What Darwin Got Wrong, the new book by Jerry Fodor and Massimo Piattelli-Palmarini (not to be confused with Massimo Pigliucci), came out two days ago. Its thesis is that while evolution may be true, natural selection plays at best a minor role in evolutionary transformation. Selection, say F&P-P, can be rejected on two grounds: it is empirically untenable and philosophically unsupportable. Both of its authors are respected academics (Fodor is a philosopher, Piattelli-Palmerini a cognitive scientist) and neither is a creationist—or even religious—so we can expect this misguided critique of evolution to be warmly received and touted by creationists of all stripes. In other words, it will damage evolutionary biology, although I don’t think Fodor is worried about this in the slightest.
Because of this, I’ll be highlighting some of the reviews before my own piece, a long one, comes out in a while. The first is by the philosopher Michael Ruse in the Feb. 14 Boston Globe. I’ve had, and suspect I’ll continue to have, my differences with Ruse. We don’t see eye to eye about accommodationism, or about faith, or about anything concerning the intersection of science and religion. But damn if he didn’t produce a good review of What Darwin Got Wrong. From the outset it hits the nail on the head:
“What Darwin Got Wrong’’ is an intensely irritating book. Jerry Fodor, a well-known philosopher, with coauthor Massimo Piattelli-Palmarini, a cognitive scientist, has written a whole book trashing Darwinian evolutionary theory – the theory that makes natural selection the main force of change in organisms through the ages.
You would think that somewhere in the pages there would be one – just one – discussion of the work that evolutionists are doing today to give a sense of how the field itself has evolved. Peter and Rosemary Grant on Darwin’s finches for example; Edward O. Wilson and Bert Hölldobler on ant social structures perhaps; David Reznick on Trinidadian guppies perchance? But no such luck. A whole book putting in the boot and absolutely no serious understanding of where the boot is aimed. . .
Read it; it’s a deft, albeit brief, dissection of F&P-P’s specious arguments. (The review, in fact, is titled “The Origin of the Specious”, presumably referring to F&P-P’s motivations, discussed in the last paragraph of the piece.)
On the other hand, I can’t say much good about philosopher Mary Midgley’s review in the Feb. 6 Guardian. Midgley, who is infamous for reviewing The Selfish Gene while completely failing to understand its premise, still fails to grasp modern biology. Look at this postmodern analysis, claiming that all we’ve recently learned about biology and inheritance militates against Darwinism (the use of “privilege” as a verb immediately tips you off that you’re in academic La-La land):
Its authors do not, of course, deny that this kind of classical natural selection happens. But they argue strongly that there is now no reason to privilege it over a crowd of other possible causes. Not only are most mutations known to be destructive but the material of inheritance itself has turned out to be far more complex, and to provide a much wider repertoire of untapped possibilities, than used to be thought. To an impressive extent, organisms provide the materials for changes in their own future.
Surprise! Most mutations are bad! Lord, we didn’t know that before, did we? It’s unclear what she means by “organisms providing the materials for changes in their own future.” In one sense that’s trivially true—organisms are the repository of mutation, which is the raw material for evolution. But I suspect that Midgley, bamboozled by F&P-P’s long and arcane discussion of stuff like genetic assimilation, epigenetics, and modularity, simply doesn’t know what she’s talking about.
She then invokes the self-organization of individuals by physical and chemical laws as an explanation of evolutionary change. (We’re going to hear a lot more of this; trust me.):
Besides this – perhaps even more interestingly – the laws of physics and chemistry themselves take a hand in the developmental process. Matter itself behaves in characteristic ways which are distinctly non-random. Many natural patterns, such as the arrangement of buds on a stem, accord with the series of Fibonacci numbers, and Fibonacci spirals are also observed in spiral nebulae.
I’m going to hurl if I hear this stuff about Fibonacci spirals in plants one more time. I’d be more impressed if Professor Midgley could tell me how “self organization,” without the intervention of natural selection, produced the bodies of whales (who evolved from terrestrial artiodactyls) or the camouflage of stick insects.
