I'm just stopping by briefly. I don't have time to follow email much more
than once a week (probably less), so I'm not subscribed to reflector.
Browsing via Netscape I saw a question come up about the number of
differences between humans and apes. Steve Clark wondered if I might
have anything to add...
I think that Jim Behnke's and Paul Nelson's posts covered most of the
details about where the numbers originated and what they compare. It
was good to see people reading the late Alan Wilson's paper (with
Mary Claire-King... now of breast cancer research fame), on human/chimp
similarities.
I think it's pretty clear now that a lot of morphological change in
animals would be expected to be regulatory in nature. We know from
biochemistry that organisms share a high degree of common processes
and that these similarities increase as more closely related organisms
or compared. As one source mentioned by Paul says, the dramatic
genetic similarities between humans and apes suggests that the
differences in the basic, or core biologies/biochemistries are probably
trivial. In _most_ cases I'd bet that we could swap protein coding
sequences between chimps and humans with no observable differences
in overall function. This would likely occur because either the
enzymes do no differ at all in function or because they differ to an
extent that the robustness of feedback systems can easily compensate.
(Heck, you can sometimes pop human genes into yeast and get them
to work).
---There were a few other issues raised about whether even these changes would block primate -> hominid evolution. One issue was whether evolution could produce the "new designs" found in humans. I wonder, "What new designs?" I'm not terribly knowledgable in this field but I've never heard anything that claims there were "new designs" involved in that transition. From what little I've seen, I thought that these differences appear mostly as modification of existing (or shared) structures.
Also, there was some question about whether inversions or transpositions in the chromosomes might produce infertility and thus "prevent" evolution. I am aware that many diseases can be attributed to rearrangements. Still, I wonder if some sense we have about the relative proportion of negative effects is somewhat biased by sampling error (again, this is not my field). For example, we often only look for differences when we see a problem. Asymptomatic variation tends to receive less examination. I've just bounced this question off a biosystematics friend of mine and she can't think of many large, systematic surveys in humans to investigate it. She suggested Drosophila work where some workers have compared the genomes of the many fruit fly species, many of which exhibit numerous genetic rearrangements (I've got to comment that if one thinks that the Hawaiian fruit flies -and others- are reasonable examples of evolution, then I think that from the crude standpoint of comparative genetics, the descent of humans from the last common ancestor with chimps is significantly less of a set of steps).
I don't know how the possibilities of surviving the specific events that lead to humans could be determined today. However, I do know that infertility is _not_ an inevitable product of chromosomal rearrangements. For example, an inversion in part of a chromosome might not prevent the rest of the chromosome from alignment -- perhaps it would affect the rate of recombination locally. There was a brief thread awhile ago in sci.bio.evolution about how chromosomal fusions may arise -- such as the one proposed during hominid evolution. Perhaps one could look it up the new archives.
---Finally, Brian Harper makes a good point from Yockey's papers. Sequence comparisons are not the end-all of evolutionary phylogeny. Also Paul Nelson mentions, there are many things to consider that operate at higher levels than simple sequence ("Context" is a good buzz word in that field). Some things, such as the timing and propagation of regulatory signals and how they relate to overall morphology are probably decades from being understood. I know from work in my lab's group that all the sequence data that is coming out of genome sequencing projects is just the beginning of the research. For this to make "heavy sense" will require better understanding of cell physiology and etc.
Still, I think it would be a mistake to disregard the sequence comparisons simply because we don't know everything about cell biology. I think that in many cases, and with justifiable elimination of many known caveats, real progress is currently possible in evolutionary phylogeny. For example, even though the work of the time was cutting edge, Alan Wilson's work with the rate of sequence divergence correctly identified an important window of time in which the split between humans and chimps probably began. While this sort of work is neither perfect nor always better than other means of comparison, it has proven to be useful many times. It's certainly a useful tool.
Regards, Tim Ikeda (timi@mendel.berkeley.edu)