David Dobbs mucks up evolution, part II

If you’ve been following this site, you’ll know that yesterday I wrote a long critique of David Dobbs’s recent article in Aeon magazine, an article called “Die, selfish gene, die” (the subtitle is “The selfish gene is one of the most successful science metaphors ever invented. Unfortunately, it’s wrong”). Actually, there were a fair number of comments on that piece (127 up to now!), so I was pleased that readers took the time to digest a long science post.

Sadly, I couldn’t analyze Dobbs’s entire article in one go, both because of the “TL/DR” syndrome and because I simply didn’t have time: almost all these posts are written strictly between 6 and 8 a.m., after which I start my day job. So today I’ll finish my critique by discussing the second contention of Dobbs: that conventional natural selection, in which existing genetic variation is sorted out according to the gene copies’ ability to replicate, is wrong. As he said, “Die, selfish gene, die.”

I gather that Dobbs has backpedaled on his own website, but I am not going to read whatever clarification or retraction he issued until I’ve finished writing this. As I said yesterday, I want to discuss the original piece, not some subsequent gloss on it.  I’ll then have a look at what Dobbs wrote.  But he should know by now that, regardless of whatever encomiums other science writers (or scientists) gave him, his piece was a bad job. If he were an honest man, he would say that it was indeed full of misleading statements, and apologize for it.  But we know that won’t happen!

Today’s discussion is on what Dobbs and some of the heroes of his piece (especially Dr. Mary Jane West-Eberhard) see as the truly novel and non-Darwinian refutation of the selfish gene idea: the idea of genetic accommodation.  “Genetic accommodation” has other names: it’s also been called “The Baldwin Effect” and “genetic assimilation.”  But all of these names refer to a single mechanism: instead of existing genetic variation being subject to natural selection in an existing or changing environment, the environment itself evokes phenotypic (not genetic) variation, which is then somehow fixed in the species’ genome.

This idea was first suggested in 1896 by the American psychologist James Baldwin, although little was known about genetics then.  The idea was worked out in nearly its present form in a paper by George Gaylord Simpson in 1953, and then made famous by geneticist Conrad Waddington, who demonstrated how it might work using a fruit fly experiment.  The idea has been altered and refined—in a way that makes it truly non-Darwinian—by Mary Jane West-Eberhard. Finally, Dobbs misrepresented the whole notion in his piece: not only misleading people about how it works, but by claiming that it makes hash of Dawkins’s “selfish gene” idea.

Now there are really three versions of genetic accommodation. The first of these falls firmly within the purview of neo-Darwinism, and in no way violates the “selfish gene” idea, as Dobbs mistakenly trumpets.  The second, the one that West-Eberhard has proposed, does have non-Darwinian features, but there’s simply no evidence for it.  The third, which seems to be Dobbs’s own garbled version of West-Eberhard’s idea, is non-Darwinian in two ways, and again there’s no evidence for it. Here are the three versions.

1.  A change in the environment exposes a bunch of mutations whose effects were masked in the previous environment.  This exposes a lot of new genetic variation, some of which could be adaptive in the new environment.  The genes that replicate better in the new environment (let’s just say they improve the reproduction of their carriers), sweep through the population via natural selection.

The classic example of this was Conrad Waddington’s artificial selection experiments with fruit flies. He exposed the pupae to heat shock, and this screwed up the development of the flies, so that some of the adults who hatched from the pupal cases had broken veins in their wings.  Waddington then selected the broken-veined flies and bred them to create a new generation, whose pupae were also subject to heat shock.  There were, in their offspring, a higher percentage of broken-veined flies. Waddington continued this selection for several generations. Eventually he saw that broken-winged flies were appearing even when their parents weren’t heat-shocked.  Although this looks like Lamarckian inheritance—the inheritance of acquired characteristics—what was happening was eminently neo-Darwinian. The explanation was simple: the heat shock simply exposed those individuals carrying genes that gave them a propensity for broken wing veins. These effects weren’t expressed at normal temperatures: it took a heat shock for the genes’ effects on wing veins to be seen (that shock might have done this by altering the expression of those genes).  Eventually, via continued selection, Waddington accumulated enough “broken wing vein” genes that they showed their expression without the need for a heat shock.

That, of course, and this form of genetic accommodation, is totally in harmony with Dawkins’s idea of “selfish genes”. The broken-vein genes were indeed “selfish” in the artificial selection experiment, for Waddington selected their carriers to breed.  The only novelty here is that the “selfish” genes were exposed by an environmental change.

Now Waddington’s experiment was done in the lab. Does this happen in nature? My answer is hedged: “Probably, but the evidence is thin.” I can think of only one really convincing demonstrated example: that described in a paper by Scoville and Pfrender in Proc. Nat. Acad. Sci. in 2010.  These authors looked at the small crustacean Daphnia in two lakes in which fish were introduced about 50 and 90 years ago, respectively, and contrasted them with Daphnia in fishless lakes. Normally Daphnia have a plastic response to the environment: if there is high ultraviolet light, they become pigmented to protect themselves (a crustacean sunscreen). But if put in a lake with fish, individuals can get rid of their pigmentation. This “developmental plasticity” is adaptive, because darker individuals are more easily seen by fish and eaten. Presumably natural selection favored the ability of an individual to change its color based on the environment it “perceives,” just as cats grow longer fur in colder weather and shed it when the weather gets warm.

These authors found, though, that in the permanent-fish lakes, where predation was high, the absence of color became “canalized”: that is, individual Daphnia were no longer able to make as much pigmentation when exposed to UV light. What presumably happened is that, when fish were constantly around, they selected for those individuals that didn’t have the ability to change color at all (a mistake like that would get you spotted and eaten, and there’s also a metabolic cost to maintaining flexibility)—those individuals who, though natural selection, simply lost their ability to alter their color in response to intense sunlight.  That, of course, involves “selfish gene-ery”: the preferential replication of those gene variants that have lost the ability to effect color change. You don’t need to become pigmented in lakes where it never pays to lose your pigment, and you pay a metabolic (and presumably reproductive) cost to keep that flexibility.

But that’s the only example of genetic assimilation I find convincing.  It has undoubtedly happened in other cases, but we can’t know for sure because we weren’t there to observe  the evolutionary history. That’s important because, to make a convincing case for genetic accommodation, you need to know whether the genetic variation was there in the first place, and simply selected in the new environment (normal natural selection), or was actually revealed by the new environment.

There are other possible cases, but these are purely speculative.  For example, if an early Tiktaalik-like fish were to walk temporarily on the land, and gain an advantage by so doing (e.g., get more stuff to eat or the ability to scuttle from a drying pond to a more permanent one), those individuals who were able to develop more muscular “fin-legs” during their terrestrial sojourn, due to exertion, would be favored. If that difference in ability to develop musculature had a genetic basis, then eventually such sojourns could select for a better ability to walk on land. Perhaps that is how terrestriality evolved. But of course there’s an alternative scenario: those individuals who had stronger fin-legs to begin with would have an advantage walking on land. That’s not genetic accommodation, but simple natural selection. But neither example violates the notion of the selfish gene.

In contrast, we know of many cases in which existing genetic variation, not revealed by an environmental change, responded to selection: antibiotic resistance in bacteria (the mutations are there before the antibiotic is given), the evolutionary change in color of the peppered moth Biston betularia from white to black during industrialization in England (the black moths were there in low frequency before the polluting began), and the increase in size of finch beaks in the Galapagos in the seventies when there was a drought, killing plants with small seeds so that only finches with the larger beaks were able to eat (finches with bigger beaks were there before the drought).  So the existing evidence supports conventional selection, not genetic accommodation. My guess is that the conventional mechanism would be far commoner, simply because there are few environmental changes that expose new genetic variation that could adaptively respond to that change. (Ancestral brown bears moving north would not get whiter coats due to developmental plasticity.) But regardless, this doesn’t, contra Dobbs, suggest that the “selfish gene” notion is wrong. I say that so often because Dobbs says the opposite so often.

2. A change in the environment alters the phenotype in a directional and adaptive way, and genes are not initially involved. Later, that phenotypic change becomes read into the DNA by selection of genes that promote the adaptive phenotype.  This is, I think, Mary Jane West-Eberhard’s view of how genetic accommodation works. This seems less probable to me than version #1, simply because I can’t envision an environmental change preferentially invoking an organismal change that’s useful in that environment. Instead, like the effects of heat on variants of the heat-shock protein Hsp 90, an environmental change (in this case the heat shock) simply exposes a bunch of genetic variants with random effects on the organism, nearly all of which are maladaptive (deformities and the like).  Heat-shock doesn’t expose mainly those variants that are resistant to heat.  It’s is “non-Darwinian” to envision an organism being able to respond adaptively to an environmental change UNLESS it’s prevously evolved adaptive plasticity, as in the Daphnia case above. But in that case the situation reverts to scenario #1, the exposure of a bunch of genetic variation, only some of which is adaptive, followed by selection among the adaptive variants.

I know of no case of this type of genetic accommodation, and none are really given in West-Eberhard’s 800-page book, Developmental Plasticity and Evolution, which I’ve read.

Despite this, Dobbs not only touts the views given in that book, but quotes West-Eberhard as saying that, in light of her ideas, Dawkins’s selfish gene idea “risks ending up on the wrong side of history.”  Pardon me, but that’s a rather presumptuous thing to say about one’s own theories.  She also says, “the gene does not lead; it follows”, which is not really accurate in her situation if the plastic response of the organism to the new environment evolved through natural selection. In that case the gene originally led, and then follows after the plastic response is expressed in a new environment. But here again no violation of the “selfish gene” paradigm is seen: the environmental changes eventually become fixed in the genome via the selection of genes that promote a response.

3. Dobbs’s Lamarckian view of genetic accommodation.  Dobbs’s characterization of how genetic accommodation works is deeply muddled, for it invokes a Lamarckian process in which a developmental change gets read into the genome, but not by selection among pre-existing variants. It also involves an environmentally invoked phenotype being inherited across generations—that is, the inheritance of acquired characters.

Dobbs’s scenario begins by describing selection for predators that ambush their prey by leaping on them (e.g., a serval).  Then the environment changes: there’s a forest fire. This changes the situation: now to catch prey you must run them down over open ground.  But instead of proposing the simple theory that predators with longer legs, better endurance, and so on, have a selective advantage—conventional natural selection—Dobbs postulates a combination of non-genetic adaptive change of phenotype based on changed gene expression, followed by Lamarckian inheritance of that change, and then, finally, the occurrence of some mutations that favor that phenotype. (Why doesn’t he just cut out the middleman and assume that mutations were there at the outset? Also, why would fire just happen to change the expression of your genes to make you a better open-ground predator? Dobbs does not explain.)

Read his explanation and see if it makes sense to you.  The first part does, because it evokes conventional natural selection:

For example, suppose you’re a predator. You live with others of your ilk in dense forest. Your kind hunts by stealth: you hide among trees, then jump out and snag your meat. You needn’t be fast, just quick and sneaky.

But comes the muddled non-Darwinian part (my emphasis):

Then a big event — maybe a forest fire, or a plague that kills all your normal prey — forces you into a new environment. This new place is more open, which nixes your jump-and-grab tactic, but it contains plump, juicy animals, the slowest of which you can outrun if you sprint hard. You start running down these critters. As you do, certain genes ramp up expression to build more muscle and fire the muscles more quickly. You get faster. You’re becoming a different animal. You mate with another fast hunter, and your kids, hunting with you from early on, soon run faster than you ever did. Via gene expression, they develop leaner torsos and more muscular, powerful legs. By the time your grandchildren show up, they seem almost like different animals: stronger legs, leaner torsos, and they run way faster than you ever did. And all this has happened without taking on any new genes.