Finally, she buys F&P-P’s call for a multiplicity of mechanisms causing evolution:
If we now ask what will take its place, their answer is that this question does not arise. There is not – and does not have to be – any single, central mechanism of evolution. There are many such mechanisms, which all need to be investigated on their own terms.
True, there are processes besides selection that can cause genetic change—meiotic drive and genetic drift are two of them—but no process other than natural selection can yield those remarkable features of organisms—the apparent “design” of plants and animals—that used to be explained by God.
I’ll start paying attention to these radical revisions of Darwinism, including attacks on natural selection, when they tell me how non-Darwinian processes can yield the appearance of design. I’ll exit the flock of “hidebound Darwinists” (a term Steve Gould once applied to me) when I hear how modularity, epigenesis, self-organization, or evo-devo constitute self-contained explanations for the elephant’s trunk.
Fibonacci spirals — setting standards for theological botanists since 1170 AD.
But where are the futurist balloon models of metazoans?
I’m not going to defend Fodor and Piattelli-Palmarini because I think some of their arguments are silly. However, your position is not helpful.
Nobody seriously questions the role of natural selection in adaptation. That’s just not an issue among evolutionary biologists. What’s up for grabs is whether everything is an adaptation or whether everything in biology exhibits the “appearance of design.”
To me, there are lots of things in biology that don’t look designed—unless you think Rube Goldberg is a good designer!
It’s about time that “hidebound Darwinists” concede that EVOLUTION can only be explained by invoking multiple mechanisms, especially random genetic drift. The debate is over explanations of EVOLUTION and not explanations of ADAPTATION. You are not contributing to the discussion if you keep confusing the two. Is it deliberate?
I’ll exit the flock of pluralists (like Gould) when the adaptationists explain molecular evolution and molecular clocks, the prevalence of variation in populations, junk DNA, and why Indian and African elephants are different.
Umm. . . I am addressing Fodor and Piattelli-Palmerini here, not evolutionary biology in general. As you should know from my critiques of evolutionary psychology, I don’t think that every feature of species can be explained by selection!
Who are these mythical people who claim that natural selection and adaptation are the only method of evolution? I am just a layman but I know of no one who dismisses everything else.
Fodor and Piattelli-Palmerini wrote a book in which people can not even agree what point they are trying to address. I guess I’ll just re-categorize the book in my mind as fiction or mystery.
translation: I resent your strawman and much prefer my own.
Don’t feed the trolls, people.
If Larry isn’t even going to bother reading or understanding what Jerry wrote before he replies, it’s not worth arguing with him. He’s just looking for a place to lecture about “pan-adaptationism” as if it were still 1979.
Have you ever sat in on an undergrad biochemistry or cell biology lecture?
You obviously wouldn’t be claiming that pan-adaptationism is dead if you had, not in my institution anyway…
As someone who hangs around people who actually understand the very mechanisms of evolution (*molecular* evolutionary biologists, not birdwatchers), I get really annoyed when taught that all the complexity of the ridiculous MAP kinase cascades is ‘adaptive’ and evolved so that “evolution could have more flexibility to use the pathway for different things” and “evolution likes to conserve energy” (direct quotes from class, by the way), when I know that to be wrong, or at least as wrong of an approach to explaining its origins as you can get. (Of course, in the same class — well, tutorial — we learned that if we take a pair of primers for human DNA, and run it against turkey DNA, the correct answer is that we won’t get any product (nothing was mentioned about how conserved a region was). I asked the TA how barcoding works, and got a bewildered look in response, mumbling something about how ‘obviously’ humans and turkeys are too distant for the primers to match.)
What irks me is the assumption that complexity can only arise through natural selection. That is wrong. (Stoltzfus 1999 J Mol Evol and examples cited therein; Lynch 2007 PNAS, Lynch 2007 Nat Rev Genet, Koonin 2009 Biol Direct, Lukes et al 2009 PNAS, etc) Not only can even inorganic self-organisation achieve a fairly impressive level of complexity (however, not heritable and therefore not evolution), but processes like constructive neutral evolution, in tandem with selection, can yield some rather awkwardly complicated solutions to problems closely related lineages can solve much simpler (eg. RNA editing in trypanosome kinetoplasts)
Of course, F&P-P have ways to go to understand any of that, judging from their rather mangled ‘understanding’ of natural selection (didn’t realise it was so bloody difficult), but what Larry Moran is saying is not trolling material, but a highly valid point that must be reiterated again and again until it gets into some rather thick skulls that selection is not the sole mechanism for increasing complexity!
