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The Descent of Edward Wilson (with Polish translation) - Comments

antipodesman's Avatar Comment 1 by antipodesman

Thanks Richard for this review of the controversy concerning kin vs group selection. Can you explain whether a suicide gene could be attributed to kin selection?

Thu, 24 May 2012 15:56:03 UTC | #943298

Serdan's Avatar Comment 2 by Serdan

Beautifully written and very informative, as always. :)

@antipodesman: I'm not an expert, but I believe he already did. Can you find some circumstances under which rB>C, where C is suicide?

Thu, 24 May 2012 16:09:55 UTC | #943302

candide94's Avatar Comment 3 by candide94

@Serdan @Antipodesman

Here is a lovely (as in fascinating) example of ants sacrificing themselves to help their kin.

http://www.newscientist.com/article/dn14821-heroic-ants-pay-the-ultimate-price-to-safeguard-nest.html

Every evening at sunset the ants seal the door to their nest. But a few ants always stay outside to kick sand over the entrance to disguise it better. A large proportion of the ants left outside die of the cold, are blown away or eaten by predators. Hence, every night a number of ants must sacrifice themselves to ensure the protection of the rest of the colony.

This is very interesting as there is no caste that does this, it seems to be a behaviour wired into all the ants which is activated by certain circumstances, i.e. being of the right age to be last in the door. (so they don't get in the door at all!)

Now if we consider Hamilton's rule, this all makes perfect sense. Think of all those genes for "sacrificing yourself to lock the door" swarming inside the colony (or rather inside the queen in the colony, and in the potential queens in the colony). The cost to the individual may be huge (i.e. death) but rB >>>>>>> C because of, first, the fact there are individuals carrying that gene in the nest who will go onto reproduce a helluva lot and second, the fact this behaviour is very important in letting the queen go onto reproduce as it prevents predators sneaking in and attacking the nest (and her) at night.

Obviously RD's book explain this far better than me, but I thought this was a good example.

Thu, 24 May 2012 16:31:04 UTC | #943305

Serdan's Avatar Comment 4 by Serdan

Thank you for that example. It is, indeed, very lovely. :)

Thu, 24 May 2012 16:46:34 UTC | #943309

brighterstill's Avatar Comment 5 by brighterstill

"This is very interesting as there is no caste that does this, it seems to be a behaviour wired into all the ants which is activated by certain circumstances."

I immediately began to think about a species of ant which might devolop a "suicide" caste, where the door-lockers followed a genetic path to use fewer ressources than other ants, since they were going to die anyway, then I immediately though "That's awful! What a barbaric species!" Then I laughed.

Thu, 24 May 2012 16:52:58 UTC | #943311

Cartomancer's Avatar Comment 6 by Cartomancer

How do identical twins affect the working out of this Hamiltonian equation then? Surely in the case of twins who share 100% of DNA factor r is 1 and any genes for altruistic behaviour towards siblings will be selected for on a simple one to one cost/benefit analysis if the recipient benefits more than the donor loses out?

Obviously human beings do not produce twins very often, so perhaps there is only a minor effect from this in humans, which gets swamped by regular sibling-strategy genes. But am I correct in thinking that some species (Polar Bears?) pretty much always produce twins, and therefore are much more likely to exhibit sibling-altruism phenotypes than species that don't?

Thu, 24 May 2012 17:17:13 UTC | #943315

candide94's Avatar Comment 7 by candide94

@ brighterstill

Well, the door lockers wouldn't follow a specific genetic path because door lockers are never going to have children. The door lockers will have sisters who are going to grow up to be queens, who will often carry the door locking genes and spread them to the colonies they set up. In ants, caste is determined by either how an ant was raised or by its age. (e.g in some species, the youngest ants are the nursemaids, the next oldest are the nearby foragers, the oldest are the scouts). So (generalizing hugely) in most species every female ant has the potential to be of any caste, and depending on the temperature the egg from which she hatched was incubated will either be queen or worker) and the depending on her age will be of that caste or this. In a sense, there is a doorlocking caste in that on the evening the elderly ants happen to be last in the door, a behavioural switch is triiggered and the stereotypic responses locked in their genes are brought to life by the situation...