Then a mutation occurs in one grandkid. This mutation happens to create stronger, faster muscle fibres. This grandchild of yours can naturally and easily run faster than her fastest siblings and cousins. She flies. Her children inherit the gene, and because their speed wows their mating prospects, they mate early and often, and bear lots of kids. Through the generations, this sprinter’s gene thus spreads through the population.

Now the thing is complete. Your descendants have a new gene that helps secure the adaptive trait you originally developed through gene expression alone. But the new gene didn’t create the new trait. It just made it easier to keep a trait that a change in the environment made valuable.

Note the bold part, which invokes adaptive change in gene expression that was not due to a pre-evolved plasticity (or perhaps it was, in which case the genes were leading!), and, especially, the Lamarckian notion that “your kids run faster than you do” because the changes in gene expression are inherited. But how does that work? It’s Lamarckian, an adaptive and purely epigenetic change in phenotype that can be passed on for at least two generations (“grandchildren).

Now I suppose this is possible, but it is unparsimonious, evoking as it does a concatenation of unlikely circumstances: an “adaptive” plasticity that might not have rested on genes, the Lamarckian inheritance of an adaptive but nongenetic change for several generations, and then a new mutation that is somehow connected with the plastic response.  Why the unnecessarily multiplication of entities? Had Dobbs started this scenario with the mutation in paragraph 2, he wouldn’t need to suggest this convoluted scenario.

And it’s not that the data demand that we invoke this complicated scenario. It’s simply concocted out of thin air, with no evidence supporting it (and no known examples), and then waved around like a flag, with the flag-bearer crying “Horray! Hooray! The selfish gene is dead!”

Parsimony, my dear Dobbs, parsimony. We need not concoct such convoluted scenarios unless we have evidence showing that the present theory is inadequate. But we don’t have that evidence: there is no “black body radiation” phenomenon in evolutionary biology.

Dobbs’s piece goes on to further tout this idea and drag in some scientists (many of whom I’ve criticized before) who like the idea, but I’ve done my job now and must rest (or rather, work on my book).

Let me add one thing, though. I’m constantly puzzled these days by how often people argue that the neo-Darwinian synthesis is wrong, and that we need a new paradigm. Genetic assimilation, epigenetics, horizontal gene transfer—all of these buzzwords are evoked as reasons to jettison our “conventional” view of evolution. But always, when you look at the data, the evidence that these phenomena will overturn neo-Darwinism is nonexistent.

I’ve already written a lot on the epigenetics hype, and have shown that there’s no evidence that a single adaptation in nature involves the fixation in the DNA of an epigenetic alteration of the genome that isn’t initially inherited.  Yet people keep banging on about epigenetics.

I’m not sure why the hype continues, but perhaps it has to do with the fact that the main paradigm of evolution—the neo-Darwinian synthesis—is largely consolidated, and is correct. Sure, there are surprises to come, and interesting new phenomena, but there’s no “quantum mechanics” of evolution on the horizon.  Some theories don’t need to be overthrown because they’re generally right. Perhaps people don’t like working in a field where there’s no new “paradigm” to forge, and Kuhn has ruined us all!

The “neo-Darwinism is dead” trend may have to do with ambition, or perhaps with boredom. I don’t know. What I do know is that the many recent challenges to neo-Darwinism have all failed to hold water, but people keep pouring liquid into that sieve.

148 Comments

  1. Jesper Both Pedersen
    Posted December 6, 2013 at 7:17 am | Permalink

    sub

    • NewEnglandBob
      Posted December 6, 2013 at 9:54 am | Permalink

      ditto

  2. Posted December 6, 2013 at 7:31 am | Permalink

    In an attempt at being charitable towards Dobbs, I tried to think of ways of salvaging his example.

    At every step, I failed.

    The hunters with the genetic plasticity were the ones that developed muscles they normally wouldn’t, the same way that a human couch potato who becomes active might. Fine so far. And those who develop more muscles catch and eat prey and thus survive.

    But what of those who don’t develop more muscles? Or, if all members develop more muscles, why mention this change in the first place?

    …and so it goes, at every step.

    Dobbs is trying to get to infinity by dividing by zero, and not truly understanding why the value is undefined — in part, because he never noticed that the division function is asymptotic negatively for negative numbers….

    Cheers,

    b&

    • sean
      Posted December 6, 2013 at 8:57 am | Permalink

      My sentiments exactly. I feel like Dobbs’ argument was just bad enough that, with my very limited understanding of natural selection, I could grok why it was wrong. Thus his article wasn’t useless after all, which maybe should help him take heart.

    • Frank
      Posted December 6, 2013 at 9:09 am | Permalink

      Hasn’t this sort of thing become rampant in popular science writing? It seems, unfortunately, that one has to at least engage in hyperbole, or engage in outright distortion, in order to “sell” the article as revolutionary (and therefore worth reading). In the field of human evolution, in particular, each new discovery is INEVITABLY touted as “completely changing” our picture of our evolutionary history. Some of these findings do shake things up a bit, but even incremental increases in knowledge are hyped to the limit. This is why I cherish the minority of science writers/journalists who keep their feet firmly on the ground.

      • Posted December 6, 2013 at 11:21 am | Permalink

        I know! Someone should write a book about this problem, titled ‘Most Scientific Paradigms are (not) Wrong‘.

      • Posted December 6, 2013 at 2:47 pm | Permalink

        It’s not just science writing.

        Journalists — and especially entertainers pretending to be journalists — increasingly think they must use tabloid-style sensationalism to get people to pay attention to them.

        Maybe they’re right, and maybe there aren’t enough people left who just want to know the facts for real journalism to survive. If so, the lasting harm done to our society will be oppressive, indeed.

        Then again, maybe it’s not such a new phenomenon. The Romans had their bread and circuses, too….

        b&

        • Diana MacPherson
          Posted December 6, 2013 at 4:09 pm | Permalink

          Yeah, I think they’re mistaken. Most likely people interested in an article about evolution would prefer accuracy over controversy. I would happily read a “Why the Selfish Gene Is Seminal” article.

          Maybe I’m an outlier, but there is a large readership on this site and I have to believe many here would feel the same.

          • Posted December 6, 2013 at 5:25 pm | Permalink

            If nothing else, we’re certainly part of the “long tail.” But I suspect it’s much more the case that we’re a sizable minority, and likely one that could prove quite profitable.

            Mom has a subscription to Science News, which I read religiously when I go to my parents’s place for dinner. Sensationalism is vanishingly rare; when used, it’s either deserved or clearly tongs-in-cheek. There’s rarely anything significant to criticize, and they’re not shy about ‘fessing up when the fuck up — which, again, is damned rare.

            Indeed, I’d go so far as to state that the journalism in Science News is significantly more responsible than that in Science, regardless of the reputation of the latter.

            Cheers,

            b&

    • Posted December 10, 2013 at 8:07 am | Permalink

      >But what of those who don’t develop more muscles? Or, if all members develop more muscles, why mention this change in the first place?

      Presumably some will develop muscle better than the others, and will have a higher chance of survival.

      What I don’t understand, still, is how this goes against TSG. Presumably this kind of muscle adaptivity is still an expression of genes. You can concoct a hypothetical situation and reason that two fast runners who mate, wouldn’t necessarily be passing “fast running” genes to their young, but rather genes that allow muscles to adapt to the fast-running environment more easily. At some point, a ‘real’ fast-running gene mutation may show up and be selected for.

      I suppose in this hypothetical situation it looks as if fast-running gene followed the fast-running gene expression but that’s just semantics. It’s interesting but like Jerry Coyne wrote, it all started with the gene for fast-running adaptation. So we’re back firmly into the TSG world.

  3. Diana MacPherson
    Posted December 6, 2013 at 7:34 am | Permalink

    This was a very clear explanation & I loved reading it. I’m glad I took a vacation day today so that I could give it the time that it deserved!

  4. gbjames
    Posted December 6, 2013 at 7:37 am | Permalink

    Perhaps, bored by the established nature of Darwinian paradigm, these guys want to establish a replacement. Well, OK, but why do their attempts always seem to fall back on Lamarckain stories?

    Die, Lamarck, die!

    • DV
      Posted December 6, 2013 at 8:29 am | Permalink

      Um..Lamarck is long dead I believe.

      • gbjames
        Posted December 6, 2013 at 8:36 am | Permalink

        Yes, I know. But there seem to be quite a few who haven’t gotten the memo.

      • Achrachno
        Posted December 6, 2013 at 10:32 am | Permalink

        But not as dead as he should be, it seems. How does one kill zombies again?

  5. Erik Verbruggen
    Posted December 6, 2013 at 7:40 am | Permalink

    Good piece! Another problem with theory 2 is that it might hamper actual genetic adaptation by masking beneficial mutations from natural selection. So it may be less accommodating than these authors assume, but I haven’t read the book :-)

  6. Posted December 6, 2013 at 7:46 am | Permalink

    Jerry, your first link to the first part of your reply points simply to WEIT, not to the reply.

  7. Dominic
    Posted December 6, 2013 at 7:56 am | Permalink

    If he had called it the Baldwin Effect I would have known straight away what was meant. There is a recent book on that
    Evolution and Learning: The Baldwin Effect Reconsidered. Edited by Bruce H. Weber and David J. Depew

    There is a chapter by Dan Dennett, Peter Godfrey-Smith & Terry Deacon

    http://www.epjournal.net/wp-content/uploads/ep02105107.pdf

    • Dominic
      Posted December 6, 2013 at 8:49 am | Permalink

      In fact I think it was Douglas Spalding who first said learnt behaviour becomes instinct in 1873,
      http://en.wikipedia.org/wiki/Douglas_Spalding
      See Patrick Bateson (yes, that same family!) -
      The Evolution of Evolutionary Theory, European Review. 2010, 18 (3):287-96
      Seems to be freely available…
      Also other Bateson articles & I suppose his book The Adaptability Driver

    • DV
      Posted December 6, 2013 at 9:02 am | Permalink

      As I understand it, the Baldwin effect is specifically involves learning. So I commented yesterday that it is related. But not really just another name for genetic accomodation. Jerry’s discussion above is about genetic accomodation that involves no learned behaviour contributing to the selection pressure. Genetic accomodation may be the more general phenomenon of which the Baldwin effect is just a special case.

      Actually the Baldwin effects probably makes more sense since the learning ability of the brain provides the “plasticity” factor.

      • DV
        Posted December 6, 2013 at 9:05 am | Permalink

        forgive the grammar mistakes – didn’t proofread

        • Dominic
          Posted December 6, 2013 at 10:19 am | Permalink

          No you are right – I just thought it might be of additional related interest.

  8. Posted December 6, 2013 at 7:59 am | Permalink

    Thanks again for such clear and readable explanation.

  9. John
    Posted December 6, 2013 at 8:05 am | Permalink

    I suspect that the recent ‘neo-darwinism is dead’ rumble is a phenomenon that takes place largely only among journalists, who lean toward sensationalism to get more reads.

    I would wager that among serious academics there are very few that consider the selfish gene out-dated given the current evidence.

    I suspect Dobbs simply saw what he thought was a crack, so as journalist, he pounced. Only to discover that it wasn’t a crack at all, just his own misunderstanding of the model.

    I’m not calling Dobbs a troll, but I’m surprised that a man with such talents a science writer has made such an obvious error. Suffice to say its slightly suspicious I had not so much heard of him until his article erupted. Could he be deliberately disingenuous in order to profit from a controversy? maybe he’s the Katie Hopkins of science communication.

    • Rob
      Posted December 6, 2013 at 8:36 am | Permalink

      And even if it was a crack, so what?

      More data, model changes. Isn’t that inherent to science?

