Over my time as a dilettante observer of the science blogging community, I have noticed a certain frisson of controversy over the idea of random genetic drift. Sewall Wright, who with Ronald Fisher and J. B. S. Haldane (Bill Bryson’s observations on Haldane’s research into diving and decompression are entertaining) established the science of population genetics, is credited with coining the phrase in 1929. Thanks to Professor Joe Felsenstein for pointing out his seminal paper.
Will Provine has written a much admired biography of Sewall Wright, Sewall Wright and Evolutionary Biology, and yet has expressed doubt about the significance of genetic drift, culminating in his recent work, The “Random Genetic Drift” Fallacy, available as an E book here. This has caused a storm of comment on the internet. At the ID-friendly blog currently run by lawyer Barry Arrington, there was a portentous post by “News” which generated immense interest and four comments that I failed to notice and it was only when Larry Moran criticized Provine’s book recently at The Sandwalk that I became aware of its existence.
In ignorance of Provine’s doubts, I’ve recently expressed my own inability to grasp the significance of the effect for evolution. Allan Miller has been very gentle and patient with me and OM’s computer simulation was most helpful. In the commments, Joe Felsenstein links to his 1971 paper which should give the mathematically inclined food for thought. It just made my head spin!
So I’m hoping that someone can gently take me by the hand and lead me to the promised land where the effects of random genetic drift are clear to all. I have purchased Provine’s book. At less than three dollars and only 180 pages, why would I not?
How about you give us your review of Provine’s book. Then I’ll decide whether it’s worth the time to read it.
Personally, I don’t doubt that there is random genetic drift, and I found OM’s simulation very helpful. But I have a gnawing feeling that some people are trying to use random drift to explain too much.
I’ll put stuff in the comments if you like. I’ve skimmed through and started to read properly. The formatting is sort of unfinished. The early chapters are more of a history than an argument. He is convinced that meiosis in sexually reproducing populations is the issue.
I agree.
Exactly!
PS Provine also suggests there is confusion over the result of inbreeding and whether random genetic drift is merely the result of inbreeding.
I bought Provine’s book on Kindle (it’s cheap). It reads more like a memoir than a scientific argument. It’s self-published and really badly edited.
I will parrot something said by Larry Moran that seems apt: Most evolution took place in the first three billion years of life, in microbes. Evolution since the Cambrian has mostly been the evolution of regulatory networks. The genes were already there. Most criticisms of evolution talk about animals, and that’s not where the really tough sledding has been.
That would be fine.
You are whetting my appetite. I see meiosis as very important.
For myself, I’m inclined to say that maintaining variation in the gene pool is the most important aspect of evolution. And meiosis is part of that.
Aren’t you talking about drift via another route? If stuff hides from selection, isn’t it drifting?
I see drift as a side effect of having variation.
The presence of variation in a changing environment is what I see as mainly important. Drift is the special case of that when the environment is stable.
I would agree with Moran that drift is the dominant mode and that occasionally the presence of variation makes serendipitous adaptations possible.
I suspect that the most likely response to environmental change is extinction. Followed by radiation. But I would think that most new species arise opportunistically, because niches are left vacant by extinction events.
But I think our attitudes toward speciation are biased toward evolution of vertebrates or other animals. That’s a bit like reconstructing human society based on the lives of the Astors and Rockefellers.
Statistically, drift is a certainty (almost). But knowing with almost certainty that drift exists is one thing. Identifying instances where you can conclusively say that fixation was the result of drift is far more difficult.
As a yEC i think random drfit was needed because natural selection on mutations didn’t seem to be able to explain things. its really a “withdrawl” from the first trenches. I predict more reteats to trenches in the back.
OM’s simulation has one important lack that would make what drift can do more apparant, It needs to include randomly arising mutations and then let them drift (either to eventual fixiation, or lost back out the population again as most will do).
Creationists in particular have a hard time seeing how drift can contribute anything constructive to evolution. But new mutations arise every generation. Is OMagain still around?
