will be closed on the 24th and 26th and all activities are canceled on the 21st, 22nd, and 23rd.

Here's The Bare Naked Ladies singing "If I had a million dollars" (With many interruptions). Go to Jennifer Smith's blog Runesmith's Canadian Content to see the new lyrics for [If I Had a Billion Dollars].

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Jonathan Wells Weighs in on Alternative Splicing

You can read his contribution at Evolution News & Views (sic): The Fact-Free “Science” of Matheson, Hunt and Moran: Ridicule Instead of Reason, Authority Instead of Evidence.

What I find so interesting is the willingness of Wells and Sternberg to believe whatever they find in the scientific literature. (Yeah, right.) In this case, they've found a few papers claiming that the vast majority of human genes exhibit alternative splicing. They claim this refutes the idea that introns are mostly junk.¹

Do they really believe everything that's published in the scientific literature? I don't think so. They are very selective in what they believe. They only believe the papers that criticize evolution or support their belief in intelligent design. That's why they have no credibility. That's why they deserve ridicule. That's why reasoning with an Intelligent Design Creationist is a waste of time.

Don't believe me? Try reading Icons of Evolution by Jonathan Wells. It's the example we use in my course to illustrate how NOT to do science.

Here's Wells standing up for his friend ...

So why are Matheson and Moran so sure that huge portions of introns don’t have functions? According to Matheson, it’s because “Larry Moran and I clearly know a whole lot more about molecular genetics” than Sternberg.

A more naked appeal to authority would be hard to find. It sounds like an undergraduate trying to score points in a late-night bull session (“I know all about that; I took a course in it…”), not a college professor engaged in a scientific debate.

But Matheson didn’t stop there. He demeaned Sternberg by calling him “poor Richard.” He also claimed that Sternberg is “disastrously clueless” because he doesn’t understand “the important and very basic distinction between a transcript and an intron.” Since every undergraduate biology student learns that an intron is a segment of DNA, while a transcript is a segment of RNA encoded by DNA, this last jibe is on a par with Moran’s insult that Sternberg can’t do elementary arithmetic. And it is equally unjustified.

Here's what undergraduates learn when they read what I wrote in my textbook. Maybe I should send copies to Wells and Sternberg?

Internal sequences that are removed from the primary RNA transcript are called introns. Sequences that are present in the primary transcript and in the mature RNA molecule are called exons. The words intron and exon also refer to the regions of the gene (DNA) that encode corresponding RNA introns and exons. Since DNA introns are transcribed, they are considered part of the gene.

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1. I'm ignoring the fact that Sternberg's calculation assumed that every intron in a gene must be alternatively spliced. That assumption is/was not based on anything in the scientific literature but it's unlikely that Sternberg will admit his error.

Watch This Movie

 
PZ Myers want to see Agora [I want to see this movie]. So do I. Here's the website [Agora] and here's the synopsis.

A historical drama set in Roman Egypt, concerning a slave who turns to the rising tide of Christianity in the hopes of pursuing freedom while also falling in love with his master, the famous female philosophy professor and atheist Hypatia of Alexandria.

I hear that the producers are having trouble getting widespread distribution in America. I wonder why? It's a movie about an atheist woman standing up to a Christian mob hell bent on destroying Alexandria and the library.

What's wrong with that? Sounds like Texas, or parts of Alberta.

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The Academic Discipline of Science & Religion Studies

 
Joshua Rosenau thinks that science and religion are different ways of knowing. This means that, at some level, they can't conflict. I'm a skeptic and a scientist. I want some evidence before accepting that religion offers a valid way of knowing the truth. Please give me an example of some kind of "knowing" that religion offers. Be prepared to explain why millions of atheists can get along just fine without this way of knowing. It certainly seems as though the religious way of "knowing" is completely dispensable.

While you're at it, please explain why different religions arrive at different conclusions. If religion is a valid way of knowing, then why don't all religions arrive at the same conclusions about, say, the divinity of Jesus, or the morality of abortion, or how the universe originated? If only some religions have a lock on valid ways of knowing about truth, then which ones are correct?

Josh's latest foray into this minefield is over the composition of the Science & Faith panel at the World Science Festival [A fair point]. He says, ...

In the field of science/religion studies, there's a consensus statement that's been widely circulated and agreed to, and it states: "in most instances, biology and religion operate at different and non-competing levels… natural theology may be a legitimate enterprise in its own right, but we resist the insistence of intelligent-design advocates that their enterprise be taken as genuine science - just as we oppose efforts of others to elevate science into a comprehensive world view (so-called scientism)." The New Atheists reject this consensus, as they are entitled to do. But they reject it without going through the academic literature of the relevant field, preferring pop-culture books to academic engagement.

There's so much wrong with that statement that it's hard to know where to begin. Let me just mention two problems before moving on to a third one.

1. Atheists don't believe in supernatural beings. They have not been convinced by any of the arguments offered up by religious scholars or passionate friends and relatives. This does not mean they "elevate science into a comprehensive world view (so-called scientism)." Speaking as one of those atheists, if anyone wants to argue for another valid way of knowing (other than science) then I'm more than happy to pay attention. Just don't ask me to make the assumption that supernatural beings exist. You have to convince me of that first.


2. There are perfectly valid, rational, objections to accommodationism. Josh insults all of us by saying that we don't read the academic literature. That's just not true and I expect an apology.

Finally, let's look at the so-called "consensus" view that Josh quotes. He provides a link to its source—it's the International Society for Science & Religion's Statement on the Concept of 'Intelligent Design'.

Who is this group and why should their statement be considered the consensus view in studying the possible conflicts between science and religion? Looking at their website, I find this statement about their purpose.