      • John
        Posted December 6, 2013 at 9:25 am | Permalink

        yes if there were a crack then I’d be thrilled, we’d have advanced toward the truth in a true scientific fashion.

        Unfortunately there wasn’t one, Dobb was sensationalizing a well-known fact; namely that genes are switched on and off, and phenotypes often result from this epigenetic phenomenon. This has been well addressed within the selfish gene model already, Dawkins specifically addressed this in the book. It’s nothing new, unfortunately Dobb, perhaps knowingly, tried to dress this up as a revelation and the beginning of the end for selfish gene theory.

        As a scientist I relish the idea of well-established idea, or theory, being displaced, if the evidence warrants. But when this evidence is not sufficient then I will remain content with the established notions.

  10. Posted December 6, 2013 at 8:25 am | Permalink

    Excellent response! Thanks for investing the early-morning time and effort.

    Just FYI: your link to Part 1 needs to be fixed.

  11. Posted December 6, 2013 at 8:25 am | Permalink

    Ah, it seems to work now. Nevermind.

  12. fivegreenleafs
    Posted December 6, 2013 at 8:29 am | Permalink

    I would just, like so many others, add my deep appreciation for these critiques regarding Dobbs article.

    I would say that not all questions can, in a resposible way be answered with a few well formulated sentences, (or should ever try to be); and I for one, enjoyed every bit of these clear and lucid responses.

    Thanks!

  13. johnjacoblyons
    Posted December 6, 2013 at 8:36 am | Permalink

    https://www.academia.edu/2551188/GENETIC_PRIMING_HOW_ADAPTIVE_BEHAVIOUR_SHAPES_THE_GENOME

    Please take a look at this paper that I was recently invited to write by The Linnean Society. In this paper, I describe how an adaptive behaviour that is positively associated with genetically mediated propensities can spread in a population via a inter-generational positive feedback loop between the incidence of that behaviour and the under-lying propensities.
    This challenges neither the selfish gene paradigm nor Darwinian Natural Selection. It simply suggests another evolutionary process that I call ‘Genetic priming’.

  14. Posted December 6, 2013 at 8:40 am | Permalink

    Really perfect (it answered all of my questions, esp about the epigenetics connection) response!

    I often tell folks who wonder about the veracity of evolution articles to head over to WEIT to check if Jerry has covered the controversy because that’s what I do or if I know he has, give them the link(s).

    Jerry has given Dobbs a chance to grow as a writer/journalist in a positive direction. Let’s hope he takes it.

  15. lamacher
    Posted December 6, 2013 at 8:42 am | Permalink

    Two outstanding posts, Jerry! Thank you. Clearly stated, well-reasoned, and for me, educational.

  16. AJ
    Posted December 6, 2013 at 8:47 am | Permalink

    “Perhaps people don’t like working in a field where there’s no new “paradigm” to forge, and Popper has ruined us all!”

    Don’t you mean Kuhn instead of Popper?

  17. Lenny Darnell
    Posted December 6, 2013 at 9:10 am | Permalink

    fyi

  18. Posted December 6, 2013 at 9:33 am | Permalink

    Dr Coyne, let me offer a correction and a question. No, make that a correction, a rhetoriacal question, and a correction.

    The first correction is fairly minor: You say I quoted West-Eberhard as saying Dawkins would end up “on the wrong side of history.” I did not4. That quote, attributed to another geneticist who said it in reference to Dawkins’ resistance to expanding more flexibly the gene-centric paradigm, appeared in the article only briefly. A few hours after the story was published, the source quoted contacted me and argued, convincingly, that while the quote was accurate, its close proximity to a different quote from West-Eberhard might make some people think that the source was allied with West-Eberhard in a broader sense (which he is not), rather than just about this resistance to altering dominant framings of genetic evolution. I found that a completely reasonable concern. The source and I very briefly discussed whether to use the quote elsewhere, but as the source had a truly all-consuming family situation to deal with, and it might take some time to find another right spot for the quote, we agreed that the most sensible thing to do was just cut it. So I cut it.

    I point this out so that no one puts in West-Eberhard’s mouth words that she did not say.

    The idea ofo putting words in mouths brings me to my rhetorial question and correction:

    Where o where, in my account of the quickening hunters that you excerpt above, do I say the faster-running hunters gene-expression changes were passed to offspring in some Lamarckian way? Look for it. It’s not there and never was. I never said or wrote or thought any such thing. Having described how the parents grew faster through gene-expression changes due to what amounts to steady training, I continued the scenario by describing how the kids in each generation grow up running faster essentially because they started training earlier, and this phenotypic change is then locked in when a friendly mutation shows up in a grandchild. I thought that would be clear, but apparently it’s not. But even if things in this passage are less than dead clear, I do not see any reader, except one who hopes to see me advocating a Lamarckianism inheritance, can conclude that I said the parents passed their training-increased speed on via some Lamarckian voodoo. Here are the words in question:

    “Your kids, hunting with you from early on, soon run faster than you ever did. Via gene expression, they develop leaner torsos and more muscular, powerful legs.”

    I then describe how, in the next generation, a mutation arose that essentially locked in that change. (Just as a similar gene that was available via standing variation could have done the same.)

    You say that passage “postulates … .a Lamarckian inheritance of change.” It says no such thing. Nowhere. You have to force such a meaning on the passage. Yet you do. And then you build much of your dismissal around a statement I never made andn a postulate I never offered.

    THIS is what I meant, in my comment below your first post on my story, by deliberate misreading. And it’s everywhere in both of your posts. And your misreadings are not peripheral to your argument; they are central and necessary to most of it.

    You lead this post, for instance, by stating I contend “that conventional natural selection, in which existing genetic variation is sorted out according to the gene copies’ ability to replicate, is wrong.” This is just as manufactured as my non-existent call on Lamarck. Nowhere do I say conventional natural selection is wrong. I simply point out, first, other ways that sharply different traits can be built during a lifetime via gene expression changes (no news to geneticists, but complete, startling, and exciting news to many lay readers), and, second, other ideas about how a trait can develop first through gene expression changes and then be locked in via a gene distinctly friendly to that trait. As both you and Dawkins have said, those dynamics and ideas are utterly compatible, fron a what’s-happpening-in-the-organism point of view, with conventional views of genetic natural selection. And while I do argue that the Selfish Gene’s gene-centric framing discourages most nonscientists from seeing these dynamics, I never say these other ideas disprove or should shove aside genetic selection. Only that the emphasis on selection can obscure them.

    But I never said genetic natural selection is wrong. Yet you accuse me flatly and plainly of saying exactly that. You seem determined to paint me as rejecting all of established conventional genetics. And you do so despite this passage, which comes immediately after a sentence saying that Dawkins’ “gorgeous argument” is wrong. I truly don’t see how an attentive reader, especially one who reads my article curious about whether I’m rejecting all of conventional genetics or Dawkins’ ideas, reads this and decides I’ve’ done so:

    “Wray and West-Eberhard don’t say that Dawkins is dead wrong. They and other evolutionary theories … have been calling for an ‘extended modern synnthesis’ for more than two decades. They do so even thought they agree with most of what Dawkins says a gene does.”

    Read the last sentence twice if you have to. Then try to square it with your thesis statement above that I contend, “that conventional natural selection, in which existing genetic variation is sorted out according to the gene copies’ ability to replicate, is wrong.”

    You can’t square it. Your main thesis here is a fabrication and a strawman. And it’s wrong.

    • Posted December 6, 2013 at 9:49 am | Permalink

      Could you explain how your scenario is any different from entirely orthodox Darwinism?

      You seem to be saying that, in a changed environment, animals make use of whatever phenotypic plasticity their current genome allows them (phenotypic plasticity that itself will be an evolved trait).

      Then, over time, genetic mutations and natural selection operate to produce descendants that are more capable in that environment.

      What is novel about that idea? What is being over-turned?

      • Michael Fugate
        Posted December 6, 2013 at 1:03 pm | Permalink

        “Wray and West-Eberhard don’t say that Dawkins is dead wrong. They and other evolutionary theories … have been calling for an ‘extended modern synnthesis’ for more than two decades. They do so even thought they agree with most of what Dawkins says a gene does.”

        Then why a headline that says something completely different?

    • Posted December 6, 2013 at 10:06 am | Permalink

      1. The printed version I have seems to show that the quote came from West-Eberhard, but that could be an error in spacing on my printer since the quote appears by itself directly above one by her. If she didn’t say it, then I retract my claim that she did. But it’s still an arrogant quote, no matter who did say it. And it still supports my claim that you’re taking out after Dawkins in a snarky manner. That kind of statement is out of place in an article of your type.

      2. As for your claim that you don’t adduce Lamarckism: there’s no reason why your kids, over TWO generations, should run faster than you did—that your grandchildren “seem almost like different animals: stronger legs, leaner torsos” and so on, UNLESS there is inheritance of nongenetic running ability among generations. Why should your kids run faster than you, and your grandkids run faster than your kids, unless there is not only inheritance of running ability, but nongenetic inheritance of running ability, i.e.,inheritance of the gene expression changes that induce faster running? That reads to me like Lamarckism. You clearly imply an increase, across not one but two generations. Now you can say that’s due to “training”,but it’s not clear how training along could lead to a two-generation increase in running ability. By the third generation, the grandchildren are characterized, without yet having experienced the the mutation, as seeming “almost like different animals: stronger legs, leaner torsos, and they run way faster than you ever did. Why the two-generation increase if just “training” is involved? Would Usain Bolt’s grandchildren run faster than he did? Even explaining it as you do, the least you are guilty of is muddled explanation.

      3. You do say that the conventional view of natural selection, in which the gene leads, is wrong. Nowhere did I accuse you of simply saying that natural selection is wrong. Note again that how I characterize your argument: you say “that conventional natural selection, in which existing genetic variation is sorted out according to the gene copies’ ability to replicate, is wrong.” That is NOT the same as arguing that you deny natural selection. And in fact you do indeed rejecct that conventional view, because you tout a view in which the variation arises AFTER the selection pressure comes to bear.

      4. Finally, yes, your article does argue repeatedly that the gene-centered view is dead wrong. You quote Eisen as saying that “The gene-centric view is an artifact of history”: that “Mendel stumbled over the wrong chunk of gold” (your word); that “we need to replace this gene-centric view with one that more heavily emphasizes the role of gene expression” (your characterization of other biologists, but one you tout repeatedly (you don’t give any extensive views of the critics); you quote Wray as saying “We’re stuck in an outmoded way of thinking that should have fallen long ago” (obviously the point of your pieces), and so on and so on. Your whole article is meant to despose the primacy of the gene in natural selection, and you failed to do so. Now you’re angry because scientists have pointed that out to you.

      And of course you’ve neglected all my criticisms about how the difference between cows and humans can’t be due to genes, and that gene expression makes hash of the selfish gene view. Both claims are bogus.

      Finally, you might consider that you are backpedalling, and everybody sees that this is what you have done. You are now claiming that you didn’t say what everybody thinks you did. If that’s the case, then you might consider that such misinterpretation is due more to your muddled thinking and writing and not to the misreadings of multiple readers.

      I stand by my characterization of your piece as scientifically incorrect, misleading, and damaging to the popular understanding of evolutionary biology. Trying to make a splash by arguing that a revolutionary new view of evolution is in the offing, you’ve fallen into the mud puddle.

      • Curt Cameron
        Posted December 6, 2013 at 11:49 am | Permalink

        Why should your kids run faster than you, and your grandkids run faster than your kids, unless there is not only inheritance of running ability, but nongenetic inheritance of running ability, i.e.,inheritance of the gene expression changes that induce faster running? That reads to me like Lamarckism.

        This seems to me to be the central point of disagreement. Dobbs may not have used the “L” word to describe this idea, but to my non-biologist understanding of the subject, that’s exactly what Lamarckism is!