Which is the opposite of what drift appears to do, according to Provine. He sees “drift” as synonymous with inbreeding in small populations and the usual result being extinction. Indeed there is some interesting correspondence quoted between Wright and Julian Huxley, who was then director of the London Zoo, Huxley seeking advice regarding minimum captive breeding populations.
But what does “drift achieve? It reduces variability in small breeding populations. How does that contribute to evolutionary change?
The evidence is with you on that one. 🙂
Whether populations find or fall into new niches, I guess they ideally need to be empty, at least of bigger, fiercer, hungrier species. (Unless you can dodge between their legs)
Excellent point. Wright spent most of his time working with guinea pigs. The possibly up to three billion years of evolution to arrive at eukaryotes (I’m only half way through as RL has only allowed me to read in snippets) seems to have been overlooked by Provine in this book.
There’s a sort of between-the-lines challenge from Provine to cite or propose an experiment that clearly demonstrates drift and does not confuse it with inbreeding.
I’m sure OM will take up that thrown gauntlet if he has time!
Not just Creationists! Will Provine is skeptical. I’m as yet unconvinced but open to persuasion.
Sure but drift in small populations reduces allelic variation except for the one that fixes Homozygosity looms.
Let’s hope so.
Alan Fox:
I don’t see how it reduces variability. The rate of fixation — in general — equals the rate of non-lethal mutation. Drift is a bit like a sliding window on viable sequences.
Oops just put in a missing tag for you but made it worse before better.
petrushka,
By reducing the alleles at a locus until one fixes, given enough time in small populations. Mutations work in spite of drift rather than because of drift. Unless I’ve misunderstood, which is more than likely.
What issue do you have with drift? It seems pretty obvious to me that it would occur but if you can’t mentally visualize it you could try one of the undergrad exercises they do in first semester classes; you put 50 red beans ( or chips or whatever) in a bag along with 50 white beans ( or chips etc) You then take out pairs of beans at random to represent the genotypes of the next generation. After repeating it a few times you’ll see the proportions change randomly. ( you’ll need extra beans of course)
If you cant see why variation is important heres the simplest example I can think of. Imagine that in a population of organisms a particular protein contains the amino acid leucine at a particular position specified by the codon CUG. If that leucine could be converted to a phenylalanine that would be beneficial for the organism ( now or at some time in the future) The codons for phenylalanine are UUU and UUC so no single mutation would suffice. Lets say in one individual the CUG is converted to UUG by mutation. This would probably be neutral since UUG also specifies leucine. Drift could remove this mutation or expand it in the population. If it expands it there would be more and more individuals that could potentially harbor a UUG —> UUU mutation.
I would think of it as something of a leaky bucket being refilled at the same rate as the leak. the level remains the same, but the fluid is being replaced. Allele frequencies change, but the overall level of diversity does not change.
If the alleles affect visible traits, the population changes appearance over time, but the overall level of diversity does not necessarily change.
I am busy at a week-long tutorial course in Tennessee which I am co-running. Let me just copy part of what I wrote when Provine’s book came up at Sandwalk:
(quoted from my comment at Sandwalk).
Provine is the major biographer of Sewall Wright. He was in charge of disposition and preservation of Wright’s scientific archives after Wright’s death.
(My involvement in all this was that, when Will and I were graduate students at the University of Chicago, he in history of science, I in zoology, I was one of the first people to suggest he go talk to Wright. At that point he was surprised to hear that Wright was alive. He was indeed alive, and continued to be for about another 23 years.)
Will used Wright as a major source for his first book The Origins of Theoretical Population Genetics, then later he more extensively covered Wright’s life, with Wright’s cooperation, in his major work Sewall Wright and Evolutionary Biology.
I think Will has always felt that even then, he had a more correct understanding of genetic drift than Wright did. Now you had to get up awfully early in the morning to outthink Wright on that. I suppose Will is either brave or foolhardy.
Will sent me a copy of his book for comments, but I was busy and have not been through it yet. Until I read it and understand Will’s argument, I’ll stick with Sewall Wright for now.