Admittedly, in species where caste is determined by morphological differences (usually size), you make a soldier of an ant by feeding more, a cleaner by feeding it less. So you could imagine that in a hypothetical ant colony evolution might have favoured for the nursemaids to feed the least food to the ants who were going to grow up to become the doorlockers. And by virtue of feeding them so little, a behaviour was triggered and the ants naturally did the door locking when left their by the nursemaids. Imagine that, kids being raised to go and die for the greater good...

Anyway, too much speculation is addictive!!!

Thu, 24 May 2012 17:19:10 UTC | #943316

Zeuglodon's Avatar Comment 8 by Zeuglodon

As much as I enjoyed the deconstruction of the group selection model by explaining how kin selection and inclusive fitness work, it would have been more appropriate if the review had gone into detail about Wilson's own argument. A comment at the bottom of the page gave a link to a Nature article which claimed that the kin selection model was "inadequate" outside of a few cases. Unfortunately, I couldn't access the article because you have to pay to see the whole thing, so I never saw Wilson et al.'s argument. In which cases did he think kin selection didn't work?

I also keep thinking that the benefit units in formulae like Br>C feel a little disembodied from the material units like number of genes. Are there any books on this genetic-mathematic subject? It might be that the workings are all done elsewhere, or are staring me in the face, but Br>C feels a bit disembodied at the moment, and I don't know what I'm supposed to be visualizing in terms of "benefit". Is it an increase in the proportion of that allele in the population relative to other alleles, with "all genes have only one allele" being the endgame?

Thu, 24 May 2012 18:21:30 UTC | #943328

kriton's Avatar Comment 9 by kriton

You cannot say the same of individual organisms (they die after passing on their genes and never make copies of themselves)

Never? So what about all those organisms that reproduce by division, such as bacteria?

In numbers, we sexually reproducing organisms are just a tiny minority.

Thu, 24 May 2012 18:24:21 UTC | #943329

Zeuglodon's Avatar Comment 10 by Zeuglodon

Comment 9 by kriton

You cannot say the same of individual organisms (they die after passing on their genes and never make copies of themselves)

Never? So what about all those organisms that reproduce by division, such as bacteria? In numbers, we sexually reproducing organisms are just a tiny minority.

Yes to the second (sexually-reproducing organisms are a tiny minority), but the argument works whether organisms sexually reproduce or not, because it's gene-centred, not organism-centred.

No to the first (bacteria make copies of themselves). Bacteria are actually a poor example because the cell bodies and protein molecules are all shaped by the genes riding inside them, and bacteria can exchange genes for differing phenotypes. I admit "never" wasn't the best word choice, but genes are atomically identical to their copies. No two individuals can be so (give or take sheer luck) because of complex environmental factors destroying the exact atomic similarities. Genes are digital, bodies are analogue.

But let's grant that organisms could make clones of themselves. Would this hurt Dawkins' argument? No, because to make your point you have to acknowledge that the genes are the salient connection. Clones (physically identical individuals) would be relevant because of the kin selection rule, not in spite of it. Of course, if r=1, then altruism would favour looking out for a clone as well as yourself in theory. They'd still be altruistic solely for genetic reasons. In practice, an individual can't be 100% certain that the thing living alongside it is genetically identical and has to base its "behaviour" on second-hand information, which are ripe fields for deception by other organisms driven by different genes.

Thu, 24 May 2012 18:47:25 UTC | #943331

Zeuglodon's Avatar Comment 11 by Zeuglodon

Yes to the second (sexually-reproducing organisms are a tiny minority), but the argument works whether organisms sexually reproduce or not, because it's gene-centred, not organism-centred.