        • Posted December 6, 2013 at 12:14 pm | Permalink

          I think the difference would be that in Lamarckism, the parent would develop a trait out of the blue and then pass it on to its offspring somehow, while in the view expressed by Dobbs the ability was always there but merely latent, and gets activated by an environmental change, and the later generations get more of it not from any genetic change in them, but simply due to them using it more or experiencing those facets of the environment more. So, in the latter case, it would be that the parents would be starting to chase down animals more, their children would be regularly chasing down animals, and for their grandchildren chasing down animals would be a way of life. Then the genetic shift would come in — and it wouldn’t have to be in the grandchildren, I think; there could be a longer time before the genetic mutation arrives — and produces a massive leap forward of that trait, and then actually solidifies that trait in the species.

          What this would seem to challenge is the idea that you can look in the genetic code for the code that “produces” a trait and say that that code really does directly produce that trait and that that code itself was selected for because it produced that specific trait and that trait was useful. If the expression story is true, one genetic sequence might possibly produce many different traits depending on the environment the organism is in, and it might exist for completely different reasons than that it directly produced the trait in question.

          • eric
            Posted December 6, 2013 at 2:13 pm | Permalink

            in the view expressed by Dobbs the ability was always there but merely latent, and gets activated by an environmental change, and the later generations get more of it not from any genetic change in them, but simply due to them using it more or experiencing those facets of the environment more.

            What do later generations get more of? There’s a gene. You seem to be saying they don’t get more of the gene. There’s the expression. Maybe you’re saying it expresses itself more in the child due to the environment’s affect on the child, but what does that have to do with the parent’s training?

            Parents pass on genes to children through sperm and egg. For a Dobbsian-like heritability, something the parents do must be showing up in the genes of the sperm or egg. No change in sperm or egg means that whatever training the parents do makes no difference to the genetic potential of their kid. There is no increase in child-musculature due to the parents actions, or whatever.

            I am having a really hard time seeing any heritable change in Dobbs’ model (or, your interpretation of Dobbs’ model).

            • Posted December 6, 2013 at 2:23 pm | Permalink

              I already gave an example of what I mean. Whether it counts as a “heritable” change or not might be debatable, but I think it does explain what the children and grandchildren have “more of”:

              …it would be that the parents would be starting to chase down animals more, their children would be regularly chasing down animals, and for their grandchildren chasing down animals would be a way of life.

              At that point, the grandchildren would probably develop about as far as their current genome would allow and so you’d need a change in the genome to get further, which would then lock it in. One error Dobbs might make in the article is not pointing out that the mutation might never happen, but you’d still get a dramatically different organism with respect to the traits he mentions.

    • Posted December 6, 2013 at 10:34 am | Permalink

      The Lamackian part is here in the highlighted part of the forest fire story:

      “You mate with another fast hunter, and your kids, hunting with you from early on, soon run faster than you ever did. Via gene expression, they develop leaner torsos and more muscular, powerful legs. By the time your grandchildren show up, they seem almost like different animals: stronger legs, leaner torsos, and they run way faster than you ever did. And all this has happened without taking on any new genes.”

      This passage implies inheritance of gene expression and phenotype without genetic change, doesn’t it?

      Cheers,

      m.

      • Posted December 6, 2013 at 11:41 am | Permalink

        Yes, and then the crux of this problem is how can gene expression in body muscles transfer to changing the future program of gene expression passed on in egg and sperm cells? One does not have to say ‘Lamarckian’ to be using a Lamarckian model. I suppose this can also be read to imply Darwins’ view of inheritance of traits by gemmules.

    • lkr
      Posted December 6, 2013 at 10:36 am | Permalink

      By the way,“your kids run faster than you do” seems to be backwards for modern humans — kids in 40 countries around the world have become 5% slower per decade over the past 40 years, so 11% slower per generation for two generations…

      With genetic assimilation, I trust that the 2112 Olympic 100m champ will come in at about 20 seconds.

      But their thumbs will be a lot faster.

      • Tim T
        Posted December 6, 2013 at 12:37 pm | Permalink

        Huh, so Usain Bolt must be much older than he looks.

      • Posted December 6, 2013 at 3:11 pm | Permalink

        I think, if I were to be optimally charitable to Dobbs, what he is proposing is that a change in environment can lead to a memetic cultural change which can, in turn, further change an organism’s reproductive environment in ways that will lead to selective pressures that favor further enhancements upon the physical expressions of the new culture.

        If that’s the case, I think he’d have better luck finding real-world examples not with predators catching prey but with sexual selection — for example, a mating dance, with mutations favoring individuals with physiologies better adapted to performing the dance.

        However, it would seem to be a most contrived example. Indeed, I think you’d need a culture as sophisticated as that seen at least in great apes, if not modern humans, for something like that to manifest itself. In this case, I’m thinking, perhaps, of extreme body modifications, such as neck rings or foot binding. Even still, the number of generations it would take for mutations to appear and dominate…well, human cultures evolve far too rapidly for that sort of thing to even have a theoretical chance of getting fixed in the genome. And, more to the point, humans are not and never have been as isolated as would be necessary for that type of evolution…even the most insular tribes still have enough contact with the outside world for genes to flow in both directions — and certainly over evolutionary timescales.

        Come to think of it, we have the perfect experimental case to consider: circumcision. And I am unaware of even any hints of genetic or phenotypic differentiations between cultures that circumcise and those that don’t.

        And…again, even if we were to grant Dobbs such an unlikely example…well, it’s still entirely and classically Darwinian, so I don’t know what the brouhaha would be all about.

        Cheers,

        b&

        • DV
          Posted December 6, 2013 at 3:54 pm | Permalink

          Interesting idea of circumcision as a perfect test case. Even if a mutation does arise for lack of foreskin, how would this be selected for? The ladies won’t presumbably be able to tell an inborn endowment from a surgical one, and cutting is probably negligible as a cost to overall fitness.

          We need something that requires more work than just a quick snip, so that any mutation avoiding the work would be truly beneficial.

          • Posted December 6, 2013 at 4:53 pm | Permalink

            It wouldn’t even need to be anything related to lack of foreskin; it could just as well be something related to resistance to infection.

            The point is that it’s a physical change made nearly universally to a large and somewhat insular portion of the population. And it’s even something closely related to reproduction.

            If there’s no genetic signature as a result, Dodd’s nice theory has, unfortunately for him, been tested.

            Cheers,

            b&

    • Gregory Kusnick
      Posted December 6, 2013 at 11:24 am | Permalink

      Her children inherit the gene, and because their speed wows their mating prospects, they mate early and often, and bear lots of kids.

      How does this follow? The postulated mutation had to do with muscle strength. Why do you assume that this would automatically entail sexual selection in a parallel direction?

      • pacopicopiedra
        Posted December 6, 2013 at 10:47 pm | Permalink

        It is a very, very confused article.

    • Posted December 6, 2013 at 11:45 am | Permalink

      From your article,

      Unfortunately, say Wray, West-Eberhard and others, it’s (Dawkins’ selfish gene theory) wrong.”

      and, in the next sentence,

      “Wray, West-Eberhard and don’t say that Dawkins is dead wrong.”

      Unless you’re simply trying to have your cake and eat it, too, could you please explain for us the distinction between “wrong” and “dead wrong?”

      If Prof. Coyne has actually fabricated a strawman argument, it’s one that’s charitable to you. In other words, if you’re not actually invoking Lamarckian arguments, your article boils down to nothing. You’re not actually taking issue with Dawkins on anything, for the very good reasons cited in the above post. Where, exactly, in “The Selfish Gene,” does Dawkins argue that you can’t strengthen muscles by training them? Where, exactly, does he say that genetic mutations can’t further strengthen those already trained muscles? In fine, where does he actually say anything that contradicts the scenarios you describe in your article? If you will recall, the title of your article is “Die, Selfish Gene, Die,” and you approvingly quote West-Eberhard’s assertion that Dawkins is “wrong,” (albeit not “dead wrong.”) All right, where is he “wrong”? How is it, exactly, that you’re trying to enlighten the lay public about things that, assuming they have a passing interest in the field of epigenetics, they haven’t already been thoroughly enlightened already?

      More to the point, where in your article is there any support whatsoever for phrases such as,

      “And ‘evolution is not about single genes,’ she says. ‘It’s about genes working together.”

      “It’s not a selfish gene or a solitary genome. It’s a social genome.”

      and,

      “(Mendel) might have discovered not just genes, but genetic accommodation. Not the selfish gene, but the social genome.”

      I find none. On the other hand, all this becomes entirely comprehensible if one views your article, not as popular science, but as an ideological tract.

    • DV
      Posted December 6, 2013 at 1:30 pm | Permalink

      >>“Wray and West-Eberhard don’t say that Dawkins is dead wrong. They and other evolutionary theories … have been calling for an ‘extended modern synnthesis’ for more than two decades. They do so even thought they agree with most of what Dawkins says a gene does.”
      <<

      Can you be specific. Exactly what is it that Dawkins says a gene does, that Wray and West-Eberhard doesn't agree with?

    • eric
      Posted December 6, 2013 at 2:01 pm | Permalink

      Having described how the parents grew faster through gene-expression changes due to what amounts to steady training,

      Mr. Dobbs, how does training affect gene expression?

      And from what scientific study are you drawing the idea that training ever could affect gene expression?

      I can sort of imagine some very basic changes that could happen this way (i.e, starvation alters cell chemistry, leading to different genetic expressions – like turning grasshoppers into locusts), but nothing anything as specific as what you’re proposing.

    • Peter Beattie
      Posted December 6, 2013 at 6:03 pm | Permalink

      The idea ofo putting words in mouths brings me to my rhetorial question and correction:

      Where o where, in my account of the quickening hunters that you excerpt above, do I say the faster-running hunters gene-expression changes were passed to offspring in some Lamarckian way?

      That’s a pretty bad defence, David. Of course you don’t say that your scenario is Lamarckian, and nobody said you did. To make that your defence—while at the same time vociferously complaining that people aren’t reading your texts closely enough—is ludicrous. What Jerry says, and pretty unambiguously so, is that your scenario amounts to a Lamarckian story. And that judgement is based on the logic of the story—judgement and logic which you curiously (and rather suspiciously) do not engage with.

      You say you want to learn, that it’s about a scientific exchange, and yet you put up bluster and (frankly, a little whiny) complaints about people you accuse of hoping to be able to accuse you of holding ridiculous ideas. You keep pointing to people who support you as confirmation that either your ideas are not muddled or that your text wasn’t. To me, that says one thing: you don’t understand the first principle of science, which is (in Feynman’s phrase) “you mustn’t fool yourself”—and science is the systematic process of trying to avoid that. I should say you’ll have to try quite a bit harder.

    • CJ
      Posted December 6, 2013 at 9:27 pm | Permalink

      Mr. Dobbs

      This kind of special pleading, intellectual dishonesty is not going to bode well for your career as a science journalist. It’s obvious that you’re now grasping at straws. It’s not just that you’re wrong from a technical standpoint; you’re wrong from a moral one as well, and your articles on this manner have been poorly written and researched. You’re attempts to save face will only make things worse for you. An apology is in order.

  19. Posted December 6, 2013 at 9:34 am | Permalink

    For info, Dawkins has posted a reply to Dobbs. See Adversarial Journalism and The Selfish Gene

    • Michael Fugate
      Posted December 6, 2013 at 2:24 pm | Permalink

      A very clear commentary by the good Dr.

      • Posted December 6, 2013 at 2:38 pm | Permalink

        Yes, it’s notable that when reading Dawkins (and indeed Prof Coyne) that the clarity and logic shine through and we’re in no doubt what they’re claiming.