Our central aim is the facilitation of dialogue between the two academic disciplines of science and religion, one of the most important current areas of debate in terms of understanding the nature of humanity. This includes both the enhancement of the profile of the science-religion interface in the public eye, as well as the safeguarding of the quality and rigour of the debate in the more formal, academic arena.

Interesting. I wonder how many members are atheists and how many think that science and religion are in conflict? After all, one of the hallmarks of a true academic discipline is that it welcomes all points of view.

What do they have to say about membership?

While maintaining rigorous qualifications for membership (membership is through nomination by existing members only) the Society has now grown to over 140 members, including many of the leading scholars in the science and religion field. Indeed the last two presidents, George Ellis, a theoretical cosmologist and Professor of Applied Mathematics at the University of Cape Town, and John Polkinghorne, are both recipients of the Templeton Prize for Progress Toward Research or Discoveries about Spiritual Realities - the world's best-known religion prize, awarded each year to a living person to encourage and honour those who advance spiritual matters.

Membership of the society is truly universal: the society incorporates, and welcomes, representatives from a variety of faith traditions including Buddhism, Hinduism, Judaism, and Islam in addition to Christianity. Membership is also widely distributed geographically, with representatives from countries as diverse as South Korea, India, Australia, New Zealand and South Africa as well as from Europe and America.

Now I get it. It's a group of accommodationists. No wonder Josh thinks this is the consensus view in the field. No wonder he accuses atheists of being ignorant because they disagree with the "consensus" view of the International Society for Science & Religion.

Is this what passes for an true academic discipline in the eyes of accommodationists? No wonder we have trouble communicating.

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What Is Scientific Literacy?

 
Neil deGrasse Tyson explains it as well as anyone could. Hint: it's not about knowing the names of the planets, the valence of oxygen, or the enzymes of glycolysis.

Chad Orzel is as excited about this video as I am—and for the same reason [Neil deGrasse Tyson Agrees With Me About The Innumeracy of Intellectuals]. It's bad enough that so many people are scientifically illiterate but even worse is the fact that many of our so-called "intellectuals" are actually proud of the fact that they are stupid about mathematics and science. Last year I went to a conference on The Two Cultures where many people were trying to convince me that the problem was solved. They were wrong and I'm glad to see that Tyson agrees.

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Creationist Fairy Tales

 
Cornelius Hunter has a Ph.D. in Biophysics and Computational Biology.¹ He's an adjunct Professor at Biola University where, presumably, he teaches undergraduates.

Dr. Hunter has recently learned about transposons and this promoted him to write something on his blog, Darwin's God [Retrotransposons are not Free].

Transposons, as most of you know, are bits of selfish DNA than insert themselves into genomes. There are several different kinds of transposons but Hunter concentrates on retrotranspsons in his example. Most of the time when transposons insert themselves into a genome they cause problems because they disrupt a gene. The exceptions are those species with large genomes containing lots of junk DNA where the insertions are usually harmless.

Every now and then, a transposon will insert near, or within, a gene causing a mutation that may become beneficial. This is what caught Hunter's attention.

Consider the retrotransposons that, in addition to its promoter sequence that helps initiate the copying of its DNA into an single-stranded RNA molecule, carries its own handy reverse transcriptase gene which encodes the protein machine that copies the RNA back into a DNA molecule, for later insertion into the genome. This can certainly cause biological variation, but it is anything but free.

With evolution we must believe that so many of the sophisticated biological variation mechanisms, such as in retrotransposons, were produced by evolution. Do you see the problem? In this circular tale that even Hans Christian Andersen could never have imagined, evolution produces the intricate mechanisms that produce evolution.

Evolutionists insist that there is no problem because none of this is impossible. Why can’t evolution produce mechanisms that produce evolution? Unless one can prove this is impossible, evolution wins (an argument that goes back to the sage of Kent himself). Though the evidence fails to prove evolution, it nonetheless must be a fact. In this Alice-in-Wonderland world, that which is not false is a fact (if it is evolution, that is).

Does this sound like a fairy tale. Yes, it does. The scary part of Hunter's fairy tale is that so many people will believe it, including his students. That's more like the Grimm brothers than Hans Christian Anderson.

Seriously, there's an interesting problem here. We often make fun of the stupidity of creationists like Hunter and Richard Sternberg because they are clearly out of their depth when they write about biology and evolution. But why are their fellow creationists so silent? If it were an evolutionist writing such nonsense we would be just as critical—in fact the blogs are full of such critical debate about science.

Why aren't there any intelligent creationists who speak out against the fairy tales that permeate their blogs and their publications? Is it because there aren't any intelligent creationists? Or, is it because they are extremely reluctant to criticize their own kind? Don't they realize that their cause is being damaged by propagating nonsense?

Maybe they're not worried because they know their audience.

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1. He can't be a very good creationist because, as far as I know, he has only one Ph.D.

IDiots Do Arithmetic a Second Time - Same Result

Yesterday I wrote an article about Richard Sternberg and his lack of knowledge of molecular biology. I also took a swipe at his poor arithmetic skills, based on his misunderstanding of biology [Creationists, Introns, and Fairly Tales]. Read the comments to see why we still refer to Intelligent Design Creationists as IDiots.

Imagine my surprise when Sternberg responded with a "correction"! [Let's Do the Math Again].

Earlier today I criticized Calvin College biologist Steve Matheson’s incorrect view of “junk” DNA. Matheson had argued in February that the human genome contains about 190,000 introns (stretches of non-protein-coding DNA that interrupt protein-coding genes), of which “only a handful” had important functional roles. “How many? Oh, probably a dozen,” he wrote, “but let's be really generous. Let's say that a hundred introns in the human genome are known to have ‘important functional roles.’ Oh fine, let's make it a thousand.”