Sorry, kriton, this was badly worded on my part. What I should have said is that the criterion for identical copies does superficially work on individuals when the population includes clone bodies, because their copies do look similar. However, the argument for individuals being the replicating entity falls down because of sexual reproduction - body structures change dramatically as a result so that each body is unique, not identical. Sexual reproducers may be a minority, but they make it harder to insist on the individual being the replicating entity, and they also show us that the genes are responsible for the phenotypes. What Dawkins should have said was that no one can say individuals are always the replicator.

Thu, 24 May 2012 19:24:32 UTC | #943337

Stafford Gordon's Avatar Comment 12 by Stafford Gordon

Although I can't recall whether the Latin definition is Trematoda or Monogenea, there is a fluke which enters the brain of the ant, causing it to cling to the top of a blade of grass in the noonday sun, when it should be underground with its pals, and which results in it being gobbled up by a passing grazing, sheep perhaps, in order for the parasite's life cycle to continue via the gut of the ruminent; perhaps this could be thought of as producing a suicidal ant?

The fluke causes a phenotypical effect I believe.

As always, I stand to be corrected.

Thu, 24 May 2012 19:40:57 UTC | #943342

Jos Gibbons's Avatar Comment 13 by Jos Gibbons

The other problem with thinking clones are replicated individuals, which RD points out in TSG, is that if individuals genuinely replicated acquired characteristics would be inherited, which isn't the case.

Thu, 24 May 2012 19:49:56 UTC | #943343

kriton's Avatar Comment 14 by kriton

Zeuglodon, I'm not sure, are you agreeing that bacteria can make genetical copies of themselves?

Either way, I'm wondering about this r part. Is there empirical evidence that says those numbers 1/2, 1/4 and so on present themselves in nature? I read the Wikipedia article, but that only said

In 2011, experimentalists found empirically that Hamilton's rule describes very accurately the conditions under which altruism emerged in simulated populations of foraging robots. The accuracy of this first quantitative corroboration of Hamilton's rule is all the more impressive given that Hamilton's model made several simplifications that did not apply to the foraging robots.

But simulated populations of robots isn't really the stuff I'm interested in.

After all, if we were to sequence my genes and my sisters genes, and compare the sequences, we would find that they were much more than 50% similar. Genes are conserved, and my parents would have lots of genes in common that are identical even if they are not related in the everyday sense.

Suppose I have a half-sister, and we look at a gene where the sequence is identical between us. A gene has no clue were it came from, so from a genetic point of view, what does it matter if my half-sister got an identical gene from the same parent as I did, or from another parent?

Thu, 24 May 2012 19:50:32 UTC | #943344

kriton's Avatar Comment 15 by kriton

Comment 13 by Jos Gibbons :

The other problem with thinking clones are replicated individuals, which RD points out in TSG, is that if individuals genuinely replicated acquired characteristics would be inherited, which isn't the case.

Can you prove then that there is no epigenetic inheritance in bacteria...?

Or perhaps you mean "It's only a replicated individual if all characteristics are copied!" ?

Thu, 24 May 2012 20:05:20 UTC | #943346

Jos Gibbons's Avatar Comment 16 by Jos Gibbons

Of course I do; that's what replication is about. "Like begets like" is one thing; "identical begets identical" is another. Remember, "it replicates at least in some parts" is true of sexual reproduction, too; I have half my father's genes.

As for the r thing, its definition is the conditional probability$ that the recipient of altruism contains an altruism-causing gene given that the altruist does. Therefore, it'll naturally be a dyadic fraction. The reason it "matters" is because, while a gene can't find out whether or not it's present in an individual, a probabilistic altruism rule is successful on average (which is what selection requires) iff it accords with Hamilton's rule.

$ More precisely, the limit thereof as the gene's frequency tends to 0.

Thu, 24 May 2012 20:54:05 UTC | #943354

kriton's Avatar Comment 17 by kriton

Jos Gibbons, of course you do what? Do you mean that all characteristics must be copied? But what has such an overly stringent definition to do with evolution?