        With Dobbs, despite the original article, a blog-post clarification, and the above comment, I for one am unclear whether he is simply espousing accepted Darwinism that is entirely in line with Dawkins (but with Dobbs either not realising that or pretending otherwise for journalistic reasons), or whether he is claiming some form of Lamarckism, or something else. I suspect that he hasn’t got clear in his own mind what he is espousing, and is simply muddled.

        • pacopicopiedra
          Posted December 6, 2013 at 11:10 pm | Permalink

          Yes. Hundreds of comments (and multiple addendums from the original author) in, no one is really sure what he was trying to say. It’s also now beginning to look like Dobbs isn’t really sure what he was trying to say.

  20. NewEnglandBob
    Posted December 6, 2013 at 10:08 am | Permalink

    “Why do people do this kind of stuff?”

    People want to be recognized. They want to be to Darwin as Einstein is to Newton. (Darwin’s Einstein?)

    Who wouldn’t want to be known as the one who revolutionized a field, taking it to a higher level?

  21. Posted December 6, 2013 at 12:28 pm | Permalink

    Well, he admitted finally on Twitter that there is no link between the phenotypical development of previous generations and the ‘locking in through’ mutation of later ones, which was the central point of his ‘argument.’

    So I think we can safely admit even he doesn’t believe what he was saying.

    • Posted December 6, 2013 at 12:29 pm | Permalink

      You’ll need to click the date at the bottom to see the whole convo. But it got quite ridiculous.

    • gbjames
      Posted December 6, 2013 at 12:36 pm | Permalink

      Now that just seems silly. This makes no sense. Even if a mutation came along that gave some critter some phenotypic “lock in”, on what bias would this mutation spread through the population? There would be no selective advantage for it since everyone else was presumably displaying the same trait.

      • DV
        Posted December 6, 2013 at 1:21 pm | Permalink

        Presumably having the genes “lock in” the trait has selective advantage in that you don’t need the training or learning effort to get that trait.

        I think the way to think about this is that once you have most of the population training and learning to have this new skill, it increases the selection pressure such that if someone happens to have a mutation conferring innate akill, then that mutation spreads quickly. The mutation doesn’t have to be all or nothing. You can get something that gets you X% fit, so you only need to train 100-X%, that’s still an advantage.

        Needless to say this doesn’t mean that “selfish genes” – gene-centric view – is wrong.

  22. Posted December 6, 2013 at 12:37 pm | Permalink

    The description above about the research of Waddington reminded me of my old work on Drosophila. This was during my former life as a post-doc in San Diego (sigh), working on the genetics of wing vein development in insects. I had obtained a number of the standard mutant lines from a stock center, and among these was the abrupt mutant which was supposed to be uniformly homozygous for a recessive mutation that caused most of wing vein #2 to be missing. However, these flies all looked like normal, or ‘wild type’ flies. My boss told me that these probably had accumulated alleles at other genes that repressed the phenotype while in culture, presumably because flies with normal phenotypes can out-compete the abrupt phenotype in culture. This selection might not be due to veins, but it could be b/c the mutation affects other things. So I outcrossed the stock, which is where one crosses them to wild type flies, and then I crossed the heterozygotes to each other. This makes about ¼ of the flies homozygous again for abrupt, and most of these will have exchanged various combinations of their original chromosomes with chromosomes from the wild type stock. Sure enough, I got many flies with the abrupt vein loss phenotype to establish an abrupt stock. But I also noticed that there were several flies coming out with extra wing veins! A few had wings that reminded me of dragonfly wings, they were so ‘veiny’. These were likely homozygotes for chromosomes that had genes which repressed the abrupt phenotype. That is, genes that cause extra veins cancel out the effect of genes that cause vein loss, resulting in normal wings. I became very interesting in propagating some of these extra vein mutants as well, just to later learn what genes they might be (probably all already known), but try as I might they all became normal looking over several generations and I had to give it up.
    I do not know if I was doing a demonstration of natural selection, but it sure seemed like it might be.

  23. Posted December 6, 2013 at 12:43 pm | Permalink

    I train horses. I explain to my clients how each horse comes equipped with the behavior to either be the leader or the follower in the herd, and also comes equipped with a behavior to determine when to lead and who to follow. I suppose this could be described as ‘plasticity’, but both behaviors — Lead, Follow — are already there, in the genes. Nor would constantly letting your horse push you around result in its offspring being naturally more assertive.

    Now, we can, and do, selectively breed horses for docility, and for a lack of “spookiness” that would get them quickly eaten in the wild. (Which is why mustangs so often prove an handful for most amateur owners.) But growing up in a barn most certainly does not in and of itself alter the gene pool.

    As you’ve exposed so eloquently in these two post, everything that West-Eberhard, Dobbs, et al. describe is either actually neo-darwinism, or Lamarckism.

    • John Scanlon, FCD
      Posted December 9, 2013 at 9:23 am | Permalink

      …either actually neo-darwinism [and right], or Lamarckism [and wrong].

      But it’s all about re-branding, so it’s more important to come up with a catchphrase and hype it on Tw***er than to be technically correct.

      • Posted December 9, 2013 at 10:03 am | Permalink

        Yeah. I see Dobbs’ article as the science journalism equivalent of the Paris Hilton sex tape. Something that ought to be embarrassing, except was done for the expressed purpose of becoming famous.

        As for PZ Myers’ incoherent defense of Dobbs, that’s just Lindsay Lohan making a fool of herself in public yet again.

  24. Posted December 6, 2013 at 1:32 pm | Permalink

    I will start listening when they discover a DNA write-back mechanism that allows for gene expression information to be written back to the genome. As it stands each generation has the same approximate potential without a random mutation changing the game.

    Date: Fri, 6 Dec 2013 14:13:02 +0000 To: t_aid@hotmail.com

  25. superatheist
    Posted December 6, 2013 at 1:41 pm | Permalink

    This reminds me of the debate between Steve rose and dawkins posted on youtube. http://www.youtube.com/watch?v=Ir64odzG98Q

    I think quite a few of Rose’s ideas – which I agree with – are shared with some of Dobbs’ arguments.

    I disagree with Jerry on the idea that gene regulation doesn’t render the selfish gene a bogus idea. I think it does phenotypically, though maybe not genetically. However, I said this before, the phenotype isn’t a vehicle of the gene, it much more complicated than that, and I don’t think the gene is the unit of selection, though I would say – as Hamilton – did it is one of them.

    • Achrachno
      Posted December 6, 2013 at 2:31 pm | Permalink

      “I disagree with Jerry on the idea that gene regulation doesn’t render the selfish gene a bogus idea. I think it does phenotypically, though maybe not genetically.”

      Huh? The selfish gene is not bogus genetically but is is phenotypically? What is it that builds the phenotype? Sounds to me like Jerry and Dawkins are right, to little general surprise around here.

      • superatheist
        Posted December 6, 2013 at 2:36 pm | Permalink

        Yah, the characterization of phenotype being a vehicle for the selfish replicator is an extreme reduction of the complex relationship between phenotype-genotype. What make a phenotype? what do you think does? the gene?? as an undergrad studying embryology we learn that complex genetic networks with environmental factors and embryological history – like historical and embryological constraint – make a phenotype.

        • DV
          Posted December 6, 2013 at 3:13 pm | Permalink

          Are you disputing that the gene is the replicator? It cannot be anything else, because it’s the genes that survive identity through the generations.
          And it is not accurate to say the the phenotype is the vehicle. Rather it is the organism that is the vehicle of the genes. The metaphor is pretty straightforward – the organism carries the genes through reproduction to the next generation. The phenotype is the properties of the organism, the expression of the genes in the physical body, but more than that, as Dawkins explained in the Extended Phenotype, the phenotype doesn’t need to be limited only within the organism. The classic example is the beaver dam as a phenotype of beaver genes. But clearly beaver dams don’t carry beaver genes. Beaver genes are inside the cells in the beaver bodies. That is why it is wrong to say the phenotype is the vehicle. And Dawkins didn’t say that the phenotype is the vehicle. He said it is the individuals that are the vehicles of the genes.

          • superatheist
            Posted December 6, 2013 at 3:24 pm | Permalink

            Well this depends on emphasis, Dawkins cares about bookkeeping as Gould called it, other biologists worry about the interaction. It is not just the gene that is passed on, the genome is passed on, which include genetic interactions that are highly context dependant. 2ndly, no the phenotype is what the gene expresses according to how mendel thought of it, like purple genes produce a purple flower colour, but embryologically what on earth is the purple gene? the purple colour is a result of complex interactions that produce the colour on the flower. 3rdly, could you give me the nucleotide sequence for the dam-building gene, I would love to see it. Dawkins interpreted Niche construction theory as Niche engineering, which ignores the whole point about niche construction. Saying that the individual is a vehicle gives the individual a passive role in process of evolution; i.e. interaction with the environment and the embryological constraint that tells genes to jump in a lake – sth called cryptic variation – aren’t important.

            • DV
              Posted December 6, 2013 at 3:41 pm | Permalink

              You’re reading too much into the metaphor of individuals as vehicles. It doesn’t mean any of the gene interactions aren’t important. Even Dawkins talked at length about gangs of compatible genes and other genes being part of the environment of each gene, in The Selfish Gene book itself.

              You’re being inaccurate when you say the genome is passed on. The particular genome of an individual is unique. Your genome is not the same genome, not even a copy, of the genome of any of your parents. It is most definitely not the genome that replicates in any sense. The only thing that replicates with fidelity is the gene. It is the gene that survives intact through generations. It is the thing that is passed on.

              • superatheist
                Posted December 6, 2013 at 3:45 pm | Permalink

                I meant chromosomes which contain genes in them.

    • DV
      Posted December 6, 2013 at 3:00 pm | Permalink

      The gene is not the unit of selection? Just one of them? Please don’t keep the suspense. Tell us what are the other units of selection that gets handed down between generations.

      • superatheist
        Posted December 6, 2013 at 3:24 pm | Permalink

        I would refer you to David Wilson’s multi-level selection theory.

        • superatheist
          Posted December 6, 2013 at 3:28 pm | Permalink

          For another criticism of the selfish gene that is very good, I refer you to Larry Moran’s recent post: http://sandwalk.blogspot.ca/2013/12/die-selfish-gene-die.html

          • gbjames
            Posted December 6, 2013 at 3:31 pm | Permalink

            Perhaps Jerry will offer a response to Larry’s comments. I look forward to it.

        • gbjames
          Posted December 6, 2013 at 3:29 pm | Permalink

          And we might refer you to critiques of David Wilson’s multi-level selection theory. (Perhaps even those made by our host.)

          • superatheist
            Posted December 6, 2013 at 3:42 pm | Permalink

            Yes, I am aware of it. I understand that the level of selection argument isn’t settled in the field. But isn’t ironic that Hamilton whose work influenced dawkins a great deal, doesn’t think there is one level of selection: http://www.youtube.com/watch?v=kRmOVeXU3zQ

        • DV
          Posted December 6, 2013 at 3:44 pm | Permalink

          It is even worse than I thought. Multi-level selection has been critiqued thoroughly.

          • superatheist
            Posted December 6, 2013 at 3:48 pm | Permalink

            Massimo piglucci published a wonderful recent book called “The extended Synthesis” which explains the current status of Multilevel selection theory. I would also refer you the spandrel’s paper by Gould and Lewontin and “The concept of a character in Evolutionary Biology” that talks about levels of selection.

  26. George
    Posted December 6, 2013 at 1:46 pm | Permalink

    Dobbs got into it with another Coyne in September – James Coyne. He is at the University of Pennsylvania,Department of Psychiatry.

