There seems to be little doubt that most of the fixed alleles at the molecular level are probably neutral in their effect. Thus, they have been fixed by random genetic drift. This includes many amino acid substitutions in proteins. Even though these substitutions change the structure of a protein by a small amount, it does not seem reasonable to assume that they have all been selected.
Most adaptationists are content to concede this point (although there are holdouts). However, they draw the line at more "visible" mutations. According to this group, the vast majority of "visible" mutations are subject to natural selection and therefore most fixed alleles with a "visible" phenotype are adaptations. The argument seems to be that once a mutation produces a "visible" phenotype then it is not appropriate to suggest that it might be neutral with respect to natural selection. The line seems to be drawn somewhere above differences in the amino acid composition of proteins but it's not clear exactly where.
p-ter is one of those who are very reluctant to admit that a visible character could have been fixed by accident. He has posted a short article on Gene Expression [Do phenotypes evolve neutrally?]. I recommend that you read the comments to see examples of the extreme version of adaptationism. Most of these adaptationists will even argue that human blood types are adaptive. The idea that most native North Americans have type O blood is due to some undefined selective advantage and not to accident.
This argument has been going on for several decades. As usual, it's not about the existence of natural selection or random genetic drift. It's about their relative importance in evolution. To reiterate, the adaptationists believe that almost all mutations with a visible phenotype have been fixed by natural selection. The pluralists think that many of them are neutral and have been fixed by accident. The adaptationists make a distinction between what happens at the molecular level and what happens at the "visible" level while the pluralists think the same mechanims are operating at both levels.
Richard Lewontin uses the example of the Indian and African rhinoceros to focus the debate. The African rhinoceros has two horns while the Indian rhinoceros has only one. The question is whether this difference is due to natural selection—is two horns better than one in Africa? Or, is it just an accident of evolution that one species has two horns while the other has only one?
I don't understand why the adaptationist camp is so reluctant to admit that some visible characters can be fixed by random genetic drift. The idea that every feature of an organism has to be an adaptation seems so out of touch with our modern understanding of evolution that I'm really puzzled by the vehemence with which adaptationists defend their orthodoxy. It seems as though admitting that visible phenotypes might be non-adaptive is a major threat to their worldview.
Here's something for you and Jeffrey Shallit to argue over:
ReplyDeleteMost Canadians would fail own citizenship test
Um, okay, I don't know enough about fixation mechanisms to follow the science. But is it possible to concur on null hypotheses for each level, say for a large but finite population? p-ter claims in the other thread that "...a priori your preference for neutrality [is] a defensible preference...", which doesn't really help me here.
ReplyDeleteThe argument seems to be that once a mutation produces a "visible" phenotype then it is not appropriate to suggest that it might be neutral with respect to natural selection.
ReplyDeletenot exactly. this is a population genetics question. the parameters that control the probability of fixation of a new mutation are the selection coefficient and the effective population size (and the mode of action-- recessive, dominant, etc). assuming selection on the individual level (i.e. the mutation doesn't cause meiotic drive or something), the selection coefficient cannot be ignored. If the selection coefficient is 0 (the mutation is neutral), that's one thing. but it should be demonstrated. this is possible, you know. see this, for example:
"In a comparison of amino-acid replacements among species of the mustard weed Arabidopsis with those among species of the fruitfly Drosophila, we find evidence for predominantly beneficial gene substitutions in Drosophila but predominantly detrimental substitutions in Arabidopsis. We attribute this difference to the Arabidopsis mating system of partial self-fertilization, which corroborates a prediction of population genetics theory that species with a high frequency of inbreeding are less efficient in eliminating deleterious mutations owing to their reduced effective population size.""
Most of these adaptationists will even argue that human blood types are adaptive. The idea that most native North Americans have type O blood is due to some undefined selective advantage and not to accident.
again, this is a population genetics question. Native Americans have lower MHC diversity (and high frequencies of things like the O blood group) likely because of a population bottleneck, a neutral process. This does not mean, however, that selection doesn't operate on blood groups- it does not mean that the selection coefficient is 0; that would have to be demonstrated. The duffy blood group, of course, has high frequency in Africa likely due to the fact it confers some resistance to malaria. Note that the distribution of this phenotype is somewhat similar to the O group you mentioned in Native Americans.