Obviously a bacteria doesn't copy itself molecule for molecule. But so what? It can still make a genetically identical copy of itself, and that is what should matter. I'm not exactly the same individual I was a year ago if we look at all characteristics, and molecule for molecule, but how is that relevant for evolution?

I don't really understand what you are saying about r, but it does not seem to answer my request for empirical evidence for the 1/2 and 1/4 numbers.

It seems to me that it's only "the conditional probability that the recipient of altruism contains an altruism-causing gene given that the altruist does", if the altruist is the only source of that gene. But I just pointed out that in real life we have no reason to assume that the altruist is the only source.

So when a successful gene spreads through the population, the 1/2 and 1/4 stuff should no longer be relevant. It only holds for a newly introduced gene, right ...?

Thu, 24 May 2012 21:54:30 UTC | #943361

Zeuglodon's Avatar Comment 18 by Zeuglodon

Comment 14 by kriton

Zeuglodon, I'm not sure, are you agreeing that bacteria can make genetical copies of themselves?

I think you're confused. Our aim is to identify what the unit of replication is. This requires that the unit is unambiguously capable of creating atomic-scale identical copies of itself. In fact, a bacterium's ability to split is itself a consequence of the replication process of this unit. Without genetic mechanisms to regulate and time the mitosis of the cells, you wouldn't get the division of cells in the first place. After all, a cell body deprived of its genes does not create copies of itself. It would simply sit there and do nothing.

Either way, I'm wondering about this r part. Is there empirical evidence that says those numbers 1/2, 1/4 and so on present themselves in nature?

Yes. The process of meiosis and genetic recombination in sexually-reproducing organisms is a basic fact of biology. Between parents and offspring, for example, the probability is on average 50% that a parent provided any particular gene. The 50% threshold applies mostly to those genetic loci that still vary within the population, for instance for variables that can, by the process of pleiotropy, also express themselves as eye colour. Either you got your eye colour gene from your mother or from your father. Averaged out, 50% of your genes will come from any one parent. Of course, there will be cases where a person may have more genes from one parent, but these are statistical anomalies to be expected as part of the recombination process. To the rest of the family tree, you simply implement an extension of this basic fact.

I read the Wikipedia article, but that only said... simulated populations of robots isn't really the stuff I'm interested in.

Why not? Simulations may not always map onto real life, but to dismiss them out of hand is to stack the deck. You forget that kin selection was not only an answer to a known phenomenon, but needed to be mathematically verified. In any case, the empirical evidence comes from, for example, genetic studies of animals like social insects.

After all, if we were to sequence my genes and my sisters genes, and compare the sequences, we would find that they were much more than 50% similar. Genes are conserved, and my parents would have lots of genes in common that are identical even if they are not related in the everyday sense.

If they are identical at the same genetic loci, then they are practically copies. In any case, the 50%, 25% and 12.5% relatedness figures are more usually invoked for the set of genes that are not included in a "species threshold". Say, for instance, 99.9% of human genes were identical. The remaining 0.1% would be where the relatedness figures would be present. It isn't hard to see why: obviously, if the genomes were 100%, genes would have nothing to compete with because whichever individual wins means the genes win anyway. You have to remember that the genetic competition is between alleles competing for the same spot on the genome, not genes fighting any old gene.

Suppose I have a half-sister, and we look at a gene where the sequence is identical between us. A gene has no clue were it came from, so from a genetic point of view, what does it matter if my half-sister got an identical gene from the same parent as I did, or from another parent?