    He reviewed Dobbs’ ‘Social Life of Genes’ -
    http://blogs.plos.org/mindthebrain/2013/09/23/social-life-of-genes-david-dobbs-dinner-with-andre/

    Dobbs commented on the review and James Coyne responded.

  27. eric
    Posted December 6, 2013 at 1:57 pm | Permalink

    This is, I think, Mary Jane West-Eberhard’s view of how genetic accommodation works. This seems less probable to me than version #1, simply because I can’t envision an environmental change preferentially invoking an organismal change that’s useful in that environment.

    I suppose its possible, but it would be more of a luck thing than a systematic thing. For example, its theoretically possible that heat shock affects certain mutational mechanisms more than others, and the mutational mechanisms it effects might just be those which would lead to greater heat tolerance. But it is really hard to see how this could happen in real life.

  28. Posted December 6, 2013 at 1:57 pm | Permalink

    On his “ask me anything on Reddit” session, Dawkins recommended anyone trying to escape creationism to read both “Why Evolution Is True” and “The Greatest Show on Earth.”

  29. Posted December 6, 2013 at 3:13 pm | Permalink

    Dawkins’ point about Dobbs’ attempt to “adversarialise” (good word; I’m nicking it) his article as clickbait is a good one. It’s certainly not the first time an article about science has been presented in a sensationalist fashion to grab attention (we probably all recall New Scientist’s infamous “Darwin was wrong” cover, endless articles about the “God particle” and a thousand other examples).

    It seems to have worked, in a limited way at least – yes, people are discussing the article, but mostly to criticise its badly-worded arguments and question its unnecessarily combative tone. Dobbs almost seems embarrassed by the sort of attention his piece has attracted, going by the fact of his blog post and lengthy comment here, both intended to clarify his original points. It’s trivial to point out that neither of those responses would have been necessary had Dobbs focused more on clarity and facts than on winding up a controversy.

    • Diana MacPherson
      Posted December 6, 2013 at 4:22 pm | Permalink

      Yes, I like how he put it to – harvest links. It was such a good burn delivered so skillfully.

  30. John Harshman
    Posted December 6, 2013 at 3:36 pm | Permalink

    What presumably happened is that, when fish were constantly around, they selected for those individuals that didn’t have the ability to change color at all (a mistake like that would get you spotted and eaten, and there’s also a metabolic cost to maintaining flexibility)—those individuals who, though natural selection, simply lost their ability to alter their color in response to intense sunlight. That, of course, involves “selfish gene-ery”: the preferential replication of those gene variants that have lost the ability to effect color change. You don’t need to become pigmented in lakes where it never pays to lose your pigment, and you pay a metabolic (and presumably reproductive) cost to keep that flexibility.

    Just to make Larry Moran happy, I have to respond to this. Why not just assume the simpler scenario that any genes affecting genetic plasticity that’s unused for a lengthy period, and so never subject to selection, will tend to decay through genetic drift? No need to invoke either metabolic cost of plasticity or any other selective advantage to loss of plasticity.

    • Posted December 6, 2013 at 5:19 pm | Permalink

      I don’t think Jerry would at all rule out the possibility that drift plays a role.

      However, we have other examples, especially of cave-dwelling animals, where metabolic cost definitely plays a role, and it’d be just as foolish to prematurely rule that out, as well.

      Of course, in practice, the two really interact with each other. It is primarily going to be drift that provides the raw material for evolution in the first place. Even if there’s no metabolic cost to retaining the trait, without active selective pressure maintaining it the trait will likely tend to disappear. The lack of selective pressure for a trait can just as easily be understood as a selective disadvantage to the trait, especially from the gene’s own perspective.

      Cheers,

      b&

      • John Harshman
        Posted December 7, 2013 at 7:02 am | Permalink

        The lack of selective pressure for a trait can just as easily be understood as a selective disadvantage to the trait, especially from the gene’s own perspective.

        No, it can’t. Wherever would you get such an idea?

        • gbjames
          Posted December 7, 2013 at 7:24 am | Permalink

          Because advantage/disadvantage is relative. When you end selection for a trait there is nothing to keep it in place.

          Over time, the genes that encode for it will suffer damage and that damage will not be removed. Genetic drift can cause the now-damaged version to spread through a population. Gradually the trait will evaporate.

          • Posted December 7, 2013 at 8:37 am | Permalink

            Exactly.

            Or, even more succinctly, it’s the Red Queen hypothesis.

            Cheers,

            b&

            • John Harshman
              Posted December 7, 2013 at 11:59 am | Permalink

              What? That has absolutely nothing to do with the Red Queen hypothesis, which is all about coevolution under mutual selection in competing populations.

          • John Harshman
            Posted December 7, 2013 at 11:58 am | Permalink

            Sure. But in what way does that mean the trait is selectively disadvantageous? The absence of selection — neutrality — and advantage/disadvantage are antithetical.

            • gbjames
              Posted December 7, 2013 at 12:06 pm | Permalink

              Remember the phrase at the end of the quote we are disputing?

              “…from the gene’s own perspective.”

              The gene(s) decay and evaporate over time. It definitional that this is not in the long term interest of the gene(s).

              Selection (for) is required to maintain genes over time. Selection (against) is one way to purge genes over time. Doing neither is like selecting against, only slower.

              • Posted December 7, 2013 at 12:14 pm | Permalink

                …which, to answer John’s reply to me, is why I brought up the Red Queen: you have to run as fast as you can just to stay in place. The genes in this example aren’t running at all, which is why they fall behind and lose their place.

                b&

              • John Harshman
                Posted December 7, 2013 at 6:05 pm | Permalink

                You folks are extending the selfish gene metaphor into territory that Dawkins never intended and that is not biologically meaningful. (And also extending “Red Queen” far beyond Van Valen’s intentions.) If that’s what “selfish gene” means to you, then perhaps it should die.

              • gbjames
                Posted December 7, 2013 at 6:23 pm | Permalink

                It isn’t a question of what it means to me. That’s what it means. That’s how Dawkins uses it. Go back and re-read The Selfish Gene.

              • John Harshman
                Posted December 7, 2013 at 9:16 pm | Permalink

                Can you find me anything in any of Dawkins’ writings that says anything like “The lack of selective pressure for a trait can just as easily be understood as a selective disadvantage to the trait…”? If you can I will certainly correct my views.

              • gbjames
                Posted December 8, 2013 at 7:02 am | Permalink

                John, let me introduce you to my friend, Mr. Google. He can help you at times like this. For example, I asked him your question and he pointed me at this page.

                Two patterns are described that contribute to the loss of traits. One is selection. The other is drift in the absence of selection.

              • John Harshman
                Posted December 8, 2013 at 7:10 am | Permalink

                That’s nothing like I asked for. It’s nothing like what Ben said. In fact, it’s exactly what I said, to which he was responding.

              • gbjames
                Posted December 8, 2013 at 7:19 am | Permalink

                No, John. You are misreading Ben somehow. That is exactly what Ben is saying. Something is preventing you from understanding him.

              • Posted December 8, 2013 at 7:36 am | Permalink

                Indeed, I even used the example of cave species in my original response on this thread….

                b&

            • John Harshman
              Posted December 8, 2013 at 9:09 am | Permalink

              If I’m misunderstanding what Ben said, in what way was he disagreeing with my original comment?

              • gbjames
                Posted December 8, 2013 at 9:23 am | Permalink

                Please review the transcript, John.

                Ben made a statement. You quoted it along with “No it can’t. Wherever would you get such an idea?”. Everything since has been an attempt to correct that somewhat snark-ridden response.

              • John Harshman
                Posted December 9, 2013 at 11:32 am | Permalink

                No, Ben’s original comment was a reply to me. So, what was he disagreeing with in that original comment?

                I maintain that there’s no way to make “The lack of selective pressure for a trait can just as easily be understood as a selective disadvantage to the trait, especially from the gene’s own perspective.” sound sensible. Drift isn’t selection. Not from anyone’s perspective.

              • Posted December 9, 2013 at 11:59 am | Permalink

                What’s the difference between subtracting one from a number and adding negative one to that same number?

                Perspective, is all.

                Cheers,

                b&

              • gbjames
                Posted December 9, 2013 at 12:22 pm | Permalink

                I’m sorry, John, but I’ve concluded that you are being obstreperous for no apparent reason. I don’t think that this exchange can go anywhere since you insist on disagreement where none seems to really exist.

                Catch you later.

              • John Harshman
                Posted December 9, 2013 at 1:51 pm | Permalink

                Ben, that was not illuminating in the slightest.

                gbjames, if there is no disagreement, I don’t understand the point of Ben’s comment, and neither of you is clarifying it.

              • gbjames
                Posted December 9, 2013 at 3:19 pm | Permalink

                Yes, John. You are misunderstanding. But I’m done trying to clarify it. You seem to be intentionally misunderstanding, but I could be wrong. Still, I’m done trying.

              • John Harshman
                Posted December 9, 2013 at 4:15 pm | Permalink

                Yes, you’re wrong that my misunderstanding is intentional. And it’s very annoying of you to depart without any actual explanation of what you think my misunderstanding is.

              • John Harshman
                Posted December 12, 2013 at 11:45 am | Permalink

                Why don’t you leave in a huff? If that’s too soon, make it a minute and a huff. Or you could leave in a taxi.

    • W.Benson
      Posted December 7, 2013 at 11:28 am | Permalink

      If mutation is entropy, selection is Darwin’s demon.

  31. Posted December 6, 2013 at 4:37 pm | Permalink

    As a botanist, I always wonder how Lamarckism is supposed to work in plants.

    • Posted December 6, 2013 at 5:28 pm | Permalink

      Well, you see, while the giraffe is stretching its neck to reach the acacia leaves, the acacia is stretching its branches so it doesn’t get eaten, leading to taller and taller trees.

      What, you’ve never seen a tree stretch its limbs? And you call yourself a botanist? How do you think they grow so big and strong and tall if they don’t get plenty of exercise and drink lots of milk and eat all its spinach?

      Sheesh. Kids these days….

      b&

      • John Scanlon, FCD
        Posted December 9, 2013 at 9:35 am | Permalink

        But of course the immediate effectiveness of the plant’s attempts to (inter alia) widen its leaves, reduce the density of its stomata, and grow thorns in the path of hungry folivores, is beside the point as long as the will to change has a beneficial effect on succeeding generations.

        So Lamarckian evolution works in pretty much the same way for plants as for animals, but with a lag of approximately one generation. I’m sure this can be demonstrated with suitable experiments. :)

        • Posted December 9, 2013 at 9:47 am | Permalink

          Word — salad.

          No, I’m not accusing you of writing word salad. Well, I mean, of course, you did write word salad, but obviously intentionally so for comedic effect, which is something els —

          <ahem />

          What I mean, is that the word for the suitable experiments would be, “salad.” We should encourage the cabbage to think of its impending doom…er, “harvest,” as the ultimate expression of its Lamarckian fulfillment, and can’t it do something to pack those leaves a bit tighter and keep them from wilting? Carrots, too: don’t let those roots get too woody! Nice and tender is the ticket — but, of course, with a particularly crisp snap. And pass the word on to the celery that it needs to keep its strings under control, hmm? Nothing worse than getting celery guts caught between your teeth.

          Veggies, we eagerly await your answers!

          b&

  32. Eduardo
    Posted December 6, 2013 at 5:32 pm | Permalink

    Excellent critique, Prof. Ceiling Cat.

  33. fellytone84
    Posted December 6, 2013 at 10:09 pm | Permalink

    “This seems less probable to me than version #1, simply because I can’t envision an environmental change preferentially invoking an organismal change that’s useful in that environment.”

    Does this still apply when the environment is a product of natural selection?

  34. kirkwillmarth
    Posted December 7, 2013 at 1:01 am | Permalink

    I think there is more evidence to your version #2 of genetic accommodation than you claim.