I don't understand why the adaptationist camp is so reluctant to admit that some visible characters can be fixed by random genetic drift. The idea that every feature of an organism has to be an adaptation seems so out of touch with our modern understanding of evolution that I'm really puzzled by the vehemence with which adaptationists defend their orthodoxy.
it's not reluctance to admit that characters can be fixed by neutral processes; it's reluctance to assume neutrality without evidence (you assumed PTC tasting was neutral, but it's not. If everyone had assumed that, we would have missed out on some interesting biology). the "orthodoxy" is simply basic population genetics-- in some situations, neutral processes swamp selection, and in other situations selection is more efficient. these are *empirical* questions. I agree your example of the rhino horns sounds like drift, but show me the locus that controls horn number and give me some sequence to analyse, then we can talk.
It seems to me that the relative importance of selection and drift has been debated extensively rather than everyone assuming that all phenotpes are adaptive.
ReplyDeleteUntil relatively recently many evolutionary biologists in fact thought selection acting on phenotypic traits was extremely weak and that evolution by natural selection was a very slow process. Only recently have we started to accept that selection can be very strong and act very quickly, (e.g Kinsolver et al 2001).
It is not simply the "adaptationists" that are guilty of assuming a mechanism. Wright famously argued that the variation in flower color between populations in Lianthus parryae was due to drift, this was his best example of drift acting on a phenotypic trait. However we know have pretty strong evidence that the differences in flower color between these populations is driven by selection (Schemske and Bierzychudek 2001). I think selection actually acts on a much finer phenotypic scale and a much broader integrative scale than most people think.
I think that there is indeed a danger both in simply assuming that traits are either due to selection or drift and that both possibilities need to be examined. However, there is probably a bias in that people studying phenotypic selection are more likely to study phenotypes that appear to be functionally important to an organism.
Rather than fix phenotypes within a population I wonder if drift does indeed have an unnapreciated role in determining the early fate of mutations. Two populations could differ dramatically in some character simply because drift influenced the variation in the trait and then selection acted on that variation.
But is it possible to concur on null hypotheses for each level, say for a large but finite population?
ReplyDeleteabsolutely. in that example-- a large but finite population, the math has been done. for a diploid, the probability of fixation of a neutral allele is 1/2N, where N is the population size. For a selected allele, most of the time it disappears immediately as well, but as N increases, the probability of fixation approaches 2s, where s is the selection coefficient (likely <= 0.01). For very large N, then, the vast majority of fixed alleles should be due to selection.
for smaller N, it gets trickier, and there's no a lot of work done incorporating demography (like would be necessary for modeling human races, for example). But don't worry, I have a feeling people are working on it :)
Rather than fix phenotypes within a population I wonder if drift does indeed have an unnapreciated role in determining the early fate of mutations.
ReplyDeleteyeah, most mutations are lost in those initial first generations. Razib posted on this:
http://scienceblogs.com/gnxp/2006/10/you_only_go_extinct_once.php
sorry, link here
ReplyDeleteI don't think that is the problem with adaptationism. I think the problem is the assumption that selection explains the origin of adaptation. And by this we do not mean only how selection may increase the populational frequency of a trait in a population, but how this selective pressure, acting in a sustained and directional fashion, may come to accumulate several such mutations and extensive organic change (not only population frequency change) between early and late generations, pretty much as it is shown to occur in artficial selection. The point being that this accumulation is driven by selection and that the final result will be an adapatation to that selective prossure that would no have occurred without the direction given by selection. Hence, selection as "creator" of adaptation... not a mere restriction (which is what it really is)
ReplyDeleteNotice why mutationism is launched against darwinism; it is one thing if I select succesively lighter flies until I get white flies; a different thing is if a white fly is born at once, in which case I do not require selection. Then, if adaptations originates in a single step, no matter how "good", are not the result of selection, but of a mutation with a high effect.