This is one place where I think you're really confused. The altruism of an individual is a product of the combined phenotypes of several genes, each of which is either competing with rival alleles or had to compete with them at one point. Imagine two alleles competing for the same spot. One allele makes its host organisms behave more altruistically to its genetic relatives. The other does not. Under certain conditions - for instance, when organisms would benefit from staying in isolated groups - the altruistic allele would simply become more widespread in the population until it reached fixation (i.e. choked out its rival). The mathematical rules of kin selection theory would shape both the survival of further mutations and the direction of natural selection. The population would consist of increasingly more "intelligent" altruists who would be willing to do altruistic things when faced with certain situations. This might take many speciation events before it reached pitch perfection, and several versions at varying stages could be found during the same time interval (hymenopterans are a particularly rich source of examples, from lone digger wasps to huge colonies of bees and ants).

Thu, 24 May 2012 22:08:52 UTC | #943362

Peter Grant's Avatar Comment 19 by Peter Grant

The Descent of Edward Wilson http://www.prospectmagazine.co.uk/science/edward-wilson-social-conquest-earth-evolutionary-errors-origin-species/

This is sort of sad, but I imagine it must also be quite irritating for Professor Dawkins and his peers to have to keep correcting the same mistakes over and over again. Thank you.

Thu, 24 May 2012 22:26:34 UTC | #943368

decius's Avatar Comment 20 by decius

Kin may or may not cling together in a group. Kin selection works whether they do or not.

That's it, in a nutshell. Funny Hamilton should invoke parsimony.

Thu, 24 May 2012 22:52:32 UTC | #943371

kriton's Avatar Comment 21 by kriton

Zeuglodon, the unit of replication would be either the individual gene or the whole bacterial genome. But the individual gene is expressed as a protein and the genome is expressed as an individual organism. I argue that genomes can make identical copies of themselves. Why would the resulting organism have to be identical atom for atom? As I said before, I'm not exactly the same as one year ago, but I'm still the same individual from an evolutionary point of view.

And that's not the empirical evidence I'm asking for. I'm asking about altruistic behaviour.

If the 1/2, 1/4 and so on only applies when genes or gene variants are not already widespread in the population, then I think I get it.

But if that is the case, I would say this is something that should be pointed out MUCH more. If altruistic gene variants have been successful, they should be widespread in the human population already. And then those 1/2 and 1/4 numbers should be irrelevant for the current human situation. I don't think I'm the only one who gets confused. It seems you are explaining things I'm not asking about.

Thu, 24 May 2012 22:55:22 UTC | #943372

decius's Avatar Comment 22 by decius

Correction to my previous post: I meant Wilson, not Hamilton.

Thu, 24 May 2012 23:12:59 UTC | #943379

Zeuglodon's Avatar Comment 23 by Zeuglodon

Comment 21 by kriton

Zeuglodon, the unit of replication would be either the individual gene or the whole bacterial genome.

In Comment 9, you were talking about bacteria and organisms. At least concede you've just changed tracks.

But the individual gene is expressed as a protein

Do you know that the cellular processes inside and outside the nucleus are regulated by these things? Again, you can't have the reproducing organism without genes.

and the genome is expressed as an individual organism. I argue that genomes can make identical copies of themselves.

Except that the genome suffers the same problem as the organism - recombination quickly "destroys" it, and the process is only an extension of genetic-level replication in the first place. How would you explain viruses and non-inherited gene-exchange (I believe it is called epigenetics) on this genome-centric model?

Why would the resulting organism have to be identical atom for atom? As I said before, I'm not exactly the same as one year ago, but I'm still the same individual from an evolutionary point of view.

Because that's what replication means. The errors per replication can't be so severe that they'd never have identical copies yet distinct generations, otherwise there's no selecting going on at any point. It would be a random process and the resulting organisms would be increasingly likely to die off. Vehicles have less requirement for atomic exactitude because their job is simply to square off with the environment, and that involves changing and taking changes. A replicator needs to be stable over several generations. Jos Gibbons made the same point when he described acquired characteristics earlier.

And that's not the empirical evidence I'm asking for. I'm asking about altruistic behaviour.

What a strange request. The altruistic behaviour was what the theory was invoked to explain in the first place.