Larry Moran: I’ll exit the flock of pluralists (like Gould) when the adaptationists … why Indian and African elephants are different.
I don’t study elephants, so I can’t tell you why they are different. But I can tell you why green anoles and brown anoles are different. Their differences in size, shape, color, and scalation are due largely to differences in the microhabitats they’re adapted to– so adaptation is quite important in understanding their differences. I’d be surprised if elephants differ signally from anoles in this regard. And, for another pair of elephants, the mammoth and the mastodon, I can tell you a lot about their differences– it’s because mammoths are grazers, and mastodons are browsers (I have no special expertise on fossil elelphants– Cuvier worked this all out in the early 1800s).
You might have confused elephants with Dick Lewontin’s famous, but essentially hypothetical, example of the adaptive differences between Asian and African rhinoceroses. Lewontin intended to contrast one- vs. two-horned rhinos, but this does not correspond to an Asian vs. African difference, and I don’t know of anyone who’s actually explored the possible adaptive differences among rhinos with different numbers of horns. So while adaptively equivalent solutions that do not require a selective explanation of the differences between them are certainly an interesting possibility, neither elephants nor rhinos provide a very compelling example of the phenomenon.
I’m going to hurl if I hear this stuff about Fibonacci spirals in sunflowers one more time.[…] I’ll exit the flock of “hidebound Darwinists” … when I hear how modularity, epigenesis, self-organization, or evo-devo constitute self-contained explanations for the elephant’s trunk.
You’re lucky that Ms. Midgley, with her scant (one presumes) knowledge of astrophysics, has not yet found out about elephant trunks in nebulae:
http://www.dias.ie/elephant/index.html
http://arxiv.org/pdf/0912.1499v1
http://arxiv.org/pdf/0808.3013v1
and, most worrisome for Darwinian evolution, the formation of elephant trunks from the Horsehead:
http://arxiv.org/pdf/0909.2614v2
From my own modest field of expertise, I can offer size/rank/frequency diagrams of medieval towns and Iron Age necropoles in Central Europe, which can be plotted in 2D as elephant trunks, or in 3D as spirals. Enough to confound Prof. Midgley? (And to boot, they are the beautiful statistical products of some of the dumbest mechanisms of self-organisation imaginable. I’d sell them to Prof. Midgley as “privileged aggregation”.)
Isn’t meiotic drive just a specific type of selection at the level of individual genes?
yes, what makes it interesting is that most genes are selected based on the phenotypic effects of their alleles, while those that show meiotic drive (or biased gene conversion, or other tricksy subcellular things) have something else going on changing their allele frequencies. so you have the possibility for evolution that is (to varying degrees) independent of organismal fitness.
ZOMFG! New Scientist was right! Darwin got it wrong! F&P-P have brought about a –wait for it (h/t OB)– paradigm shift! News at fucking eleven.
They should sell quite a few books, though, and we’ll be fighting this new misapprehension for years.
Agreed on the dummy Fodor, but I don’t understand your dismissal of non-adaptive evolution, or evo-devo? Despite the annoying grand terms in which some people discuss it, it is development that is the interesting (and constrained, and complex, and rube goldberg-y) part of producing the phenotypic variation on which selection acts. To me, the production of variation should be as central as the selection process. Mutation is random, variation is not…isn’t that something interesting to explain?
He didn’t dismiss any of those things.
As he implies, “modularity, epigenesis, self-organization, or evo-devo” may be useful additions/modifications to evolutionary theory, but as he rightfully says, none of them constitute a “self-contained explanation” for adaptations.
“… a self-contained explanation for adaptations.”