By the way, where did P-tr come up with that "8%" figure for being considered a "large efect"? We can fin examples of evolution by muations with an effect much larger than that.... not to mention all the one-step changes that are qualititative and cannot readily be assigned a percentage.
-Alipio
Here are a few reasons why selection is a more prevelent force shaping evolution than is mutation alone. The selective environment changes rapidly, a phenotype that may have had the highest fitness one year may not the next. Selection acting on existing variation will act much faster than the occurence of very large mutations.
ReplyDeleteAlso a mutation occurs only in one genetic background and only in one individual, A single mutation, even if it confers a large advantage is likely to be lost early on and may not be advantageous in different genetic backgrounds.
By the way, where did P-tr come up with that "8%" figure for being considered a "large efect"?
ReplyDelete??? what 8% figure?
sorry, maybe it wasn't you...someone did... show up! haah
ReplyDeleteAnd why should mutations with small effects stand a better chance of being favorably selected? Specially if there are non-genetic sources of variation acting on a trait that drown these effects, something not uncommon in metric traits. In artificial selection this is easier not only because of the power of the human selection itself but also because of the standarization of epigenetic conditions. But in nature...
ReplyDeleteAsides from this, I know a handful of examples of "re-organization" in vertebrate evolution that could not have been gradual (tortoise scapula under ribs, for instance). I know another handful of cases with molecular caharacterization of a high- effect mutation is behind a new adaptation.
But, I still don't know any case of a new adaptation with several small effect, molecularly characterized genes behind it.... can anyone recommend me something?
-Alipio
If directional, consistent selection does not shape adaptations, events of selection seem as contingential, "chance", as events of drift. Selective accumulation as a theory of adaptation also tends to ignore other two important and well-documented sources of adaptation: the ocurrence of exaptation, and epigenetic adaptation.
ReplyDelete-Alipio
I still don't know any case of a new adaptation with several small effect, molecularly characterized genes behind it.... can anyone recommend me something?
ReplyDeleteI think skin color in humans is a decent example of that. for example:
a review that focuses on a couple recently characterized genes
a small study of positive selection on pigmentation genes in humans
In this case the evident epigentic plasticity of this trait and the variability in that plasticity within each race has not been taken seriously nor adequately studied. And probably nobody is intending to do so. Why? I'm guessing because of the conceptual predilections of darwinism: What "rocks" are mostly adaptationist scenarios of gene selection (with no explicit epigenetic "intermediaries" considered, of course). I won't dedicate myself to prove it here..maybe I'll write something haha
ReplyDeleteI am sorry to say I cannot be convinced by that example, for that reason, as well as for the reason that basic data remains to be collected since we know this trait is affected by several other genes of which most remain unstudied. Some genes can mutate with a stronger phenotype (red hair for instance) and can be found to be "positively selected"
Now, when we find that substitution rates show "positive selection" in a pigmentation gene, does this mean that selection has shaped the evolution of human skin color? Nope.
It is good we brought this up because now we can discuss just how far can we go in creating evolutionary scenarios from observing the changes in sequence substitution rates in a gene.
In first place consider these are succesive mutations in a gene along its evolutionary history, and not so evidence of a coexistence of several genes of small effects affecting a same trait (as in the scenarios where selection is the force that accumulates genes shaping an adaptation).
I'd like to ask you, P-ter, if you think that finding "positive selection" in a genes is direct evidence that at some point in the evolution of humans and races, the situation was such, that slight differences in the capacity to taste bitternes, or slight genetic differences in skin color, was what determined succes, that is, outcompetition of those who did not have these genes. Is that the correct inference? Did "positively selected" mutations of microcephalin alleles (that now make no functional difference, by the way) once determine the diference between competitive success and extinction for those outside of africa?
In my opinion, a "positively selected" gene provides no direct evidence of a process of "bettering" or shaping of an adaptation by directional selection, which requires the coexistence of several genes of small effects.
Actually, changes in positively selected genes can have great phenotypic effects... each mutation could have been well-separated in time and not even been selected for the same function.