Parental care, sibling care, mobbing, food distribution among relatives, self-sacrifice et al. are all examples of altruistic behaviour. Hymenopterans are, again, a particularly rich source of such evidence, but mammalian caring behaviour, avian roosting behaviour, crocodilian caring behaviour, and several kinds of fish and marine species' maternal/paternal behaviour (e.g. that of seahorses and octopus mothers) would also be fine examples. Family units in nature are generally the examples of most interest. If you wanted to vindicate Hamilton's theory, however, you'd have to perform a genetic analysis at some point, and the obvious animals I would look at are hymenopterans.

If the 1/2, 1/4 and so on only applies when genes or gene variants are not already widespread in the population, then I think I get it. But if that is the case, I would say this is something that should be pointed out MUCH more. If altruistic gene variants have been successful, they should be widespread in the human population already.

Well, duh. Most of them will be. That's the point of the competition between alleles - that one of them eventually supplant the other. This isn't always clear cut, however. Sometimes, alleles are highly conditional on what's going on elsewhere in the gene, and this can hamper their performance. For instance, Gene A1 might beat its allele Gene A2 only if Gene B1 isn't around.

And then those 1/2 and 1/4 numbers should be irrelevant for the current human situation. I don't think I'm the only one who gets confused. It seems you are explaining things I'm not asking about.

Ah, I think I see where we're getting confused. You have to take into account the process by which a gene reaches fixation in the first place.

Imagine: you're a new mutant on the scene, and the process of reproduction goes like this. Copies of your altruistic allele are created in the gametes. But your reproductive partner is also shuffling their genes, including your rival allele. The shuffling means that, when copulation occurs, you have no idea whether the offspring will have a copy of your own allele or the rival. There's a fifty-fifty chance. Your offspring is born. What's the best way to treat them? The optimal would be to go along with the fifty-fifty chance that the offspring inherited your allele, so they are a half a priority compared to yourself. If you have more children, then obviously your chances have gone up that any one of them will have your gamete. In these cases, it would be worth behaving more altruistically than usual towards them, but there's still some holding back and there will be tensions between parent and child.

If the mutant allele in this case is successful, (its success is conditional), then the population of the behaviour will increase generation by generation. Obviously, the strategy can be refined by additional genetic inputs on other genetic loci, but the principle is the same because each gene on each locus is following the same general rule. Even when it reaches fixation, the allele will still be programming its host to use the rules of thumb that ensured it got there in the first place.

Your scenario can't come about by the introduction of a new pan-species altruism allele, because that would suffer against less suicidal rivals that were measured against the mendelian probabilities of being passed on to the next generation. The only way for your scenario (of pan-species altruism) to come about would be if every last copy of the fixated allele miraculously mutated such that the resulting phenotype treated every species member it met as though they were genetic clones. This is, to say the least, incredibly unlikely.

Remember, this whole competition is against rival alleles. The strategy that gave an allele an edge over its rival will stay there when it drives the rival allele to extinction. And don't forget that multiple gene interactions can make the process very complicated in the real world.

Does this make it clearer? Please say if it doesn't, as it's important you get these points.

Thu, 24 May 2012 23:53:52 UTC | #943386

Jos Gibbons's Avatar Comment 24 by Jos Gibbons

It seems to me that it's only "the conditional probability that the recipient of altruism contains an altruism-causing gene given that the altruist does", if the altruist is the only source of that gene. But I just pointed out that in real life we have no reason to assume that the altruist is the only source. So when a successful gene spreads through the population, the 1/2 and 1/4 stuff should no longer be relevant. It only holds for a newly introduced gene, right ...?

As I said, r is the limit as gene frequency tends to 0 of the conditional probability, so as it becomes more common the true conditional probability rises. Remember, however, the gene for altruism has to satisfy rB-C > 0 for all periods in which it becomes more common, including the initial brand-new period. As time passes, the "true" r will exceed that of these calculations, making the "true" rB-C greater, so it will still be positive. But because the gene will only get to that era if initially rB-C>0, the altruism policy it enacts has to be no more altruistic than the pessimistic estimate of the conditional probability warrants.