On the contrary, I pointed out that at least 90% of genes are alternatively spliced, meaning that 0.9 x 190,000 = 171,000 introns are involved in alternative splicing, an essential process that helps to ensure that the proper proteins are made at the correct developmental stage and in the appropriate cells and tissues.

Along comes University of Toronto biochemist Larry Moran, an outspoken Darwinist who hates the Center for Science and Culture so much he would probably heap abuse on us for saying that the Earth goes around the Sun. Sure enough, Moran wasted no time jumping on me for being an “Intelligent Design Creationist.” He posted the relevant portion of my critique and concluded: “It's up to you, dear readers, to figure out all the things wrong with this explanation. You can start with the math. Arithmetic isn't one of their strong points.”

A few minor corrections ...

1. I am not a Darwinist [Why I'm Not a Darwinist]
2. I don't hate the Center for Science and Culture. I mock it. It's a joke.
3. Richard Sternberg supports intelligent design and be believes in a creator who used intelligent design to create life. Therefore, he is an Intelligent Design Creationist.

So let’s do the math. Again. I will make the task easy for everyone—even Moran and Matheson:

Step 1. There are ~25,000 protein-coding genes in the human genome.
Step 2. There are 190,000 introns/25,000 protein-coding genes = 7.6 introns/gene on average.
Step 3. Ninety percent (possibly more) of gene transcripts undergo alternative splicing. Hence, 0.9 x 25,000 = 22,500 genes (actually, their RNAs) undergo alternative splicing.

Therefore, 22,500 genes x 7.6 introns/gene = 171,000 introns involved in alternative splicing.

This is just a rough estimate, of course. And as I wrote in my original critique of Matheson, even if I’m off by a factor of two we are still left with far more functional introns than Matheson acknowledges. This compels me to ask Steve Matheson: How exactly did you come up with your estimates? And what about you, Larry Moran? What sort of arithmetic are you using?

I'm using arithmetic that's based on an understanding of basic molecular biology and the scientific literature.

We could quibble about the number of introns—I think it's closer to 150,000. We could quibble about the number of protein encoding genes—the most accurate number is 20,500. We could quibble about how many genes exhibit alternative splicing—I think it's about 5%, not 95%. You can't be expected to know the facts and the controversies since this is way outside your area of expertise.

So, let's assume your facts are correct. If 90% of genes exhibit alternative splicing then this means 22,500 genes. You got that calculation right. The minimum number of introns that must be involved in alternative splicing is one (1) per gene. That means at least 22,500 introns involved in alternative splicing. You made the mistaken (and stupid) assumption that every intron in a gene had to be alternatively spliced.

The fact that you repeated this false assumption, even after being warned, does not enhance your credibility. I conclude that you don't understand RNA processing or alternative splicing. In spite of your ignorance you wrote up a posting attacking Steve Matheson and defending your colleague Steve Meyer. That's why we call you IDiots.

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Creationists, Introns, and Fairly Tales

Richard Sternberg thinks that introns are important. He has to think that way because he's an Intelligent Design Creationist and the idea that introns could be mostly junk and not have a function isn't part of his faith [Matheson’s Intron Fairy Tale].

The segments of our DNA that are commonly called "genes" consist of protein-coding exons and non-protein-coding introns. Initially, the entire DNA segment is transcribed into RNA, but between ninety and ninety-five percent of the initial RNAs are "alternatively spliced."

What is alternative splicing? Imagine that the initial RNA derived from its DNA template has the organization A—B—C—D—E—F, where the letters represent blocks that specify amino acid sequences and the dashes in between the letters stand for introns. Alternative splicing enables multiple proteins to be constructed given the same RNA precursor, say, ABCDF, ACDEF, BCDEF, and so forth. In this way, hundreds or thousands of proteins can be derived from a single gene.

There’s more. The messenger RNAs that are produced by this process—and therefore the proteins that are made in a cell—are generated in a way that depends on the stage of development as well as the cell and tissue type. In the above example, a nerve cell may express the ACDEF version of a messenger RNA whereas a pancreatic cell may produce only the BCDE version. The differences are biologically essential.

What does this have to with introns? Everything. It is the presence of introns that makes this permutative expansion of messenger RNAs possible in the first place.

So let’s do the math. At least ninety percent of gene transcripts undergo alternative splicing, and there are at least 190,000 introns in the human genome. That means we have at least 0.90 x 190,000 = 171,000 introns that participate in the alternative-splicing pathway(s) available to a cell.

It's up to you, dear readers, to figure out all the things wrong with this explanation. You can start with the math. Arithmetic isn't one of their strong points. Or maybe it's an understanding of biology that's the real weak point?

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Accommodationism and Controversy

 
The accommodationists are sometimes accused of wanting to silence their opponents. They don't like the idea of vocal atheists advocating that science and religion are incompatible. This is offensive to people of religion and it may turn off allies in the fight against fundamentalist creationism. (Theistic evolution shouldn't be attacked.)

The World Science Festival is sponsoring an event on Faith and Science this Saturday. One of the sponsors is The Templeton Foundation.

For all their historical tensions, scientists and religious scholars from a wide variety of faiths ponder many similar questions—how did the universe begin? How might it end? What is the origin of matter, energy, and life? The modes of inquiry and standards for judging progress are, to be sure, very different. But is there a common ground to be found? ABC News’ Bill Blakemore moderates a panel that includes evolutionary geneticist Francisco Ayala, astrobiologist Paul Davies, Biblical scholar Elaine Pagels and Buddhist scholar Thupten Jinpa. These leading thinkers who come at these issues from a range of perspectives will address the evolving relationship between science and faith.