-Alipio
"The African rhinoceros has two horns while the Indian rhinoceros has only one. The question is whether this difference is due to natural selection—is two horns better than one in Africa? Or, is it just an accident of evolution that one species has two horns while the other has only one?"
ReplyDeleteI don't know. You either. Barring invention of a user-friendly time machine neither of us ever will, probably. P-ter wants to see some molecular details of horn development; I'd rather have a perfect phylogeny of rhino populations and the ability to map horn phenotypes onto it, but either type of data will only offer clues. In the ansence of information it's not difficult to make up just-so stories that would impart a selective advantage to 2-horns-in-Africa and/or 1 in Asia (e.g., protection against different predators, energy costs of maintaining 2 horns when 1 would do, etc.), and sexual selection is the joker in the deck. But it's even easier to shrug and say "drift." Just so!
From Michael Lynch's PNAS paper of 15 May 2007:
ReplyDelete"Thus, as will be discussed more fully below, to the extent that an increase in gene-architectural complexity is a precondition for the emergence of greater complexity at the organismal level (including the hallmarks of multicellularity: multiple cell types, complex patterns of gene expression, and mechanisms of cell signaling), a long-term synergism may exist between nonadaptive evolution at the DNA level and adaptive evolution at the phenotypic level. There is no need to abandon the idea that many of the external morphological and/or behavioral manifestations of multicellularity in today’s organisms are adaptive.
Many external morphological characters, of course, not all. Finding good methods to discern adaptation (with neutrality as zero hypothesis) has been the focus of the "adaptationists", not telling just so stories: for 40 or what is it years?
Finding good methods to discern adaptation (with neutrality as zero hypothesis) has been the focus of the "adaptationists", not telling just so stories: for 40 or what is it years?
ReplyDeleteexactly. the debate on this blog seems to be stuck in 1970 (I'm a little amused to be called an "adaptionist". Who says that anymore, honestly?). back then, the data was sparse and people argued about basic assumptions and worldviews. Now there's data, and lots of it. There's something for everybody, Larry-- switch fields!
I'd like to ask you, P-ter, if you think that finding "positive selection" in a genes is direct evidence that at some point in the evolution of humans and races, the situation was such, that slight differences in the capacity to taste bitternes, or slight genetic differences in skin color, was what determined succes, that is, outcompetition of those who did not have these genes.
ReplyDeleteyes, to a certain extent. we're talking about small selection coefficients here. the strongest signal of selection in the human genome is at the lactase gene (on an allele that confers lactose tolerance). The selection coefficient is estimated at 0.1, meaning that people with the allele tended to have 10% more children than those without it. Most other selection coefficients are much smaller (on the order of 1%).
An allele doesn't have to "determine" success to sweep to fixation; it only has to have a slight advantage over many generations.
To a certain extent, then. The point now is exactly what are the limits. Maybe all we can do is stare at a protein sequence and say it has changed faster than neutral.
ReplyDeleteLactose intolerance is a perfect example of the one-step mutation leading to the origin of a potential adaptation. Not the result of any selective accumulation or shaping. And lactose intolerance will continue to exist.
You talk about this as if it were a standing competition. I think any greater representation of lactose intolerance in current populations probably just reflects descendance from early tribes that were very cow and milk oriented, where milk is a major source of adult food (a lactose intolerant adult is unlikely to hang out with those guys).
Observing populational frequencies of an allelle is different from observing sequences that show "positive selection" , eve if in both cases we speak of selection for a gene, in the second case we assume that accumulation of mutations has occurred, and that therefore these mutations must have become fixed, that is present in most or all of the population.
Maybe that is something we want to keep in mind that is different from how selection is proven by populational frequencies. For instance, in sickle-cell disease is simply "less rare" (not a majority!) under the right selective pressure.
I have no problem accpting that a slighter greater capacity for tasting bitterness can lead to a modest increase in population frequency under the right seletive conditions. It is a lot harder to belive that a mutation with a slight effect like this was decisive between prevailing and not prevailing at some point in human evolution.