From another comment of mine in that same thread:
Here’s a case where it seems to me genetic drift is real and does not immediately result from inbreeding. Imagine a population of 1000 individuals, 500 females and 500 males, mated in 500 pairs. Each pair has exactly two offspring. If we have a gene with gene frequency 0.5 in the parent population, the offspring generation will not necessarily have a gene frequency of 0.5. Rather the frequency will vary owing to random Mendelian segregation.
Those differences between parent and offspring generation are genetic drift, owing to Mendelian segregation at the locus. (The other possible sources of genetic drift, random births and random deaths, have been ruled out in this simplified case).
Can somebody persuade us that these random changes of gene frequency “are really inbreeding”?
ok Alan, I’ll start at the end and work back.
Population genetics is unreal in modern biology.
– Will Provine
Joe, if you get a chance, was Wright wrong when he said that no “random genetic drift” occurred in prokaryotes?
I am surprised to hear that he said such a thing. If he said it, he was wrong about that. Random deaths, plus random variation in time to reproduction, would of course produce random genetic drift.
Would love to see the reference. I have not encountered that statement. Reference, please?
Hi Joe,
According to Provine the statement was made “in the 1930s.” It’s on page 161 of the Provine book. He gets no more specific than that. In the References section he cites five sources from the 1930s by Sewall Wright. Unfortunately the Bibliography page on Wikipedia for Sewall Wright is sorely lacking.
Provine went on to say:
With discussion following.
Perhaps Provine was wrong about the former and right about the latter. 😉
Assuming Provine is correct about what Sewall Wright said about random genetic drift in prokaryotes, are you still sticking with Sewall Wright?
[ETA: Never mind. You already wrote that if he said that he was wrong about that.]
The statement is in Provine’s book. Write apparently forgot to publish the opinion.
And we must assume that nothing new has been learned since 1930.
You could believe that, by faith, or you could show how the relevant mathematics and models have in fact changed. Or not.
I have Provine’s book. Perhaps you can refer me to the mathy part. I missed it. Alternatively, you could just summarize the part where he actually addresses the mathematics of drift.
You have the book, you have the page number, you have the sources provided by Provine. You can choose to disbelieve Provine, or you can say Wright was wrong.
You can disregard what Joe said if it makes you feel better:
Why is this even being discussed? It is wrong and trivially so. Drift happens for prokaryotes too, there is random sampling.
Frankly, I’m having difficulty grasping its significance.
OM’s simulation (see OP for the link) is an excellent illustration that where alleles are competing for a locus, in the absence of any bias, eventually one will win out and move to fixation. I think I get the concept.
I have not the slightest doubt that sources of new variations are crucial to the evolutionary process.
That makes complete sense but it does not help me see the significance of drift, unfortunately. What am I missing?
So are you saying it is necessary that some variation in a breeding population is lost to make room for more? Drift makes room for more variation? Without drift, there would be too much diversity?
I’m not challenging anything. I’m just not understanding. Would you recommend any papers on the subject? I found The Repatterning of
Eukaryotic Genomes by Random Genetic Drift, a paper (PDF) by Michael Lynch and another paper from the Ochman lab.
I’m still working through Provine’s book. I hope you are able to comment further as you find time.
For a list of Wright’s papers from the 1930s, see my Bibliography of Theoretical Population Genetics which is available at my lab’s we site here.
Two points are of importance here:
1. Prokaryotes have immense population sizes. This would mean that a gene at intermediate frequencies would scarcely drift (but see qualification below). Random genetic drift would be important for genes newly arising and still in modest numbers of copies. Wright would have been aware of this — I presume that this was the basis of his opinion. (I am 2000 miles from my copy of Provine’s book so I can’t check whether Provine gives any additional details).
2. However, prokaryotes have very restricted recombination. This would not have been known in the 1930s. It was then a mystery as to how, or even whether, prokaryotic genetic systems worked. Not until the remarkable work of people like the Lederbergs and Luria and Delbrück in the late 1940s and early 1950s would it become clear how bacterial genetics worked.
The restricted recombination means that an advantageous genetic mutation arising in a bacterial population would carry with it toward fixation whatever other variant alleles happened to be on its haploid genome. There would then be large fluctuations of frequency of those other alleles. This was observed by Aaron Novick and Leo Szilard in the early 1950s [yes, that Szilard].