One of the missing "perspectives" is the idea that science and religion are not compatible. Sean Carroll (Cosmic Variance) and Jerry Coyne (Why Evolution Is True) both think this panel is a silly idea because that perspective will not be represented. They are correct. This is a "World Science Festival"—you should not take it as a given that supernatural beings exist in order to have a discussion about the compatibility of faith and science. It's called begging the question.

You might think that defending such a panel would be a tricky problem for an accommodationist. After all, I assume they are as interested as I am in getting at the truth. Not so. Chad Orzel at Uncertain Principles [Extremists Aren't Interesting] and Josh Rosenau at Thoughts from Kansas [Talking Sense] take the same position. Non-accommodationist atheists shouldn't be allowed on the panel because they are extremists who can't discuss anything calmly and rationally.

Francis Ayala is only one of many scientists who have strong opinions about the compatibility of science and religion. Others are Ken Miller and Francis Collins. For some reason, their strong opinions aren't viewed in the same light as the strong opinions of those who think science and religion are in conflict. For some reason, the accommodationists think that it's okay for people with strong opinions about their faith to have a platform but it would be disruptive to allow the other side to have a say. Does that make sense?

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The Mutationism Myth, IV: Mendelian Heterodoxies

This is the sixth in a series of postings by guest blogger, Arlin Stoltzfus. You can read the introduction to the series at: Introduction to "The Curious Disconnect". The first part is at: The "Mutationism" Myth I. The Monk's Lost Code and the Great Confusion. The second installment is: Theory vs Theory. The third part is: The Mutationism Myth, II. Revolution. The fourth installment is: The Mutationism Myth: III Foundations of Evolutionary Genetics.

There are many ways in which the so-called "Modern" Synthesis has to be revised and extended. One of them is to reinstate the concept of mutationism which was purged from evolutionary theory in the 1940s. If you want to understand why this is important then these articles are the place to start.

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The Curious Disconnect

Last month, we debunked the Mutationism Myth and learned why the discovery of genetics in 1900 led "Mendelians" to reject Darwin's view. These same Mendelians went on to lay the foundations of a genetics-based view of evolution, during a period of rapid innovation from 1900 to 1915. But this begs another question: if the Mendelians invented the 20th-century consensus, and just left it to others to work out the math, why aren't they lauded as "founders" of modern neo-Darwinism, instead of being derided as fools? We'll find out in part 4 (today), and part 5, here on on The Curious Disconnect (credits).

The Mutationism Myth, part 4. Mendelian Heterodoxies

The reader who has been following our story so far may be baffled. As we found out in part 3, the Mendelians understood how to conceptualize a population as a dynamic system of allele and genotype frequencies (the Bateson-Saunders equilibrium), how to see evolutionary change as a probabilistic 2-step process of the introduction and acceptance-or-rejection of mutations, and how to think about selection-driven changes in a quantitative trait.

Why don't the Mendelians get credit for laying the foundations of the 20th-century consensus?

As we will learn today and in part 5, the Mendelian view is not the 20th-century "neo-Darwinian" consensus. The Mendelians combined genetics with selection. By contrast, the 20th-century consensus combines genetics with Darwinism, i.e., the Modern Synthesis invokes the principles of genetics to prop up 19-century doctrines of Darwin and his followers, such as natura non facit salta, the creativity of selection, the idea of evolution as a process of adaptive adjustment initiated by changed conditions, and the notion that the course or direction of evolution is determined by selection but not by "random" variation.

When I mock the Modern Synthesis for its Darwinian excesses, I don't want to give the impression that its wrong for a theory₁ to go beyond what is demanded by the facts. All theories₁ must go beyond the facts, taking risks. While most theories, it seems, take risks in the service of conceptual simplicity, the Modern Synthesis takes risks in the service of 19th-century Darwinian doctrines. On the basis of these commitments, e.g., its rejection of the "lucky mutant" view necessary to understand molecular evolution, the Modern Synthesis later failed.

But that's getting ahead of ourselves. Our task right now is to begin sorting out why the Modern Synthesis is Darwinian, while the Mendelian view it replaced was not.

"Mutationism" vs the Mendelian "view"

My understanding of the evolutionary views of "Mendelians" is based on the works of Bateson (1894, 1900, 1902, 1909), Johannsen (1903, 1909), de Vries (1905), Morgan (1903, 1916, 1925, 1932), Punnett (1911), Vavilov (1922), Shull (1936) and, with some reservations, Goldschmidt (1940). Every time I research the Mendelians, I find new material and revise my views, e.g., I am resolving more and more to avoid the label "mutationism", which I see increasingly as a pejorative term preferred by opponents rather than supporters.

I also have come to understand more confidently that, while the Mendelians had much to say about evolution— indeed, many of them were motivated to study heredity precisely because of their interest in evolution—, they didn't have a unified "view". With the exception of de Vries, the Mendelians did not propose what we would call "a theory of evolution", i.e., a Grand Unified Theory₁ of Evolution (GUTE) that purports to be comprehensive. Instead they argued that we need to rethink how evolution works, and follow the implications of genetics wherever they led— typically away from a more Darwinian view emphasizing infinitesimalism, determinism, and selective control.

Thus, while "Mendelism" (in contrast to "mutationism") does not sound like a very good name for a theory of evolution, that's ok, because it's not: Mendelism is a theory of genetics, and the "Mendelian view of evolution" is simply what the early Mendelian geneticists thought about evolution.