Ooops error
ReplyDelete"LactoseTOLERANCE is a perfect example of the one-step mutation leading to the origin of a potential adaptation. Not the result of any selective accumulation or shaping. And lactose intolerance will continue to exist"
Sorry
I would like to thank everyone for giving a layman a decent idea of the history and current status of population genetics. The discussion on null hypotheses, a priori assumptions, levels, demographics et cetera, here as well as on R(P)M's blog, helped a lot. [And RPM has a series of posts explaining basic models and tests for selection, sweet!]
ReplyDeletep-ter:
"For very large N, then, the vast majority of fixed alleles should be due to selection."
Thank you for taking time to answer the specific question!
[Sadly, I seem to remember seeing those model equations before. To mix some metaphors, you can lead a horse to water, but you may have to hit him over the head by a two-by-four to get him to think.]
I think any greater representation of lactose intolerance [sic!] in current populations probably just reflects descendance from early tribes that were very cow and milk oriented, where milk is a major source of adult food (a lactose intolerant adult is unlikely to hang out with those guys).
ReplyDeleteAre you perhaps thinking exclusively of populations in hot climates? Because in temperate climates milk from herds (cows, yaks, reindeer) are helpful due to year round availability, replenishment and storage as cheese and butter. AFAIU winter starvation was a concern for quite large groups until recent times, and milk (and of course produce like potatoes) made a, perhaps the, difference.
p-ter says,
ReplyDeleteexactly. the debate on this blog seems to be stuck in 1970 (I'm a little amused to be called an "adaptionist". Who says that anymore, honestly?). back then, the data was sparse and people argued about basic assumptions and worldviews. Now there's data, and lots of it. There's something for everybody, Larry-- switch fields!
I agree that the debate seems to be stuck in the 1970's. I thought that the adaptationists would have seen the light after the publication of the spandrels paper. Instead, they are still insisting that every visible character has to be an adaptation. That's so 70's. It's like they never heard of random genetic drift except in biochemistry class.
Larry wrote: I don't understand why the adaptationist camp is so reluctant to admit that some visible characters can be fixed by random genetic drift.
ReplyDeleteThe 'adaptationist camp' is not reluctant to admit that some visible characters can be fixed by random genetic drift. That visible characters can be neutral is a matter of course. To show this is something different, as it is equivalent to showing absence of effect. Lewontin’s rhinos (Scientific American about 1975) might be an example, but as pointed out above, nobody really knows.
Moreover, initial neutrality and continuing neutrality might not be the same thing.
I would think the fact that all mammals have seven cervical vertebrae was neutral at initiation, given that vertebrates differ in that number. That number of seven cervical vertebrae is fixed at least since the therapsids (mentioned in Kemp). Nowadays, having seven cervical vertebrae is so enmeshed in the developmental program that it is an indication of faulty development: deviations from seven occur in spontaneous abortions, but not (AFAIK) in adult humans. Present day developmental necessity has no relevance for the question of initial selection.
Whoever studies behavioural ecology or evolutionary ecology is not going to choose a presumably neutral character to study: what would be the fun? A collection of known cases of selection should not be confused with an a priori commitment that everything whatsover is always selected.
I still don't know any case of a new adaptation with several small effect, molecularly characterized genes behind it.... can anyone recommend me something?
This raises several questions.
Apart from the difficulty of deciding what is 'new', after the initial phase of randomness in getting into a population, selection speed depends on effect size. That is, imagine identical phenotypes, either due to one mutation with large effect or to one mutation with small effect, in an otherwise identical population. The large effect mutation gets faster to fixation. The distribution of effect sizes of mutations leading to ‘new’ traits will be skewed towards larger effect size.
Next point is that for most traits that are considered an adaptation, nothing is known about genes, certainly not molecularly characterized genes. Even in cases where some molecularly characterized gene is known to be involved in a trait, as Bmp4 in Geospiza beak size, this might not be the gene that is the target of selection. Beak size differences between species seem to be a matter of differences in expression, so what regulates expression? Many genes belonging to that exasperating class called ‘transcription factors’? We don’t know for certain either whether the genetic variation within say G. fortis is related to differences in gene expression of Bmp4, because the assay has not been done..