    As a post-doc, Daniel Jarosz from the Lindquist lab at the Whitehead Institute (disclosure: he is now a faculty member at Stanford University where I study) has provided evidence for adaptive changes via non-genetic means.

    To summarize, he and his colleagues found that certain adaptive traits could be caused by replicated in yeast prions, which are inherited in a non-genetic manner. (PMID: 22337056)

    It is also worth noting that Jarosz also provided a lovely example of your version #1 during his post-doc. He shows that Hsp90 in yeast can hide variations until a stress exhausts the Hsp90 reservoir, unleashing the stored variability for a potentially adaptive response (PMID: 21205668). This is an elegant counterexample to the Creationist criticism about how new traits can emerge when an adaption that is later beneficial later may be detrimental to the current environmental conditions.

    For those who don’t like to read papers, these are briefly summarized in a Nature profile of Professor Lindquist:
    http://www.nature.com/news/prions-and-chaperones-outside-the-fold-1.10026

    There are other examples of version #2 that I’ve come across – for example non-genetic heritability of viRNAs in C. elegans (PMID: 22119442). In this case, like above, the genome isn’t modified but the acquired trait is still inherited.

    Additionally the CRISPR/Cas9 adaptive immune system in bacteria is another example of an acquired trait being inherited. In this example, the end result genome itself is adapted in response to the environment. I am not well-versed in the history of this issue, but this seems to be perfectly fit your definition of the Baldwin Effect: “the environment itself evokes phenotypic (not genetic) variation, which is then somehow fixed in the species’ genome.” Since this isn’t a field I follow actively, there may be even more examples that I am unaware of.

    Overall, these seem to be the exceptions that prove the rule. We have discovered a few (initially) non-genetic means of adaptation and inheritance, but they tend to be rare quirks that themselves relying on conditions selected for by genetic Darwinian evolution.

    Still, I think it warrants mentioning that there are a few examples for version #2, despite claims that no evidence exists. However, I don’t think this undermines your overall argument.

    By the way, my first time posting. Love your work.

    • Posted December 7, 2013 at 4:20 am | Permalink

      I’m not aware of any of the examples above except for the heat-shock proteins, which are a purely lab example and, as you surely know, there is no example of an adaptation in nature caused by heat-generated mutations. They are all “monsters,” and you recognize this by saying “potentially” adaptive variation. Well, all variation is potentially adaptive, but in this case it’s just a possibility, and not one demonstrated in nature. As for the “Lamarckian” inheritance of genetic elements like prions, I suppose one could consider those environmental effects, but they’re not genetic mutations revealed by a new environment. BUt I’ll check the other cases; thanks.

    • bobs
      Posted December 7, 2013 at 1:08 pm | Permalink

      CRISPR is pure Lamarck. Of course it’s “exceptional,” occurring only in virtually all of archae and half of bacteria…

      Oh well.

      • kirkwillmarth
        Posted December 7, 2013 at 3:49 pm | Permalink

        Bobs,

        You’re are right for criticizing me calling this an ‘exception’. I wasn’t trying to brush away the CRISPR system just because its bacterial. Clearly it is widespread by any metric (# of species, # of organisms, % of worldwide biomass) that possess this trait.

        I should have clarified that by ‘exceptions’ I meant the number of known traits that do not follow our classical conception of neo-Darwinian is small (though non-zero), despite the fact that some of them may be quite common and important.

        To Prof Coyne’s point, my inclusion of heat shock proteins was merely an aside that this is a lab that has worked on the same example you cite above. I agree that this is like horizontal gene transfer, a form of new genetic variation but not directed adaptation.

        If we are defining Lamarkian inheritance as an inherited adaptation that requires fixation in the genome, then I suppose both prions and viRNA fail as examples. They would be more similar to epigenetics in that they are inherited adaptations but not genetically fixed (though both can be reinforced across multiple generations through their own systems of replication). However, both the CRISPR system in bacteria and piRNAs in mammals would seem to fit this criteria.

  35. Graham Lyons
    Posted December 7, 2013 at 3:44 pm | Permalink

    Can someone explain why the ability to pass on acquired characteristics has never evolved? It seems to me the progeny of most organisms possessing that ability would have a pronounced advantage under natural selection.

    Darwin thought Lamarckism was a possible mechanism of evolution by natural selection.

    • gbjames
      Posted December 7, 2013 at 3:54 pm | Permalink

      Because acquired characteristics don’t alter DNA in eggs and sperm. So they can’t get passed on.

      • Posted December 7, 2013 at 4:26 pm | Permalink

        Actually, Graham’s question deserves a bit of a deeper explanation.

        gbjames is absolutely correct in that the proximal answer is, “It don’t work like that.”

        But, Graham, you’re also correct in pointing out that, if it actually did work like that, that would be an amazingly huge advantage to a species that was able to do that sort of thing.

        The reason why no species has actually evolved the capability for Lamarckian evolution is largely due to the fact that, as Richard put it, the watchmaker doing the designing is blind. There’s no striving for any particular goal in Darwinian evolution, even when species have the appearance of having been designed with some particular goal in mind. Rather, it’s something of a drunkard’s walk, and the lucky drunks who stumble along steady paths (instead of over cliffs or into bogs or brambles) are the ones who make it through the maze.

        There may well be viable hypothetical genetic mechanisms that would permit Larmarckian evolution to happen. However, we can be extremely confident in stating that, at the least, there is no viable means for Darwinian evolution of the tree of life that we have here on Earth to stumble upon such mechanisms. And, by now — and, really, for billions of years — the mechanisms of inheritance on Earth have been fixed in ways that it’s really not possible. The Central Dogma of molecular biology, indeed, states that information can be copied back and forth from DNA and RNA, and from RNA to proteins, but never from proteins to RNA or DNA. There’s just no way for that to happen.

        …with one astoundingly remarkable and most noteworthy exception: genetic engineering of the type that Craig Venter is famous for pioneering.

        At long last, after billions of years of Darwinian evolution, we are now at the dawn of a new era (however long-lived it may be) whereby life can finally intelligently design itself. Granted, the manner isn’t either in principle or practice as Lamarck described…but that’s because it’s far more sophisticated and flexible. Life isn’t just limited to genetically modifying itself to pass down those morphological changes that it was actually able to achieve through whatever means; life is able to create new life completely unrelated and unconstrained by that which came before.

        Assuming we don’t off ourselves in one of the oh-so-many ways we’re poised and seemingly eager to do, this truly is a seminal moment in the history of life on Earth, one far more radically disruptive than the invention of photosynthesis, and even more important than the invention of sex.

        Cheers,

        b&

      • gbjames
        Posted December 7, 2013 at 5:07 pm | Permalink

        Actually, there is an exception to this.

        The ability to pass on acquired characteristics has never evolved does happen, but it isn’t a strictly biological process. This is what culture is all about. We are able to pass on acquired cognitive traits to each other and to subsequent generations. So I suppose strictly speaking this capability has in fact evolved. But the mechanism for transmission isn’t genetic.

    • Gregory Kusnick
      Posted December 7, 2013 at 4:30 pm | Permalink

      Speaking as a non-specialist, I’m guessing that the answer is entropy.

      The information embodied in the genome goes through many levels of irreversible transformation in the process of producing a phenotype. In order to write phenotypic changes back into the genome, you’d need some mechanism for calculating the inverse of all those transforms and effectively reverse-engineering the gene changes needed to produce that phenotypic change.

      To use a mathematical analogy, multiplying huge prime numbers together is easy. Factoring huge composite numbers into their prime factors is ridiculously hard. That’s why we use such methods for encrypting digital data.

      So think of it as a problem in cryptography, with the genome as the plaintext message, the developmental environment as the public key, and the phenotype as the ciphertext. But there is no corresponding private key, and therefore no way to go from ciphertext (phenotype) back to plaintext (genome).

      • Posted December 7, 2013 at 4:47 pm | Permalink

        I think that’s at least an excellent hypothesis of why it doesn’t happen given the genomic mechanism life on Earth uses.

        But we don’t know that it necessarily has to be like that. And, indeed, we see two ways — first, culture (in more than just humans) and now genetic engineering — that information that the individual learns gets passed to future generations without using the genomic mechanisms. I daresay an intelligently designed genomic mechanism would have built into it encoding methods and feedback mechanisms that weren’t nearly so hostile to that sort of thing as DNA is. Indeed, an intelligently designed genomic mechanism likely would be Lamarckian through and through….

        Cheers,

        b&

    • Eduardo
      Posted December 7, 2013 at 6:02 pm | Permalink

      1) Under the only known method for permanently passing on information between generations, DNA encoding, it would be nearly inconceivable that an acquired characteristic (whether environmentally produced or due to a repetitious action, or whatever) could somehow go on to the gonads to alter a gamete’s DNA sequence exactly in the manner that would recreate the character. This is an ant trying to overcome obstacles the size of planets in it’s way.
      2) “Acquired character” is not synonym of “advantageous character”. They may or may not be favorable to future generations. So the selective pressure to evolve a mechanism that would facilitate transmission might not be there.
      3) There already is a very efficient method of passing acquired characteristics if you define these as traits that have selected over many generations that favor fitness. It’s called Darwinian natural selection.

    • johnjacoblyons
      Posted December 8, 2013 at 11:10 am | Permalink

      Hi Graham! Interesting that we have the same surname.

      Ben Goren and gbjames have given you good answers to your question. However neither has mentioned that the inability of information to flow in the ‘protein – RNA – DNA’ direction (albeit with minor exceptions) is known as ‘The Weismann Barrier’. You may be interested to Google this phrase to get even more relevant info.

      I would also like to refer you to my own hypothesis known as ‘Genetic Priming’. It explains how a spontaneous, persistent animal behaviour (a particular example of an acquired characteristic) that proves to be adaptive, can indeed – over evolutionary time – shape the genome. Please take a look at my paper https://www.academia.edu/2551188/GENETIC_PRIMING_HOW_ADAPTIVE_BEHAVIOUR_SHAPES_THE_GENOME

  36. Posted December 7, 2013 at 10:20 pm | Permalink

    Shouldn’t horizontal gene transfer be the ultimate example of the Selfish Gene that would need to be explained by a different theory? It’s literally showing that genes can move “freely.”

  37. Posted December 8, 2013 at 12:34 am | Permalink

    A recent article in Molecular Psychiatry explores several hypotheses to explain the expression of various phenotypes with a given genotype. The value for us, here, I submit, is how comprehensively they demonstrate that different phenotypes come from the same genotype, depending on additional factors. Easy to understand are transcription regulatory genes that turn on or off your candidate gene, like this blog avers; harder to grasp are trait expressions emerging when the candidate gene is “on” and in a particular gene context or in a particular functional network of other active genes (a module), or at a certain developmental phase and molecular milieu, or in a particular environment (second messenger system active within the cell and concomitant “talk” between cell membrane–proxy for outside world– and DNA, or ways in which gene-trait expression can be globally altered by environmental stimuli. I submit, all this variance makes it easy to lose sight of the genome as fixed and present from the beginning of said organism. The DNA sequence does not change! It may seem like it (epigenetic parlance) but it’s the same sequence of base pairs you get at birth that you have at death.

    For example, in this article in molecular psychiatry nov 2013, schizophrenia occurs through pleotropy. The same common genes yield many many different normal phenotypes, and only occasionally do you get schizophrenia. It depends on all these other factors, still ill-defined.

    So, I agree with this post to a point. Where I hesitate is here: some of these aforementioned factors affecting whether a gene expresses a trait are not under the
    direct control of the DNA, like second messengers, for example; the DNA is reacting to stimuli outside its control. How can that be the selfish machinations of the gene? I would think the gene is a bit hapless. It doesn’t seem like natural selection to me that different traits emerge from the relentless barrage on the DNA by stimuli. I submit that we may be giving the DNA too much credit to believe organisms are evolving simply based on transcription regulation by its own promoters. That is way too simplistic.