Recognizing the lack of a Mendelian GUTE helps us to appreciate more fully the role of the "Modern Synthesis" in the development of evolutionary thinking, and in the Mutationism Story. In the 19th century, before the discovery of genetics, scientists divided their allegiance among multiple GUTEs, most importantly, Darwinism and Lamarckism. By 1910, it was clear to leading thinkers that genetics had undermined all 19th-century GUTEs (including de Vries's "MutationsTheorie" ¹). The geneticists (for whatever reason) did not fill this gap by proposing a new GUTE. Thus, while the Mendelian era from 1900 to 1930 was not a stagnant period, it may be seen as a GUTE-less period that ended with the rise of the Modern Synthesis.²

Initiative

The view that events of mutation initiate evolutionary change contrasts with the view that evolutionary change is a series of adjustments or responses to external stimuli, as in the views of Buffon or Darwin. Punnett writes:

"With the advent of heredity as a definite science we have been led to revise our views as to the nature of variation, and consequently in some respects as to the trend of evolution. Heritable variation has a definite basis in the gamete, and it is to the gamete, therefore, not to the individual, that we must look for the initiation of this process. Somewhere or other in the course of their production is added or removed the factor upon whose removal or addition the new variation owes its existence." (p. 141)

Variation (mutation) is the locale of evolutionary initiative, to the extent that both 1) the possibilities or directions of future evolutionary change are established at the moment of the mutation (i.e., mutation as a source of creativity or direction, as addressed below); and 2) the dynamics of evolutionary change depend on the times of appearance of mutations. This second sense depends somewhat on the "new mutations" conception of evolution as a 2-step process of the introduction of a variant followed by its acceptance or rejection.

In this view, one may expect that the dynamics of evolution (adaptive or not) will depend on mutation rates. In fact, the Mendelians sometimes recognized this kinetic dependence, as when Shull (1936, p. 140) argues, "a gene produced twice by mutation has twice as good a chance to survive as if produced only once" (see also Morgan 1925, p. 142). This non-Darwinian idea that propensities of variation could make an evolutionary change more or less likely was not a new thought (indeed it was understood as the potential mechanistic basis of "orthogenesis"), but now it could be given a more precise interpretation.

The architects of the Modern Synthesis later ridiculed what they called the "lucky mutant" view (Mayr 1963, p. 101), but it was hardly an unsophisticated appeal to chance, as we saw in part 3 with the quotation illustrating Morgan's stunning grasp of the probability of acceptance of new mutations. Punnett made a similar statement in his 1911 book (online source):

"The new variation springs into being by a sudden step, not by a process of gradual and almost imperceptible augmentation. It is not continuous but discontinuous, because it is based upon the presence or absence of some definite factor or factors— upon discontinuity in the gametes from which it sprang. Once formed, its continued existence is subject to the arbitrament of natural selection. If of value in the struggle for existence[,] natural selection will decide that those who possess it shall have a better chance of survival and of leaving offspring than those who do not possess it. If it is harmful to the individual[,] natural selection will soon bring about its elimination. But if the new variation is neither harmful nor useful[,] there seems no reason why it should not persist."

By rejecting this component of the Mendelian view of evolution, the Modern Synthesis disallowed a direct link between the rate of mutation and the rate of evolution, making the theory incompatible with the results of studies of "molecular evolution" that began to emerge a half-century after the insights of Punnett and Morgan.

Discontinuity

To understand the issue of discontinuity or discreteness, again we must distinguish 2 senses. In the passage quoted above from Punnett, it's clear that Punnett is talking about what we might call a "mechanistically" discontinuous change in the sense that the mutant factor comes into existence at a specific point in time, due to an event of mutation, rather than gradually, due to an ongoing process of "imperceptible augmentation".

Mayr and others frequently misinterpret the Mendelian commitment to mechanistic discontinuity as a commitment to dramatic phenotypic saltations, but this is a different issue entirely.

In fact, the Mendelians entertained a range of views on the sizes of evolutionary changes important in evolution, excluding only the Darwinian extreme of relying wholly on "insensible" or "infinitesimal" changes. De Vries adopted an antithetical position emphasizing dramatic changes that create new species (with intra-specific variation and selection playing only a minor role). Bateson challenged

"the crude belief that living beings are plastic conglomerates of miscellaneous attributes . . . and that by Variation any of these attributes may be subtracted or any other attribute added in indefinite proportion" (Bateson 1894, p. 80)

Bateson's view was that, if we wish to understand evolution, we must move beyond speculative reconstructions of past events based on assuming variability and then assuming some adaptive rationale, and start studying what variations actually tend to occur. In pursuit of a less speculative approach to evolution, Bateson traveled the world to catalog 886 cases of discontinuous variation, published in his volume "Materials for the Study of Variation" (Bateson 1894); he planned a second volume on continuous variation but never completed it. Morgan argued that "even the smallest changes that add to or subtract from a part in the smallest measurable degree" may arise by mutation, and these are "the most probable variants that make a theory of evolution possible" (Morgan 1925, p. 129).

Both senses of "discontinuity" represent departures from late-19th-century and 20th-century versions of Darwinism. The mechanistically discretized view of the mutationists clashed with the incipient Modern Synthesis view in Punnett's (1930) Nature review of Fisher's The Genetical Theory of Natural Selection:

Throughout the book one gets the impression that Dr. Fisher views the evolutionary process as a very gradual, almost impalpable one, in spite of the discontinuous basis upon which it works. Perhaps this is because he regards a given population as an entity with its own peculiar properties as such, whereas for the geneticist it is a collection of individuals.

Much of the neo-Darwinian antipathy to "mutationists" was based on a negative reaction to the "saltationism" of de Vries and Goldschmidt, even though their views do not represent a shared commitment of the Mendelians. However, the mere fact that the Mendelians allowed some large changes distinguished them from the Darwinian view that "Natural selection can act only by the preservation and accumulation of infinitesimally small inherited modifications" (Darwin, Ch. 4, Origin of Species).