I don’t understand that point of that phrase… nothing is a self-contained explanation for adaptations, not even natural selection, because it doesn’t explain variation or trait heritability, etc. I don’t think I am wandering into the blanket pluralist camp here, and I don’t question the central and overriding importance of natural selection in adaptative evolution, but Larry, the other Massimo, Jablonka, etc, have never claimed that epigenetics, the Baldwin effect, or “evo-devo” are “self contained” anythings. Fodor and Bad Massimo are way beyond the pale of any serious discussion about evolution. So, yeah, may the best straw man win…what a fascinating discussion. Evolutionary biologists have the most stupid and weirdly personal arguments among themselves in all of biology. Though the stem cell people may yet catch up.
» Larry Moran:
What’s up for grabs is whether everything is an adaptation or whether everything in biology exhibits the “appearance of design.”
Can you quote even one marginally relevant evolutionary biologist who thinks that?
Dr. Moran is usually happy to quotemine a couple of sentences from Richard Dawkins for this purpose.
There are some evolutionary biologists who claim that evolution should be DEFINED as the product of natural selection. In that case, everything that evolved is an adaptation, by definition. That’s not a very good way to try and win an argument.
There are others who claim that non-adaptive evolution occurs but it’s just not interesting or relevant and therefore can be ignored. That’s just a reflection of the bias of the writer. There are many of us who are more interested in non-adaptive evolution than in selection. Don’t we count?
In most cases, when it’s brought to their attention, the typical adaptationist admits that there are other mechanisms of evolution. They just seem to forget it the very next day when they write their articles or give their speeches.
The point is not that adaptationists completely deny the existence of other mechanisms of evolution. You’re right to point out that there are very few examples of this type of adaptationist. The point is that the adaptationist worldview is a worldview that places far too much emphasis on adaptation and most of its adherents don’t think about anything else unless they are challenged. It’s a myopic perspective and it leads to problems when it comes to interpreting observations. In other words, it’s bad science.
Jerry gave us an example of this worldview in his posting when he said, “Surprise! Most mutations are bad! Lord, we didn’t know that before, did we?” In his book—when presumably he was focused on the problem—he admits that most of evolution is probably due to random genetic drift and that most mutations are probably neutral (in eukaryotes). But his remark above makes it clear that this is not information that he has truly assimilated into his worldview. When his guard is down he slips back into adapationist mode.
Most mutations are probably not bad in spite of Jerry’s mocking tone. That’s a pretty serious mistake to make if you really understand evolution from a pluralist perspective.
“[Jerry] admits that most of evolution is probably due to random genetic drift”
I’d be really surprised if Jerry ever said that, and he doesn’t say so in WEIT. What he does say is that “The influence of this process [genetic drift] on important evolutionary change, though, is probably minor, because it does not have the molding power of natural selection.” (p. 13). And later, on p. 124, “The relative importance of genetic drift versus selection in evolution remains a topic of hot debate among biologists. Every time we see an obvious adaptation, like the camel’s hump, we clearly see evidence for selection. But features whose evolution we don’t understand may reflect only our ignorance rather than genetic drift. Nevertheless, we know genetic drift must occur, because in any population of finite size there are always sampling effects during reproduction. And drift has probably played a substantial role in the evolution of small populations, although we can’t point to more than a few examples.” Both statements are, to me, eminently reasonable and supported by the corpus of biological evidence.
“But features whose evolution we don’t understand may reflect only our ignorance rather than genetic drift.”
Gould & Lewontin 1979 have something to say about that point, specifically. On page 586. Just sayin’. (incidentally happened to have read that recently for a project; not normally this pedantic =P)
Umm, Jerry was a student of Dick Lewontin’s. He read the 1979 paper. Probably in 1978.
I haven’t read Fodor and Piattelli-Palmarini’s book but I have some sympathy for the idea that Natural Selection has some deep conceptual problems. Both you and Ruse make the issue quite stark. Ruse claims that “design” is a metaphor and metaphors are common in science (which is, of course, abject nonsense; scientists might use metaphors but nobody creates a theory to explain a metaphor) and you claim that it’s “apparent design” that needs to explained. But “apparent design” isn’t quantifiable and isn’t something science could possibly hope to explain because it’s (at best) a subjective non-thing.
So that whole approach never gets off the ground. How would you ever know Natural Selection has successfully explained “apparent design”? How would you know if some competing theory can explain “apparent design” better than Natural Selection? If all dropping Natural Selection gets you is the inability to explain something that only exists as a judgement, there isn’t really a problem with dropping Natural Selection at all. The “apparent design” of the elephant’s trunk is no more in need of an explanation than seeing a face in a cloud.