    Some thoughts. Check out the article.

    • Posted December 8, 2013 at 7:28 am | Permalink

      So, I agree with this post to a point. Where I hesitate is here: some of these aforementioned factors affecting whether a gene expresses a trait are not under the direct control of the DNA, like second messengers, for example; the DNA is reacting to stimuli outside its control. How can that be the selfish machinations of the gene?

      You’re attributing much too much power of control to the genes. They set the stage, certainly; but organisms are not marionettes dancing to the tugs of the strings held by genes. You may also be confused by the fact that, contrary to popular usage, there really isn’t any such thing as a gene “for” anything. A gene that expresses itself in one manner in one environment is very likely to express itself differently in a different environment. Indeed, when you look at the overwhelming genetic similarity between species — let alone individuals — it becomes clear that, even at the level where the biggest factors in a gene’s environment are other genes, that environment can radically change the manner in which the gene is expressed.

      Remember Cc, the first cloned cat? She was a tabby, but her genetic mother was a calico. Clearly, therefore, there isn’t “a” gene for tabbies and “another” gene for calicos. Rather, there are genes that regulate coat patterning, and different environmental factors can influence the ways in which those patterns manifest themselves.

      But this is no different from the ancient nature v nurture argument!

      As another example that I don’t think you’ll find nearly so confusing: certain dog breeds, notoriously such as staffordshire terriers, tend to be very territorial. Two genetically-identical puppies could be raised: one treated with love and dignity and respect which grows up to be a most loyal and loving and friendly and protective and supportive companion; and another that’s tormented and beaten and abused which grows up to be the archetypal vicious pit bull attack dog of the junkyard.

      Where I suspect you’re getting hung up is with the distance between genetic composition and environmental effects. In your example, the action was right there in the primary interface between genes and their environment — protein synthesis. In my example of canine temperament, protein synthesis was several layers of abstraction prior. But, in both cases, the Central Dogma still holds: it is the genes, and only the genes that survive from the one generation to the another, and the environmental differences do not write themselves back into the genome.

      Cheers,

      b&

      • Posted December 8, 2013 at 10:39 am | Permalink

        What about maternal transmission of epigenetic modifications of the DNA like histone acetylation or methylation? The postnatal modification in the maternal DNA is directly transmitted to the offspring. The genome hasn’t been written into, no, but “information” which is non-DNA has been transmitted. Yes, the genome substrate is the primary reference, but proteins passed on are nongenetic. I see this as an challenge to your central dogma.

        • Posted December 8, 2013 at 11:39 am | Permalink

          As I understand it — and I’m not involved in the field, so I could be worng — those sorts of things never last beyond a couple generations, and never really become fixed.

          Remember, the Central Dogma — not mine, but Francis Crick’s, generally embraced by the field of molecular biology — is with respect to heritable genetic information. We already have culture (in more than just humans) and the like as ways that information survives past generations, so it’s not a prohibition on any type of information; just heritable information subject to Darwinian evolution.

          Cheers,

          b&

        • kirkwillmarth
          Posted December 8, 2013 at 11:40 am | Permalink

          You should read one of the many posts on this blog about that topic (Google “whyevolutionistrue epigenetics”).

          Evolution requires lasting heritable change. Since epigenetic modifications fade over generations, no evolution has actually occurred. Yes there is a phenotypical change for the next generation; this mechanism may be clinically relevant in a patient setting but it is not evolutionarily relevant. Transmitted information that fades after a few generations can only be for temporary adaptation (positive or negative). Since it does not result in lasting transmissible change, it cannot be a mechanism for evolution.

          A more semantic quibble: as far as I know, almost no postnatal maternal epigenetic modifications are transmitted. Don’t forget that germ cells are segregated from somatic cells prior to birth. The cells that gave rise to you were first formed while your mother was still in your grandmother’s womb and remain in a state of meiotic arrest until ovulation. As far I know, maternal behavior that impacts fetal development are almost always more environmental (exposure of the eggs and womb to the same environmental conditions as the mother) than heritable (epigenetic marks being transmitted from the mother to the child) in cause. You state this pretty strongly so if you have an example of this please correct me.

          • Posted December 8, 2013 at 6:18 pm | Permalink

            We are, I believe, both speaking of epigenetic marks (DNA methylation or histone acetylation) or, alternately, epimutations. The question is whether they persist across generations or are swept clean at meiosis. I suppose you are right in most cases meiosis resets the genome and marks do not carry forward. But, there are exceptions, such as transposon methylation in plants or hereditary colon cancer in human, in which hypermethylation of MSH2 transmits across three generations in this study:

            http://www.nature.com/ng/journal/v38/n10/full/ng1866.html

            I went to transgenerational epigenetics in Wikipedia and found this:

            Cellular mechanisms may allow for co-transmission of some epigenetic marks. During replication, DNA polymerases working on the leading and lagging strands are coupled by the DNA processivity factor proliferating cell nuclear antigen (PCNA), which has also been implicated in patterning and strand crosstalk that allows for copy fidelity of epigenetic marks.[25][26] Work on histone modification copy fidelity has remained in the model phase, but early efforts suggest that modifications of new histones are patterned on those of the old histones and that new and old histones randomly assort between the two daughter DNA strands.[27] With respect to transfer to the next generation, many marks are removed as described above.

            Emerging studies are finding patterns of epigenetic conservation across generations.

            For instance, centromeric satellites resist demethylation.[28] The mechanism responsible for this conservation is not known, though some evidence suggests that methylation of histones may contribute.[28][29]

            I am sorry to throw this out fairly undigested, but I think it’s possible that epigenetic marks can be retained.

            It does not take away your fine point, however, that there is decay of epigenetic marks within three generations, and now I can see how you and others question if epigenetics contributes to evolution.

            I will have to mull on all this:

            How about, gene A–>geneA*–> activates adaptive gene B–>adaptive trait emerges.
            In which gene A* is epigenetically modified in order to activates a highly adaptive gene B (say A is a promoter gene); gene B leads forward evolution. In this case, it would be evolution requiring epigenetics to occur. (but yes, its still the genome that is making it happen, but, no, evolution is didn’t proceed sans epigenetics, either).

            Thanks for giving me a chance to think this through! I will read the blog more thoroughly now.
            jw

  38. Posted December 8, 2013 at 2:25 pm | Permalink

    Graham Lyons #35
    “Can someone explain why the ability to pass on acquired characteristics has never evolved? It seems to me the progeny of most organisms possessing that ability would have a pronounced advantage under natural selection.”

    Lamarckism would NOT be a “pronounced advantage”, rather a reckless gamble tailoring each future generation to past conditions.

    Let’s imagine you’re born with a mutation allowing you to alter germ cell DNA to produce a thinner fur coat in response to warming conditions. Even granting that
    1) such a rewriting mechanism is feasible;
    2) your body can somehow recognize that thinner fur is advantageous in warm weather;

    it wouldn’t provide a consistent fitness advantage. Here’s why:

    * First, you yourself don’t derive any benefit from the mutation — you’re stuck with the coat you inherited from your parents;

    * If you’re so lucky as to survive long enough to breed, your offspring derive a benefit only if: 1) temperatures continue to warm; 2) the coat they would have otherwise inherited would have been less than optimal;

    * If mild winters persist, your children with the Lamarckian mutation will once again thin the already thin fur coat inherited from you, giving your grandchildren extra thin fur. (If it grows colder, we’ll assume the mutation thickens the coat a notch.) Either way, your grandchildren will have some of the thinnest coats among the population — a relative advantage if conditions keep warming, but a great disadvantage in a cold spell. Were your mutation to became prevalent or universal, the population would be at great risk of die-off were there a sudden, pronounced shift in temperatures.

    And, of course, environments are comprised of myriad conditions, all subject to fluctuation. In any one generation, Lamarckian processes are bound to guess wrong on the direction of some of the trends.

    Genes that randomly mutate don’t have to foresee what thickness of fur is optimal — they just blindly produce a range of coats distributed about a mean. The best coat wins and that trait becomes more prevalent in succeeding generations. Also, in contrast to the all Lamarckians banking on thin coats, randomly mutating genes (or any population with a range of alleles) ‘hedge their bets’ by also producing some thicker coats.

    Whereas, at the first abrupt change in conditions, all the Lamarckian individuals are at a disadvantage, some of the random mutators will always have a distinct advantage. Whatever the twists & turns of the environment, the genes that make it through — whether thick-coaters or thin-coaters — are always random mutators.

    The deftness and agility of random mutation’s response to fluctuating environmental conditions is revealed in the data collected by Grant on Darwin’s Finches. A Lamarckian process would ever be a day late and a dollar short.

  39. Posted December 9, 2013 at 4:32 am | Permalink

    Thank you so much for spending time writing this two “debunk” articles.

    I felt so uneasy after reading the original Dobbs’ piece. I knew Dobbs was wrong from how I understand self gene. But I don’t have enough knowledge and well organized words to aid me. So thanks again.

    Could you be very kind to answer a question? How to start doing research for writing a popular science book?

  40. Gallileo
    Posted December 9, 2013 at 7:38 pm | Permalink

    The observations are problems for the theory? No, of course they aren’t. We have epicycles to explain all of them. Nothing to see here! I assure you, the gene is still the center of the universe.

  41. Posted December 13, 2013 at 1:08 pm | Permalink

    I’m the author of the article under discussion. I’ve posted a revision of ‘Die, Selfish Gene, Die’(http://aeon.co/magazine/nature-and-cosmos/why-its-time-to-lay-the-selfish-gene-to-rest/) that seeks to clarify some issues and answer some of the critiques. I also put up a post at my blog (http://daviddobbs.net/smoothpebbles/die-selfish-gene-die-has-evolved/) providing some context about the revision (including its take-home) and links to resources, including a highlighted version that make it easier to spot the added and altered passages.


11 Trackbacks/Pingbacks

  1. […] David Dobbs wrote an article titled ‘Die, selfish gene, die’. My impression was that the idea that he was attack was not the one that is presented in the book The Selfish Gene, but rather some kind of strawman. In fairness, Dobbs backtracked on his twitter pretty quickly and clarified his point by restricting it quite heavily. While the writing is undeniably great, the article itself is fairly misleading which leads me to wonder whether that makes it good or bad science writing? I was going to post on it, but my fear got the better of me and I decided I didn’t know enough evolutionary theory to feel comfortable attacking the article. Jerry Coyne does the job that I wanted to do, with more authority though probably also more venom. […]

  2. […] David Dobbs mucks up evoution, part II (whyevolutionistrue.wordpress.com) […]

  3. […] Jerry Coyne: “David Dobbs Mucks Up Evolution, Part II” […]

  4. […] David Dobbs mucks up evoution, part II (whyevolutionistrue.wordpress.com) […]

  5. […] Cat, for reasons that will be obvious to anyone who visits his blog) described the idea in his second rebuttal as […]

  6. […] Part 2 […]

  7. […] Part 2 […]

  8. […] David Dobbs mucks up evoution, part II […]

  9. […] and The Selfish Gene by richard dawkins – see also David Dobbs mucks up evolution, part I and David Dobbs mucks up evolution, part II by jerry coyne – see also There is no revolution in genetics and Evolutionary orthodoxy may […]

  10. […] 62. David Hobbs Mucks Up Evolution: Part 1, Part 2 […]

  11. […] Dobbs takes on the Selfish Gene. Dawkins responds (as does Jerry Coyne, three times). I’m generally with Dawkins and Coyne on the theme (if not every detail) of this […]

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