Creativity

The mutationists held that "the function of natural selection is selection and not creation. It has nothing to do with the formation of new variation" (Punnett 1911). Likewise, Bateson (1909) writes:

"we must relegate Selection to its proper place. Selection permits the viable to continue and decides that the nonviable shall perish; just as the temperature of our atmosphere decides that no liquid carbon shall be found on the face of the earth: but we do not suppose that the form of the diamond has been gradually achieved by a process of Selection. So again, as the course of descent branches in the successive generations, Selection determines along which branch Evolution shall proceed, but it does not decide what novelties that branch shall bring forth."

The creativity of mutation or, more properly, of mutation-and-altered-development (Stoltzfus, 2006), may be illustrated (in the extreme case) by Goldschmidt's concept of a "macromutation", akin to Galton's concept (invoked repeatedly by Bateson, 1894) of a shift between "positions of organic stability". If a variant toad arises with fully formed eyes in the roof of its mouth, such that it must open its mouth to see— as in the actual toad pictured on p. 97 of Dawkins (1996)— this is an extreme yet coordinated change, and a "macromutation" if it is heritable. If such a variant supplants the parental form or becomes a separate species, this is a non-Darwinian, saltational change in which creativity is due largely to mutation-and-altered-development. In the case of less dramatic transformations, the creative role of mutation-and-altered-development is correspondingly less dramatic.

In spite of Goldschmidt's notorious belief that distinctive phenotypic transformations suggested major genetic reorganizations ("systemic mutations"), he insisted that the complexity of the underlying genetic change is not the decisive issue:

It does not make any difference whether a single macroevolutionary step is caused by a major change within the chromosomal pattern, [that is,] a systemic mutation, or by a special kind of gene mutation with generalized effect, if such is imaginable. The decisive point is the single change which affects the entire reaction system of the developing organism simultaneously, as opposed to a slow accumulation of small additive changes. (Goldschmidt 1940, p. 251)

The claim that selection is creative is one of the key claims of Darwinism, advanced and defended by supporters of Darwinism, and rejected by its critics, as Gould (1977) documents extensively. We see this argument arising again and again up to the present day, e.g., the authors of a recent "evo-devo" book echo the century-old rhetoric of Mendelians, claiming that selection is not creative and is merely a "sieve" (Kirschner and Gerhardt, 2005), and in response (in the Nature review of this book), a dyed-in-the-wool Darwinist defends the ancient orthodoxy that selection is creative (Charlesworth, 2005). Later on, we will devote an entire post (probably more than one) to the Darwinian doctrine of selective creativity, and its relation to the Darwinian doctrine known as "gradualism".

Directionality

On a one-dimensional scale of fitness or adaptedness, every change is either "up" (beneficial) or "down" (deleterious), but in a multi-dimensional space of phenotypes, every change has a distinctive direction.

Punnett invoked mutation as a source of direction in considering features such as lepidopteran wing patterns (Punnett 1911, p. 145). A more typical statement was to draw a contrast with the views of Weissman, Fisher, and others who imagine variation in all directions. For instance, in the book review cited earlier, Punnett (1930) chides Fisher for denying to mutations "any importance in determining the direction of evolutionary change"; likewise Shull takes aim at Fisher's view:

"To assert, as Fisher does, that mutation has nothing to do with the direction of evolution is like assuming that a tetrahedron may fall, at different times, with ten or a hundred points uppermost. The ten points and ten opposite sides to fall upon do not exist. How great a restriction is placed upon the course of evolution by the inability of genes to mutate in certain ways it is impossible to tell; but it may easily be much greater than any of us suppose." (Shull, 1936, p. 448)

A clearer Mendelian concept of the influence of mutation emerges in regard to parallel evolution, which was assumed to indicate non-random tendencies of variation, since "it strains one's faith in the laws of chance to imagine that identical changes should crop out again and again if the possibilities are endless and the probabilities equal" (Shull 1935, p. 448). Vavilov noted that the same varieties or polymorphisms often occur in parallel, even in distantly related species in the same genus or family, and he argued for a causal role of this "law of homologous variation" (Vavilov 1922) in parallel evolution. As an example, Vavilov reports that lentils (Ervum lens), a food crop, and vetch (Vicia sativa), a weed, have many homologous variations, and notes that vetches sometimes mimic lentils so closely in cultivated fields that their seeds cannot be separated by mechanical sorters:

the role of natural selection in this case is quite clear. Man unconsciously, year after year, by his sorting machines separated varieties of vetches similar to lentils in size and form of seeds, and ripening simultaneously with lentils. The same varieties certainly existed long before selection itself, and the appearance of their series, irrespective of any selection, was in accordance with the laws of variation. (Vavilov 1922, p. 85)

Darwin preceded Vavilov in recognizing a principle of "analogous variation" due to a similar "inherited constitution", but denied it any influence on evolutionary change:

But characters thus gained [by analogous variation] would probably be of an unimportant nature, for the presence of all important characters will be governed by natural selection, in accordance with the diverse habits of the species, and will not be left to the mutual action of the conditions of life and of a similar inherited constitution. (ch. 5, Darwin 1859)

That is, while we might recognize a kind of dualism in Darwin's view, in the sense that both fluctuation and selection are required for change as opposed to non-change, Darwin insists that selection "governs" the course of evolution, over-ruling variation. Darwin's followers, likewise, emphasize that selection, while not sufficient to cause change by itself, is the proper cause of the manner of change (that is, its directionality, dynamics, creativity, and so on). Darwin's followers have an ideological commitment to giving selection a power to control or dominate "random" mutation, and a commitment to denying internal causes of direction in evolution (if you have these commitments, you are probably a Darwinian; if you don't, you are not— or maybe you're just confused). The Mendelians did not share these ideological commitments.

