A test for claimed knowledge of how macroevolution occurs

Hi Faith.I'm still struggling to understand the disconnect here, and to get my head around what you think a genome is. You tell us to "give us a series of mutations that could change the chimp genome into the human genome"; but then say. "you can't just point out the differences".This is incoherent. Listing the differences between two genomes is listing the series of mutations that could change one into the other. Obviously we're not going to list them, because there are lots. The differences between the human and chimp genomes are thirty-five million single-nucleotide differences, five million insertions or deletions, one chromosomal fusion, and about 10 chromosomal inversions. So, the mutations needed to change one to the other would be those 35 million SNP mutation, those five million insertions or deletions, one chromosome fusion (or fission, depending on which direction we're going) and those 10 inversions.I know you don't believe that these mutations are the actual cause of the difference between the two, but that's not the point. Nor do we, since we don't think the human genome evolved from the chimp genome. You'd asked for a hypothetical list of mutations that could turn one to the other.How can we provide a hypothetical list of mutations to turn genome A into genome B if we're not allowed to list the mutations that would be necessary to turn genome A into genome B?

Several people have said this, but I think it's a bit of an exagerration. Animal breeders cannot cause mutations, of course; but there are several known examples of them taking advantage of naturally occurring mutations. The stumpy legs of sausage dogs, for example, or the hypertrophied muscles of Belgian Blue cattle, were naturally occurring mutations that breeders seized upon and preserved. I'm sure that many mutations have been involved in the creation of our domestic breeds - the examples mentioned are just particularly easy to find since they would be so obviously maladaptive in nature.And with modern knowledge of genetics, breeders don't necessarily wait for mutations, either. Plant breeders will expose plants to radiation or chemical mutagens to induce dramatically higher mutation rates. Obviously they can't target what mutations appear, so much of what's produced is worthless; but by inducing massively increased mutation rates agronomists can find in a few years useful mutants that might have taken millennia to crop up naturally (pun intended). There are thousands of commercially available strains of grains and tubers developed by this method.

Dogs have loads of mutations presumed to have arisen since domestication. The only one I can think of off the top of my head (other than the stumpy legs one) is the duplication of the amylase-producing gene. But dogs are a special case since they've been domesticated so much longer than anything else (and feral dogs don't revert to wild-type - dingoes are not wolves); so I'm not going to waste time looking up more examples in dogs.MC1R is a very famous gene, since it's effect on coloration makes its mutations obvious, and since variation in MC1R plays a role in some of the most immediately obvious variation amongst humans. For the same reasons of obvious phenotypic effect, MC1R has been extensively studied in other animals. Wild boar, for example, are monotypic for MC1R - all wild animals have the same allele. Domestic pigs, however, have at least four different MC1R alleles, which contribute to the huge variation in colour of domestic breeds. Now, it is of course possible that the ancestral wild population contained all these alleles, which have coincidentally been lost by drift in the reduced wild population. It seems much more likely to me, though, that these are all post-domestication mutations which have spread once pigs were removed from the selective constraints of camouflage. This sort of thing has presumably created the canvas from which breeders have selected in many domesticated species.A lot of the most obvious examples are about colour, but there are many other well-known examples. Check these chickens: The chap on the top right is monotypic for the wild-type allele. The other three show varied combinations of the rose-comb and pea-comb mutations. These mutations are not known in wild jungle fowl - they are unique to domestic chickens. And it's extraordinarily unlikely that these mutations exist in the wild. Breeders have tried repeatedly to establish pure rose-comb breeds (for aesthetic reasons) but keep failing; for the fairly simple reason that roosters homozygous for the rose-comb allele have sperm that can't swim straight.Texel sheep (a breed originating from an island off the north coast of the Netherlands) are renowned for their high meat content. The genetic basis of this has recently been pinpointed to a mutation in the GDF8 gene, which produces myostatin. They're not as impressive looking as Belgian blue cattle, but you can see they're kind of built Again, this is a mutation presumed to have arisen since domestication. Above are only a few examples, but I found dozens in a very quick Google search, and am pretty confident I can keep listing them for a while.To be clear, I don't think I'm proposing anything novel. I think it's pretty well established that domestic breeds incorporate a range of mutations either seized upon by breeders; or which have simply been allowed to spread by drift in the absence of the selective pressures present in the wild. Reversion to wild type often involves selection against these alleles that are beneficial or neutral in a stable, but detrimental in the wild. Or, you get something like pigeons, who even in their feral state maintain many of the phenotypes developed under domestication - just not the ones that are detrimental to survival without a human carer.Edited by caffeine, : No reason given.

I think you're very wrong. She doesn't get it. Sure, her opinion is coloured by her religious opinions; but if we approach every disagreement with Faith as if she understands all the words we're using in the same way as we do but pretending not to, we're never going to get anywhere. I do not get the impression she is intentionally misunderstanding. Rather, in constructing a model that conforms with her religious beliefs, she has come to conceive of certain biological concepts in different ways than we do.I don't think Faith is pretending to misunderstand us. I think instead that she's internalised definitions for concepts we think she understands that are different to the definitions we mean. I don't see the value in accusing her of lying. Better, like Taq is trying to do, to explain what we actually mean. And let's try to understand what Faith is trying to say - otherwise, what's the point of talking to each other?

But why would you ask for such a thing, given that we're talking about the differences between chimps and humans.Chimps and humans have exactly the same organs. All of them. We have exactly the same bones. All of them. They're all in the same place. And everything is made out of the same stuff.Not exactly the same, of course. As we discussed in a previous thread, there are slight differences between human and chimp keratins. But these differences are small and simple, and quite probably non-functional. I would be willing to bet that if you replaced the gene that produces human fingernail keratin with the gene that produces chimpanzee fingernail keratin, you would not notice - the fingernails would like the same.Few, if any, of the 40 million odd mutations separating us from chimps would have a large and noticeable effect. But 40 million is a huge number. All 40 million together have a very noticeable effect - it's the difference between a human and a chimp.But there are literally no major structural changes necessary to move between a chimp and a human. What differences do we have from chimps that are not simply changes in the colour, size and shape of existing structures?