The idea that selection has (“conceptual”) problems fail simple testing. It is AFAIU used empirically to predict changes in Darwin’s finches as well as put on robust theoretical ground by way of fitness in population genetics.
As regards “apparent design” the post clearly defined it as features of organisms. Traits as useful concepts in biology goes way back, and that such function is confused with “apparent design” is well known.
I would say that the relationship is inclusive, because creationists often dismiss lots of functional traits to seemingly haphazardly choose those that stand out or, even better, have modern technological correspondences. (Such as eyes vs cameras.)
By this inclusion we can clearly successfully explain (predict) “apparent design”. Whether of not it can be predicted better (say, more parsimonious) by rivals to selection isn’t relevant by way of the same inclusion, what is relevant for selection is to predict features (traits). There is no one-to-one relationship between a quality measure for an inclusion and for the whole set. (For example, a good car is steerable, but a good sports car has a strong engine.)
I’m still upset that I actually paid money for one of Midgley’s books (The Myths We Live By) before realising who she was. I’ve never seen anyone, even on the Internet, who manages to be so consistently wrong about every single thing she writes about.
As an interested, albeit poorly informed, observer of the science/religion conflict, it seems that too often the religious are ignorant of the evolution of evolution theory and the scientists equally uninformed of the evolution of religion. It’s as though each is using their 21st century knowledge/faith to critique a 20th century (or earlier) position as though it was current.
For me, it’s about labels and meaning. Science is about insight into the known and knowable; e.g., string theory, dark matter(energy), multiple universes. Religion, in its root meaning, is about how humans see their linkage to the past.
It was only when science began encroaching on what the rigid religious saw as sacred ground that religions moved away from the subjective and symbolic into the literal. Even then, the progressive (there must be a better word) religious saw science as objective revelation which moved their faith deeper into the unknown and unknowable.
Terms used in this discussion–religion, faith, science, truth, proof, god, theism, atheism, et. al.–are, if not meaningless unless defined, poorly employed as two disputants pose conflicting views using the same terminology with different meanings.
The question of natural selection, for instance, can have several meanings. I like it because it suggests that evolution occurs by both chance and preference.
Thanks to all who post here. It has helped me move my thinking to a better place.
It was only when science began encroaching on what the rigid religious saw as sacred ground that religions moved away from the subjective and symbolic into the literal.
This is a noble and generous view of religions, which I am tempted to call the ‘Whig view of religion’, by analogy with the ‘Whig view of history’.
Unfortunately, it is not borne out by what we know from religious history. Nor is rigid literalism a modern phenomenon in response to scientific knowledge encroaching upon religious belief. The recent discussion on these pages of pharaoh Tutankhamun’s death provides a link to a striking example.
As you know, Tutankhamun (né TutankhATEN) was an insignificant pharaoh, but the son of one of Egypt’s most outstanding kings: Akhenaten.
We can hardly grasp the depth an magnitude of the trauma caused to common Egyptians by Akhenaten’s religious revolution. The formerly tangible, visible gods were no longer in sight, no longer responding. An impalpable abstract universal principle had replaced them. This displacement of the literal by the symbolic shook and nearly shattered Egyptian civilisation. The backlash was terrible.
Jan Assmann, an eminent Egyptologist and one of the foremost scholars of the Amarna period, termed it the “Trauma of Amarna”. An introductory paper by Assmann contrasting traditional ‘literalist’ Egyptian and Amarna theologies is freely accessible here:
http://static.scribd.com/docs/4t28399kbgov6.pdf
The main problem I have with people who claim that epigenetics, genetic assimilation, modularity, etc… are in opposition to natural selection, is that they don’t realize that natural selection is often used as the mechanism that drives the selection of the traits for each one of those things.
As for Larry’s neutral theory, no one denies that this happens Larry, you need to get over this, it is getting old. As others have said above, you are creating an artificial straw-man out of your so called “opponents” that don’t exist. Sure, neutral theory is more applicable/appropriate to explain certain things such as your example of the elephants, but at the same time try explaining evolutionary arms-races by neutral theory and not natural selection.
