To: All Msg #86, Jul2493 12:52PM Subject: punk eek as artifact and my own macro theory The

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From: Chris Colby To: All Msg #86, Jul-24-93 12:52PM Subject: punk eek as artifact and my own macro theory Organization: animal -- coelomate -- deuterostome From: (Chris Colby) Message-ID: <22s7e2$> Newsgroups: There's been a little talk about punk eek recently on t.o. Since I hadn't read anything about it for a couple of years, I drug out my 'tempo and mode' folder and browsed through it. I came across one argument against punk eek that I had forgot all about. I also have come up with my own theory of macroevolution. Species in the fossil record are identified by some diagnostic characteristic. In order to be useful, this trait should be discontinuous with other morphological traits in related species. So when Gould and Eldredge state that a lot of morphological change goes on at speciation and most species level change happens rapidly, this may be because species are _defined_ in the fossil record as organisms with a distinct trait (or traits). Let me give an example to illustrate. Imagine an praying mantis lineage. We'll follow two traits through time in this (imaginary) example -- arm length and number of "spikes" (or whatever those things on a mantises arms are called). Let's say that over time, arm length increases gradually in several closely related species. As time goes on, the arm could get long enough that there is room for one or more spikes to be placed on it. Now, a paleonologist studying this group of insects doesn't know when speciation occurred in any of the species; but, following conventions would call insects with different numbers of spikes each a new species. He would focus on the discontinuous trait for ease of classification and ignore the continuously varying trait. Then, when he was gathering evidence for punk eek, he would look at the "species" and say -- yep, these characters (spike number) stayed the same throughout the life of this species, then changed abruptly at speciation. I've used a discrete trait here (can't have half spikes), but this needn't be the case. Imagine that (as before) arm length was gradually increasing, but body weight stayed the same for long periods then shot up, then stayed the same for awhile and so on. The insects would then be divided up into "species" based on size (which is discontinuous in rate of evolution). But, there is no way of knowing if the increase in body size was accompanied by a speciation event or not -- that is assumed. Any paleo types out there want to comment on this? Nedin? Here's the reference: See Levington and Simon, 1980, A critique of the punctuated equilibria model and implications for the detection of speciation in the fossil record, Syst. Zoo. 29 (2): 130-142 ----------------------------------------------------------------- And now (trumpets blare) MY OWN THEORY OF MACROEVOLUTION!!!! I will show that my theory is just as consistent with current biology as any rival theory, but has one important benefit; since I'm "publishing" on USENET and not a real scientific journal, I can easily disavow any responsibility for it by saying it was just idle speculation 8-) Many populations exist as a single gene pool over a large geographical range. But, subdivision occurs due to uneven distribution of habitats. Small subpopulations can (and do) adapt to their local surroundings, but gene flow reintroduces alleles lost to drift or selection. Constant gene flow (even at low levels) means alleles from all subpopulations can migrate to all other subpopulations. Alleles that confer a benefit in some areas may be slightly deleterious in others, so continual gene flow acts similar to mutation in depressing mean fitness. Recessive alleles that are not expressed in the individual that migrates (and his/her children if the allele is absent in the new subpopulation migrated to) could especially contribute to this fitness depression. Now, if a subpopulation suddenly acquired reproductive isolation, mean fitness would quickly rise as the population flushed out the alleles that were adaptive in other subpopulations, but present only due to gene flow in the now isolated population. How could a population suddenly become reproductively isolated? Recently, some biologists have shown that many "good" species in the wild can breed with a closely related species if one of the two are fed antibiotics. These species (most of the current examples are in insects) harbor cytoplasmic bacteria that destroys the chromosomes of non-infected sibling species. When the bacteria is killed, the barrier to reproduction is gone. It has been shown (in _D simulans_) that a cytoplasmic incompatibility (CI) factor can quickly spread through a population. The quick release from the fitness depression (due to gene flow) could also trigger more evolution. The population would be resistant to invading alleles because invading individuals would not carry the cytoplasmic factor and their matings would not produce offspring. But, any signal for individuals to pick local (infected) individuals over migrants would be favored as it would prevent the carrier from wasting energy on matings (with uninfected "outsiders") that would not produce offspring. The signal must be present in a much greater frequency in the isolated population than in neighboring subpopulations. The signal could initially be present only in low frequency in the isolated population if absent altogether in neighboring populations. If at low frequency initially, this signal will increase in frequency because individuals mating with others assured to be members of the isolated population will have a higher reproductive success than those who mate with non-signal carriers and run the risk of mating with an outsider. Thus the initial invasion of the CI factor causes at least one burst of evolution, the flushing of "outsider" alleles and possibly a second burst to evolve a mate recognition system beneficial to individuals in the population. If the signal is morphological (it wouldn't have to be), this theory would also predict more morphological change around the speciation event (although for different reasons than punk eek). My theory doesn't require the subpopulation to be either small or peripheral, just isolated enough so that the CI factor could quickly invade and confer reproductive isolation. (I've actually glossed over some details about how CI factors work, but I can elaborate on how it is possible if asked.) The release from deleterious gene flow and subsequent mating system evolution are separable -- both need not occur. The big initial population might not have local adaptations so the first part wouldn't occur. Of course, the success of my model won't depend on how well it meshes with the data. Really successful theories need splashy titles, like punctuated equilibria. Has a nice ring to it (and can be nicely shortened into cool slang -- "punk eek".) Therefore I've decided to call my theory "prophylactic flush". The CI factor shields the isolated population from "infecting" alleles and releases it to a "flushing" of deleterious alleles. Comments? Chris Colby email:


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