Larry should really look further than his own specialty here; he makes the impression of never having gotten further than the spandrels paper.
Hi Larry,
ReplyDeleteI just thought I would let you know that you've been cited by scordova (Salvador T. Cordova) over at Uncommon Descent.
Larry Moran, aptly said, “it’s going to be a challenge to refute Behe’s main claims”.
And then later in the comments,
Larry Moran points out the interesting example of rhinos having either 1 or 2 horns. Natural selection doesn’t really explain this very well!
"Nowadays, having seven cervical vertebrae is so enmeshed in the developmental program that it is an indication of faulty development: deviations from seven occur in spontaneous abortions, but not (AFAIK) in adult humans"
ReplyDeleteyeaaah, well... keep in mind that in sloths and manatees cervical number just jumped out of its enmeshment in the developmental program.
Do not misinterpret the monstrosites that may correlate with altered cervical number.
Polydactyly is also frequently associeted with stillborns, mental retardation and other nasty phenotypes. But this is not proof of any truly causal relation, other than state the fact that both can apper under abnormal developmental conditions.
Accordingly with the fact no causal link is given, we observe that it is possible to have only polydactyly, and be otherwise normal; and recently we have the case of a polidactyl fossil species of amniote, and digits have beeen shown to have been lost but then come back in the evolution of species of the Bachia genus of lizard
"Whoever studies behavioural ecology or evolutionary ecology is not going to choose a presumably neutral character to study: what would be the fun?"
Truly so. But frequently he later realizes the trait is neutral. Or epigenetic. And, for the same reason, they have no darwinian story and therefore, no publication. A "failed hypothesis". So, we never really get to know.
"Next point is that for most traits that are considered an adaptation, nothing is known about genes, certainly not molecularly characterized genes. Even in cases where some molecularly characterized gene is known to be involved in a trait, as Bmp4 in Geospiza beak size, this might not be the gene that is the target of selection. Beak size differences between species seem to be a matter of differences in expression, so what regulates expression? Many genes belonging to that exasperating class called ‘transcription factors’?"
I don't consider that case to be the molecular characterizatio of the muation that leads to beak size differnces. We ONLY know that changes in BMP4 expression were involved (yes, these HAVE been observed and compared in the embryos of the galapagos finches) so we now know part of the developmental pathway, which helps, but not the actual mutation. In any event, we already know diffierences in beak size in finch populations are not by accumulation of samll-efect genes but a few genes of great effect such that you observe two or three main beak kinds. These kinds are certainly affected by selection, but do not originate by selection.
-Alipio
I thought that the adaptationists would have seen the light after the publication of the spandrels paper. Instead, they are still insisting that every visible character has to be an adaptation.
ReplyDeleteheh. larry, honestly, if that's your contribution to this "debate", well...
1. no one's insisting all visible changes have to be adaptive, in case it's not clear from my comments (or RPM's post). of course, many visible changes are adaptive, and ruling adaptation out a priori is silly.
2. the spandrels paper was written in 1979. believe it or not, population genetics still exists. In these two threads, I've cited a number of papers from the recent popgen literature on ruling out neutrality with regards to certain phenotypes. there are ways to do this, and as i've repeated, these are *empirical questions*. You haven't cited a damn thing except a paper written in 1979. here's a review from 1995...it's old, but it details some of the methods for detecting selection that "adaptationists" use. please read something--anything--written after 1979.
you're wrong about the power of the neutral theory. it's not the end of the world, but seriously, obstinate dismissal for an entire field (apparently without bothering to read a introductory text, or at least a recent review) is unbecoming for a professor.
From Michael Lynch's PNAS paper of 15 May 2007:
ReplyDeletealso from that paper: "a long-term synergism may exist between nonadaptive evolution at the DNA level and adaptive evolution on the phenotypic level".