“…people who claim that epigenetics, genetic assimilation, modularity, etc… are in opposition to natural selection.”
Exactly, all of these things depend entirely on selection to either occur at all or have meaningful effects on evolution. However, among biologists, I don’t think these “people” exist.
This thread reminds me (very easily!) about Craig Venter yesterday here in Uppsala at his Linné seminar. Among the numerous interesting things he said (besides alluding to the fact that a good way to steer towards a Nobel prize is to take a yacht around the world!) was that they find ~ 50 % genetic variation among sea bacteria, when mammals may have an order of magnitude less.
The easiest explanation is, I believe, the one Venter ventured: that selection is important among mammals, not so much for bacteria. And who’s the ones with most traits?
[Well, as a naive layman I suspect it’s not that simple, there’s likely feedback so traits more likely begets traits, and so on. By way of complexity and/or ecology, at a guess. But there’s bound to be a root cause, perhaps along Venter’s line.]
I too should like to know the experts’ view on the amount of genetic variation among sea bacteria vs. mammals. I recall a number of papers in recent years, two of which I have right now on my laptop:
– Sogin et al., Microbial diversity in the deep sea and the underexplored “rare biosphere”; http://www.pnas.org/cgi/doi/10.1073/pnas.0605127103
– Furhman et al., A latitudinal diversity gradient in planktonic marine bacteria; http://www.pnas.org/cgi/doi/10.1073/pnas.0605127103
(No idea how good these are, my interest at the time was in the biogeostatistical frequency data.)
Sogin et al.: Differences in major populations under dissimilar biogeochemical regimes are hardly unexpected, but the idea that underrepresented populations define such enormous diversity with potential to take over a particular ecological niche has profound implications. Several ecological models that account for frequency-dependent mechanisms predict a survival advant age for rare species, which are less prone to predation and direct competition with dominant community members. The concept of a rare biosphere forces us to rethink the potential feedback mechanisms between shifts in extremely complex microbial populations and how the genomes of their constituents change over evolutionary time scales. The rare biosphere may serve as a potentially inexhaustible reservoir of genomic innovation, which could explain how microbial communities recover from environmental catastrophe and why every previously uncharacterized microbial genome offers so much genetic novelty even when compared with closely related taxa.
Fuhrman et al. : Genetic studies such as ours have been challenged as not relevant to biogeography. … We have evidence, however, indicating that the genetic variation we measure is ecologically relevant. The different bacterial taxa defined by ARISA “behave” like different species; OTUs* identified by ARISA at our San Pedro Channel study site are seasonally variable, annually repeatable, and highly predictable from environmental parameters, with different OTUs associated with different parameters (29). This indicates that the genetic variation we observe is not neutral, the different bacterial OTUs occupy different niches, and the patterns with latitude and temperature reflect underlying geographic distributions of species.
*OTU: “operational taxonomic units”
The experts, please?
Actually, according to some stuff of Effective Pop Size (I am *NOT* a population geneticist, and suck royally at anything that puts genes or organisms into an equation /disclaimer), selections acts MORE on bacteria due to their larger population size (Lynch 2007 PNAS “The fraility of adaptive hypotheses for the origins of organismal complexity”, Yi 2006 BioEssays “Non-adaptive evolution of genome complexity”); in fact, perhaps what largely enabled the runaway complexity of large multicellular eukaryotes was a reduced effective population size. Increases in complexity are for the most part a reduction in efficiency, and generally worse than simpler mechanisms…
Jerry Coyne wrote: “Surprise! Most mutations are bad! Lord, we didn’t know that before, did we?”
My understanding is that most mutations are “neutral.” Specifically, my understanding is that most mutations don’t cause an organism to be less likely or more likely to produce viable offspring. Here are two links:
http://www.talkorigins.org/indexcc/CB/CB101.html
http://www.talkorigins.org/indexcc/CB/CB101.html
It seems likely to me that most mutations don’t cause an organism to be less likely to produce viable offspring, because it is known that humans average about 130 new mutations per sexual generation. And most humans are doing fine and are able to produce many viable offspring. If most mutations were to make it less likely that the organism would produce viable offspring, then it seems unlikely that there would be any humans at all. 130 new mutations is a lot. And there are 6.7 billion humans on the planet. In comparison, most black mamba snake bites make it less likely that the organism will produce viable offspring. For instance, my understanding is that if humans get bit by one of those snakes and don’t get treated with anti-venom soon after the bite, the human generally dies soon after the bite.