Wright did not know this phenomenon, which makes random changes of neutral allele frequencies much more likely.
I’m just reporting what I understand to be facts. I may have read things wrong. I am not an expert.
But my own understanding is that any matching of mutation and fixation rates would be coincidental, or would be the result of something I don’t understand.
My intended meaning is that while fixation is the result of declining frequency of some alleles, the amount of variation in the population doesn’t change much, because other mutations are occurring. I don’t see them as replacing anything. Just happening.
Here is my understanding. I’m not an expert so if Joe or others add corrections hopefully I’ll learn something
When you first learn about evolution you tend to have a simplistic view ( a view that creationists tend to maintain throughout life) You imagine the idealized individual for the species morphing and transforming though time. But of course individuals never change during their lifetimes; entire populations with a great deal of variation change slowly over time. But mutations occur in individuals so for a population to acquire a mutation or trait in the absence of drift would require strong selection. I think one only needs reflect a while on this to see that the notion that every single minute trait and mutation is selected for is unlikely. So drift is what makes most variation useable for NS and if you accept neutral adaptive mutation it can create complexity
Alan Fox, maybe it would be helpful if you elaborated a bit on what kind of evolutionary significance you’re looking for?
From my perspective, one significant result from the presence of drift is that population size (actually, effective population size) becomes a parameter of evolutionary significance. In small populations, advantageous mutations are often times more likely to be lost due to drift than they are to reach fixation. In addition, depending on the size of the population and the magnitude of the selective effects, non-neutral alleles may behave essentially like neutral ones. That is the major result of Ohta’s Nearly-neutral theory, which I personally thinking is pretty amazing!
Whole chromosomes are crucial in evolution; geneticists know that fundamentally, but population genetics ignores them.
Fisher’s model F of 1922 should not be the foundation of population genetics. Population geneticists must invent a new science of their theories of evolution.
– William B. Provine
REW,
I’m on record here as stating individual organisms do not evolve, populations do. It’s just the rôle “random genetic drift” plays in evolution that I am not grasping at the moment.
Welcome to TSZ, Dave. What I’m asking for is an explanation or suggestion of how drift contributes to evolutionary processes.
Yes I’ve got that impression, that drift is significant in small populations
I’ll read up on it.
Just come across this 1997 paper (PDF) by Coyne, Barton & Turelli that also seems skeptical on the importance of drift.
So is inbreeding.
Mung,
Indeed! 😉
Speaking of Barton. Also mentioned by Provine:
The contribution of statistical physics to evolutionary biology
I don’t believe Provine is correct here. Work on the population genetics of frequencies of haplotypes (stretches of chromosome with multiple loci) started seriously about 1960 and was a major area of work int he 1960s and 1970s,
Whole chromosomes involve loci too far from each other to undergo restricted recombination. Loci that far apart will not show nonrandom association of presence and absence of alleles (i.e., linkage disequilibrium). LD most occur on much smaller scales.
Similarly I question his judgement about what sort of work is needed in the future.
Sorry, meant to say earlier, that Lenski’s long term E. coli experiment exploits repeated bottlenecks where new flasks are daily inoculated with a 1% sample of the previous day’s incubated flask. Is this an example of drift in action for prokaryotes?
Joe Felsenstein,
Reading Sewall Wright’s 1932 paper (linked in the OP) together with Provine’s critique in his book is enlightening (at least it seems so for me). Page 54 and on.
Alan Fox,
Not sure which paper you refer to — the 1932 paper has pages 1 to 11.
There has been some mixing here of two issues: do prokaryotes have genetic drift at all, and is it important in their evolution.
The first can be settled quickly. We watch a population of prokaryotes until the first death or the first reproduction. At any locus that has variation, one allele has then become a tiny bit more frequent or a tiny bit less frequent. That can encompass both natural selection or genetic drift.
Joe Felsenstein,
Sorry for not being clear. The page number is the point in Provine’s book where he begins his critique.
Alan,
To me, what’s most interesting about drift is that it provides a mechanism by which beneficial alleles can be lost and by which neutral and deleterious alleles can be fixed.