Fri, 25 May 2012 06:39:48 UTC | #943428

kriton's Avatar Comment 25 by kriton

Zeuglodon, how is that different tracks? The gene is useless without the protein, and the genome is useless without the organism. The organism is the vehicle for the genome, but they would not be around without each other and can't really be separated in the physical world.

The genome can be destroyed, but it is by no means necessary. It is perfectly possible for a bacterial genome to go on reproducing itself for thousands of generations. There will be changes over time, yes, just as there will be mutations in individual genes. New variants of the same gene, new variants of the same genome. I don't see how epigenetics would make a difference, since it affects both genes and genomes.

I'm not asking for evidence of altruistic behaviour in general, but evidence that the numbers 1/2, 1/4 can somehow be demonstrated to be relevant in actual such behaviour. You said:

Even when it reaches fixation, the allele will still be programming its host to use the rules of thumb that ensured it got there in the first place.

So is there empirical evidence that people or animals really treat their children like "half a priority compared to yourself"? Are there really such rules of thumb in real life, and are they stable over time?

Do the 1/2, 1/4 numbers apply only when the altruistic gene variant is new and has not yet spread in the population, or are they still relevant even after the new gene variant has spread to a large proportion (say 60%) of the population? Which one is it and why? That's what I would like a clear explanation of.

Fri, 25 May 2012 06:47:51 UTC | #943430

CEVA34's Avatar Comment 26 by CEVA34

I am not enough of a scientist to follow all the arguments in this thread so far, but one importants point strikes me:

If you read the complete review, you will find a whole bunch of direct replies attacking Dawkins and his views. Once again, I don't know enough to follow all the arguments, but in the present thread none of us seem to be addressing those often contemptuous dismissals of Dawkins and his allegedly mistaken emphasis on the gene. Dawkins describes Wilson as being in a minority; those replies seem to say it's Dawkins who is out of step. My gut feeling is that Dawkins is right, but like Sagan I don't want to think with my gut. Help me out, folks!

Fri, 25 May 2012 09:13:49 UTC | #943441

peter mayhew's Avatar Comment 27 by peter mayhew

It is true that the formal derivation of Hamilton's rule makes a bunch of assumptions, and hence that when those assumptions are broken the rule might not be expected to formally hold, but that is very different from saying that Kin Selection theory is a failure. Kin Selection also makes a huge bunch of predictions that make beautiful sense of a whole range of biological phenomena (outlined in the response to the original paper). That's the primary reason why Wilson oversteps the bounds of reason: his statements simply do not reflect the empirical success of the theory.

Fri, 25 May 2012 09:46:25 UTC | #943446

Roedy's Avatar Comment 28 by Roedy

This is the second imperious article I have read of Dawkins trashing Wilson. He just baldly states that Wilson is wrong and Dawkins is right. I said so. End of story.

It may well be true, but that is no way to argue the point.

He is is arguing like the Pope. Egad.

The article needs to be redone explaining why Wilson is wrong. What is the evidence? -- not just all the experts, especially me, say so. Part of the problem is the evidence is too familiar, too obvious to Dawkins. He has not the patience to elaborate it for a non-expert audience or even to properly recognise that it needs to be explained. Perhaps someone else should write the article for him.

Fri, 25 May 2012 11:32:43 UTC | #943460

Jussie's Avatar Comment 29 by Jussie

What CEVA34 said.

Fri, 25 May 2012 11:43:13 UTC | #943461

Peter Grant's Avatar Comment 30 by Peter Grant

The Descent of Edward Wilson http://www.prospectmagazine.co.uk/science/edward-wilson-social-conquest-earth-evolutionary-errors-origin-species/

What's so hard to understand? It's as if most of those commenting aren't even reading the article.

Fri, 25 May 2012 12:03:51 UTC | #943463