Nonetheless, the Mendelians were a long way, as we still are, from having a clear view of this issue. Shull once remarked "What the world most needs, then, is not a good five-cent cigar, but a workable— and correct— theory of orthogenesis" (p. 449), "orthogenesis" being the idea of a trend or direction due to intrinsic tendencies of variation. The Mendelians did not develop such a theory. In spite of knowing that some variations occur more often than others, they often spoke as though any conceivable variation were either possible or impossible, which I see— and I see it almost everywhere— as a sign of immature thinking on this topic.

Of course, we are not much better off today. The evo-devo field clearly needs an idea of developmental tendencies in variation as a source of direction, and leading thinkers have called (vaguely) for such an idea for 30 years, but the evo-devo field still has no theory and instead is schlepping around its clunky old "toolbox" metaphor. Apparently, this toolbox contains the tools that selection uses to build structures, revealing that evo-devoists remain Darwinians who personify selection as a craftsman. Elsewhere (Stoltzfus, 2006; Stoltzfus and Yampolsky, 2009; online source), I have argued that we manifestly need a causal theory of orthogenesis, linking tendencies of variation to tendencies of evolution, and I have outlined the conceptual and mechanistic basis for such a theory, including population-genetics modeling.

In a series of later posts, we will take up the issue of "source laws and consequence laws" of variation, i.e., source laws governing the emergence of variation, and consequence laws governing its influence on evolutionary change.

Synopsis

Upon the discovery of genetics in 1900, a new breed of scientists rejected Darwin's theory and began developing a new understanding of evolutionary change based on Mendelian principles. They combined genetics with Darwin's principle of selection, but departed from Darwin's view in arguing that evolutionary change is not composed entirely of infinitesimal increments, and in representing mutation as a source of discontinuity, directionality, creativity and initiative.

Yet, somehow, "Darwinism" returned in the form of the Modern Synthesis. This new view included all the principles of Mendelian genetics, yet rejected all the non-Darwinian innovations of the Mendelians. The restoration of Darwinism in the Modern Synthesis— an accomplishment based more on rhetorical sleight-of-hand than on population genetics theory— will be our topic next time.

References

Bateson, W. 1894. Materials for the Study of Variation, Treated with Especial Regard to Discontinuity in the Origin of Species. Macmillan, London.

Bateson, W. 1900. Problems of Heredity as a Subject for Horticultural Investigation. Journal of the Royal Horticultural Society 25:54-61.

Bateson, W. 1902. Mendel's Principles of Heredity: A Defense. Cambridge University Press, Cambridge.

Bateson, W. 1909. Heredity and Variation in Modern Light. Pp. 85-101 in A. C. Seward, ed. Darwin and Modern Science: Essays in Commemoration of the Centenary of the Birgh of Charles Darwin and of the Fiftieth Anniversary of the publication of the Origin of Species. Cambridge, London.

Bateson, W., and E. R. Saunders. 1902. Experimental Studies in the Physiology of Heredity. Reports to the Evolution Committee. Royal Society.

Charlesworth, B. 2005. On the Origins of Novelty and Variation. Science 310:1619-1620.

Dawkins, R. 1996. Climbing Mount Improbable. W.W. Norton and Company, New York.

De Vries, H. 1905. Species and Varieties: Their Origin by Mutation. The Open Court Publishing Company, Chicago.

Goldschmidt, R. 1940. The Material Basis of Evolution. Yale University Press, New Haven.

Gould, S. J. 1977. Ever Since Darwin. W.W. Norton & Co., New York.

Kirschner, M. W., and J. C. Gerhart. 2005. The Plausibility of Life: Resolving Darwin's Dilemma. Yale University Press, New Haven.

Johannsen, W. L. 1903. Erblichkeit in Populationen und in reinen Linien. Gustav Fischer, Jena.

Mayr, E. 1963. Animal Species and Evolution. Harvard University Press, Cambridge, Massachusetts.

Morgan, T. H. 1903. Evolution and Adaptation. Macmillan, New York.

Morgan, T. H. 1916. A Critique of the Theory of Evolution. Princeton University Press, Princeton, NJ.

Morgan, T. H. 1925. Evolution and Genetics. Princeton University Press, Princeton.

Morgan, T. H. 1932. The Scientific Basis of Evolution. W.W. Norton & Co., New York.

Punnett, R. C. 1911. Mendelism. MacMillan.

Punnett, R. C. 1915. Mimicry in Butterflies.

Punnett, R. C. 1930. Genetics, Mathematics, and Natural Selection. Nature 126:595-597.

Shull, A. F. 1936. Evolution. McGraw-Hill, New York.

Stoltzfus, A. 2006. Mutationism and the Dual Causation of Evolutionary Change. Evol Dev 8:304-317.

Stoltzfus, A., and L. Y. Yampolsky. 2009. Climbing mount probable: mutation as a cause of nonrandomness in evolution. J Hered 100:637-647.

Vavilov, N. I. 1922. The Law of Homologous Series in Variation. J. Heredity 12:47-89

Footnotes

¹ Although de Vries continued to promote his "MutationsTheorie" for some years after 1900, it actually was a 19th-century theory of species-selection based on his work on Oenothera varieties, not on his work as one of the 3 re-discoverers of Mendel's principles.
² The perceived need for a dominant GUTE, and the ideological immunity that develops around a dominant GUTE, are issues that we will address in a future post.

Credits: The Curious Disconnect is the blog of evolutionary biologist Arlin Stoltzfus, available at www.molevol.org/cdblog. An updated version of the post below will be maintained at www.molevol.org/cdblog/mutationism_myth4 (Arlin Stoltzfus, ©2010)

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Smart Crocodile Eaters?

National Geographic Daily News has just published an embarrassing article about early human evolution [Eating Crocodile Helped Boost Early Human Brains?].