Both of the links I posted are to the same article. I didn’t mean to post two links to the same article. I did, however, mean to post this link:
http://www.talkorigins.org/faqs/mutations.html
Hmm.. I don’t remember the numbers off the top of my head, but I believe the estimate for harmful mutations for humans is in the 50-70% rate. Still, your argument has several flaws:
– harmful mutations may have very mild effects, yet still be considered harmful
– if more harmful mutations show up early, they may cause a spontaneous abortion during fetal development. Spontaneous abortions are quite common, even so early that the woman doesn’t realize she’s become pregnant, so this may provide an explanation for what happened to the most harmful mutations, without affecting your statement that “most humans are doing fine and are able to produce many viable offspring”.
Ben W, thanks for the response.
Ben W wrote: “Hmm.. I don’t remember the numbers off the top of my head, but I believe the estimate for harmful mutations for humans is in the 50-70% rate.”
What do you mean by “harmful?” And whose estimate are you referring to? Many people have estimated that most mutations are neutral. I’ve posted two links. I may post links to other people who have claimed that most mutations are “neutral.” Moreover, just because some people have claimed X is not hugely important to whether I’m warranted in inferring that X is true. People are often mistaken.
Ben W wrote: “Still, your argument has several flaws:
– harmful mutations may have very mild effects, yet still be considered harmful…”
What do you mean by “harmful?” Also, it is unlikely that most mutations make it slightly less likely that an organism will produce viable offspring. Humans average 130 new mutations per sexual generations. If most of those mutations made it less likely that humans would produce viable offspring, then I suspect that there wouldn’t be any humans. 130 is a lot. If each of those mutations were to make it slightly less likely that any give human would reproduce, how would we have any humans?
Ben W wrote: “if more harmful mutations show up early, they may cause a spontaneous abortion during fetal development. Spontaneous abortions are quite common, even so early that the woman doesn’t realize she’s become pregnant, so this may provide an explanation for what happened to the most harmful mutations, without affecting your statement that ‘most humans are doing fine and are able to produce many viable offspring.'”
My understanding is that about 15 to 20 percent of known human pregnancies end in miscarriage. And surely many human pregnancies that are unknown end in miscarriages. But if most mutations made it less likely that the organism would reproduce, how could we have so many humans? For example, sixty percent of 130 is 78. If, on average, each of 78 new mutations per human made it less likely that the human would produce viable offspring, then how do we have 6.7 billion people on the planet? That suggests that most of those mutations do not make it less likely that humans will produce viable offspring. And I don’t see how humans could be that different that all other organisms in terms of the consequences of their mutations. For instance, my understanding is that RNA-based lytic viruses average at least one new mutation per division. And there are lots of RNA-based lytic viruses.
In addition, you said: “Still, your argument has several flaws…” You mentioned two “flaws” to in my “argument.” If you don’t mind, what are the others? We can work on this together.
Ben W wrote: “I don’t remember the numbers off the top of my head, but I believe the estimate for harmful mutations for humans is in the 50-70% rate.”
Also, for those who claim that 50% to 70% of all mutations are “harmful,” what evidence have they offered to support their assertion? And do you have any links or articles that you would recommend? Thanks
Larry Moran, Professor in the Department of Biochemistry at the University of Toronto, has argued that most mutations are “neutral.” Here is a link:
http://sandwalk.blogspot.com/2009/11/genetic-load-neutral-theory-and-junk.html
So has Motoo Kimura. I’ll see if I can find some good quotes from Kimura on the subject.
Moran and Kimura are talking about mutations at the molecular level of nucleotide sequences. Because of the redundancy and wobble in the genetic code, manynucleotide substitutions make no difference whatsoever in the amino acid coded.