That's an intriguing hypothesis-- introns are mildly deleterious, but become fixed because of small population size, but then there's selection for a nuclear membrane to allow their removal before translation. or selfish DNA elements invade (nonadaptive), creating selection for the plethora of epigenetic silencing mechanisms we have today.
helleen says,
ReplyDeleteLarry should really look further than his own specialty here; he makes the impression of never having gotten further than the spandrels paper.
Try reading Evolution by Accident. Let me know what parts you disagree with.
Heleen, I'm delighted to hear you admit that many visible characters could easily have been fixed by random genetic drift. That makes you a pluralist and it separates you from some of the other commenters who seem very reluctant to concede this point.
Whoever studies behavioural ecology or evolutionary ecology is not going to choose a presumably neutral character to study: what would be the fun?
What does this mean? Are you only interested in a single mechanism of evolution? How do you choose which characters to study if you don't know at the start whether they are adaptive or not?
p-ter says,
ReplyDeleteno one's insisting all visible changes have to be adaptive, in case it's not clear from my comments (or RPM's post). of course, many visible changes are adaptive, and ruling adaptation out a priori is silly.
At the molecular level it seems that >90% of all evolutionary change is due to random genetic drift. I suspect that a majority of visible characters are also fixed by random genetic drift and only a minority are adaptive.
What proportion of visible characters do you think are adaptive?
Nobody is ruling adaptation out. Gould and Lewontin didn't do it in 1979 and none of the pluralists since then have said anything that remotely resembles your strawman characterization of our position.
And please stop your senseless babbling about ways of detecting selection. I'm well aware of them. In fact, I've posted several articles on detection of adaptation on Sandwalk and on talk.origins, beginning in 1990. Nobody that I know is questioning the fact that natural selection exists and can be detected. What I'm questioning is the attempt to limit random genetic drift to events at the molecular level where they are uninteresting.
That tactic is a throwback to the 1970's where Gould and Lewontin addressed it head-on by saying ...
At this point, some evolutionists will protest that we are caricaturing their view of adaptation. After all, do they not admit genetic drift, allometry, and a variety of reasons for non-adaptive evolution? They do, to be sure, but we make a different point. In natural history, all possible things happen sometimes; you generally do not support your favored phenomenon by declaring rivals impossible in theory. Rather, you acknowledge the rival but circumscribe its domain of action so narrowly that it cannot have any importance in the affairs of nature. Then, you often congratulate yourself for being such an undogmatic and ecumenical chap. We maintain that alternatives to selection for best overall design have generally been relegated to unimportance by this mode of argument. Have we not all heard the catechism about genetic drift: it can only be important in populations so small that they are likely to become extinct before playing any sustained evolutionary role ...
And please stop your senseless babbling about ways of detecting selection.
ReplyDeleteshit, I thought I was making a good deal of sense. but deal. as long as you promise to read those papers :-)
p-ter keeps uselessly sputtering but but it's an empirical question.
ReplyDeleteNot in Sandwalk. The matter is settled by that paragraph from Spandrels repeated by Larry (not for the first time: ...Then, you often congratulate yourself for being such an undogmatic and ecumenical chap. ...
Of course that scenario is possible. Larry thinks it's actual for all but the few sons of light aka pluralists. That is the thesis here, not any mere empirical question.
Heleen said...
Larry wrote: I don't understand why the adaptationist camp is so reluctant to admit that some visible characters can be fixed by random genetic drift.
The 'adaptationist camp' is not reluctant to admit that some visible characters can be fixed by random genetic drift....
/Heleen
She's back to that mere empiricism.
...
Nucleo seems to make up his own rules:
In my opinion, a "positively selected" gene provides no direct evidence of a process of "bettering" or shaping of an adaptation by directional selection, which requires the coexistence of several genes of small effects.
illustrated by
"LactoseTOLERANCE is a perfect example of the one-step mutation leading to the origin of a potential adaptation. Not the result of any selective accumulation or shaping. And lactose intolerance will continue to exist".
It doesn't count unless the genetic background is what you think it ought to be?
Who mentioned 8% as a large effect? Me. Of course there has to be an arbitrary designation. 7 or 8 percent AFAIK, what do you think is used in quantitative genetics?
Pete Dunkelberg