An ancient kitchen dating back 1.95 million years was discovered in Kenya. Among the bones recovered at this were those of fish, turtles, and crocodiles. The paper has just been published in PNAS (Braun et al., 2010).

Here's what the National Geographic science writer (Christine Dell'Amore) reports ...

According to the study authors, the addition of water-based prey into early-human diets may have been what boosted brain size in certain hominins—humans plus human ancestral species and their close evolutionary relatives.

That's because reptiles and fish are particularly rich in long-chain polyunsaturated fatty acids. Some experts think this so-called good fat was "part of the package" of human brain evolution, said study leader David Braun, an archaeologist at the University of Cape Town in South Africa.

Discovering evidence for "brain food" in the late Pliocene (about 3 to 1.8 million years ago) may explain how bigger brains—for instance in our likely direct ancestor Homo erectus—arose in humans and their relatives about 1.8 million years ago, Braun said.

This is one of those cases where the press report accurately describes what's in the paper. Here's the conclusion of the PNAS paper,

The evidence from FwJj 20 indicates that hominins were very effective at securing access to a wider variety of high-quality animal tissues than has been previously documented. Some of these resources would have provided necessary dietary resources without the added predation risks associated with interactions with large mammalian carnivores that are sometimes involved with the acquisition of elements of large mammal carcasses (28, 33). In addition, although animal tissues provide nutrient-rich fuel for a growing brain, aquatic resources (e.g., fish, crocodiles, turtles) are especially rich sources of the long-chain polyunsaturated fatty acids and docosahexaenoic acid that are so critical to human brain growth (2). Therefore, the incorporation of diverse animals, especially those in the lacustrine food chain, provided critical nutritional components to the diets of hominins before the appearance of H. ergaster/erectus that could have fueled the evolution of larger brains in late Pliocene hominins.

There are so many problems here, I hardly know where to begin.

First, there's the implicit assumption that eating food rich in long chain polyunsaturated fatty acids contributes to brain growth. As far as I know, the total scientific evidence does not strongly support this assumption—although there are plenty of studies that make the claim. (Their reference 2 is to another anthropological study.) This is not an assumption that one should build a theory on, but, if you do, you'd better back it up with references to the primary biochemistry and physiology literature.

Second, it's easy to be confused about the importance of dietary lipids. For the record, you need to eat foods containing linolenate and linoleate because these are essential fatty acids. You can't synthesize them but you need them in order to make other important fatty acids. There's plenty of these essential fatty acids in plants, which is why our fellow primates (chimps and gorillas) survive quite nicely without eating crocodiles. The "magical brain food" kinds of fatty acids are the other omega-3 fatty acids that we can synthesize as long as we have an adequate supply of the essential fatty acids.

Finally, let's think about the hypothesis being put forward. The idea is that our ancient ancestors weren't very smart. They had small brains. Some of them started to eat fish and crocodiles and that made their brain get bigger. Presumably this mostly affected the children since there's no evidence that diet can make an adult brain grow bigger.

As the years passed, the entire population acquired bigger brains as a result of their diet. Maybe this group out-competed their neighbors who didn't like fish so that eventually the entire hominid population of the region had big brains and ate fish.

What has this got to do with evolution? How do you get from a cultural preference for eating fish to changes in the genes controlling brain development? Are the authors implying some kind of Lamarckian inheritance? How, exactly, does eating fish translate into genetic changes (i.e. evolution)?

Am I missing something?

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[Photo Credit: ProGolferDigest]

Braun, D.R., Harris, J.W.K., Levin, N.R., McCoy, J.T., Herries, A.I.R., Bamford, M.K., Bishop, L.C., Richmond, B.G. and Kibunjia, M. (2010) Early hominin diet included diverse terrestrial and aquatic animals 1.95 Ma in East Turkana, Kenya. Proc. Natl. Acad. Sci. (USA) 107: 10002-10007. [doi: 10.1073/pnas.1002181107]

Calibrating the Molecular Clock

John Hawks is discussing the evolution of hominids on his blog and, in particular, whether Ardipithecus (Ardi) is a hominid [Ardipithecus challenge explication: the molecular clock].

This is a complex issue. One of the problems is that Ardi is supposed to have lived 5.5 million years ago, according to John Hawks, but all estimates of the human-chimp divergence say it occurred between 3 and 5 million years ago. If that's true then Ardi is not in either the chimp or human lineages.

The human-chimp divergence is based on calibrating the molecule clock and that's what John addresses in his post. He seems to think that this calibration is accurate [Reviewing the clock, and phylogenomics] but I'm not so sure. Many of these studies (but not all) require calibrating the rate of change by using fixed time points inferred from the fossil record. For example, if you assume that primates and rodents last shared a common ancestor 100 million years ago then you can get a rate of change by adding up the number of changes in each lineage and dividing by 100 (substitutions per million years). Then you look at the number of substitutions in the human and chimp lineages and calculate the years since they diverged.

This is an over-simplification, as John explains on his blog, because the calibrations are also based on known mutation rates and population genetics. The theoretical models agree on a human-chimp divergence time of 3-5 million years.

I've been skeptical of the fossil record calibrations for many years because they give some very unreasonable divergence times and because the so-called "fixed" standards also seem unreasonable. The molecular clock ticks at an approximately constant rate but we just don't know what that rate is. I would have no problem accepting that humans and chimps diverged 6-7 million years ago.

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[Reconstructions: Copyright 2009, J.H. Matternes.]

A Young Student of Physics

 
I know you all hate it when bloggers inundate you with photos of their kids and grandkids but here's one I can't resist. It's my granddaughter Zoë (5 months old) learning vector calculus. It's never too soon to start.



She'll probably have to wait until she gets older to move on to more difficult subjects like biology. I think her mom is doing the right thing by starting out with the easiest science.

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