Even a change in the amino acid coded can have minimal effect on the functioning of the protein in many cases (e.g. substitution of one hydrophobic residue for another).
Such mutations are neutral because they do not affect phenotype and are therefore invisible to selection.
Those of use who study (the phenotypes of) organisms do not care at all about such neutral molecular sequence mutations. THey are nearly completely irrelevant to biology at the phenotypic level.
So, OK, “most mutations” are neutral or near-neutral. Most mutations that affect protein function are harmful.
Not all.
Sven DiMilo wrote: “Moran and Kimura are talking about mutations at the molecular level of nucleotide sequences. Because of the redundancy and wobble in the genetic code, manynucleotide substitutions make no difference whatsoever in the amino acid coded.
Even a change in the amino acid coded can have minimal effect on the functioning of the protein in many cases (e.g. substitution of one hydrophobic residue for another).
Such mutations are neutral because they do not affect phenotype and are therefore invisible to selection.
“Those of use who study (the phenotypes of) organisms do not care at all about such neutral molecular sequence mutations. THey are nearly completely irrelevant to biology at the phenotypic level.
“So, OK, ‘most mutations’ are neutral or near-neutral. Most mutations that affect protein function are harmful.
“Not all.”
Sven, thanks for the response. First, what do you mean by “harmful?” Also, Moran did not claim or suggest that “most mutations that affect protein function are harmful.” Here is what he wrote: “Recall that only 20% of mutations in coding regions are likely to be detrimental. That means that the effective target size for detrimental mutations is about 20% x 1.3% = 0.26% of our genome. Out of 130 mutations, only 0.3 per individual per generation will be detrimental.” Also, I don’t remember reading anything by Kimura in which he claimed or suggested that, while most mutations are neutral, most “mutations that affect protein function” are harmful. But I’m not an expert on Kimura’s work. Finally, what evidence is there that “most mutations that affect protein function are harmful?” For instance, is there an article on the subject that you would recommend? Thanks
Just to clarify an important point: the neutral theory of molecular evolution deals with the fate of genes underlying neutral traits, independently of whether they are morphological, behavioral or biochemical (also known as the molecular phenotype).
The core of the neutral theory doesn’t deal with silent mutations: they have no impact on the molecular phenotype and thus selection cannot act on them (except in particular contexts like codon usage bias and gene expression regulation). Instead, it was specifically formulated to deal with the excess of amino acid substitutions observed within and between species. (A very good read is Otha’s 2003 essay “Origin of the neutral and nearly neutral theories of evolution”.) Most substitutions are neutral is valid both for nucleotide substitutions and amino acid substitutions.
It’s fairly accepted that in many species the bulk of amino acid differences observed between species are the result of neutral evolution. However, this only tells us that these mutations had no fitness effect, not that they did not have any phenotypic effect. Which are two very different things. If any of these neutral mutations had any effect on a phenotypic trait which is not linked to survival or reproduction (i.e fitness), that trait could now appear different between species.
Therefore the adaptive/neutral scenario depends on whether it is more common for most protein changes to have no phenotypic effects or for most phenotypic changes not to have fitness effects. In fact, understanding the link between genotype and phenotype is probably the most difficult (and yet critical) aspect of working on evolutionary questions.
However, the most interesting aspect of the neutral theory is the effect of population size on evolution (this theory is ofter referred to as the nearly neutral theory): in order to be visible to natural selection (directional or stabilizing) a trait must have an absolute selection coefficient greater or equal to 1/2Ne, where Ne is the effective population size. This has the following consequences:
1) Slightly deleterious traits can be polymorphic and become fixed
2) Advantageous traits must have an effect strong enough in order to be selected on (which means that not everything that is advantageous will be fixed)
3) Population size, and therefore past demographic processes, are a major factor in evolution: in small populations natural selection is less powerful than in large ones (note: humans have an Ne of 10,000, Drosophila of 1,000,000).
The nice aspect about the neutral theory is that it provides a null hypothesis against which to test adaptive scenarios and confirm their validity.
Now throw this complication into the mix:
http://futurity.org/science-technology/new-type-of-genetic-variation-discovered/
Fucking press releases. I can’t figure out from that what is supposed to be so “new”.