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Author
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Topic: John A. Davison: An Evolutionary Manifesto: A New Hypothesis For Organic Change
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Pim van Meurs
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Member # 541
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posted 12. June 2003 22:36
Davison: I am not prepared to abandon that conclusion simply because my views are not popular or those of the contemporary majority.
Are you willing to abandon particular views when presented with evidence to the contrary? Such as your claims about speciation for instance?
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Art
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Member # 179
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posted 12. June 2003 22:53
Hi John,
If the moderator can tolerate a few quotes (sometimes it's hard for me to know who is responding to what in this thread):
quote:
As for improving the Manifesto it is a little late since most of what I have presented there has already been published.
But this document has been offered to ISCID for discussion, and in a forum that often leads to publication in the society journal. In this sense, it's most definitely not too late to revise the article, and to improve it greatly by bringing it up to date.
quote:
When you describe my references as "strawmen" you are taking exception not with me but with them.
With all due respect, John, I am inclined to ascribe the opinions in your manifesto to you, and not those you quote. I'm pretty sure that most of your sources would not deliberately ignore the vast majority of all life while making broad and sweeping claims about biology. I'm also sure they would not make such obviously incorrect characterizations as we have seen in this thread.
I still am interested in your opinion of Triticale. And speaking of sexual reproduction, I wonder if this sort of phenomenon might put the entire matter of the evolution of sex in a new light.
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Nel
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Member # 614
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posted 12. June 2003 23:03
Pim,
I'm sorry, your post is incomprehensible to me. What does this mean exactly:
quote:
Certainly the fact that Hox genes may be coding for very different parts does not disprove the fact that differences in Hox genes and genes in general can cause genetic change?
Rex's post proposed that the gene alone is what we can look that causes phenotypic change. And yet similar genetic programs cause different phenotypes, and different genetic programs cause similar phenotypes. I never said anything that Hox genes and gnees in general "cause genetic change", I don't even know what that means (are you talking about switches?).
In one sentence, my post was meant to indicate that neo-Darwinism has no theory of phenotypic origination.
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Pim van Meurs
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Member # 541
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posted 13. June 2003 00:20
Phenotypic not genetic Nelson... :-)
nelson: And yet similar genetic programs cause different phenotypes, and different genetic programs cause similar phenotypes.
and hiw does this address RBH's statement? And what examples did you have in mind? AFAIK the papers you quoted were not helpful. Surely that different genes can result in similar phenotypes does not address RBH's point nor does the fact that similar genes may code for different phenotypes either.
details please. Was something more than genes involved in causing the phenotype differences? Or was it an interaction between similar genes and different wiring? Surely delayed expression may have significant impact on the expression of lets say a limb but is the delay not encoded in the genes?
[ 13. June 2003, 00:24: Message edited by: Pim van Meurs ]
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nosivad
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Member # 767
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posted 13. June 2003 05:16
Art, my opinions are the opinions of those I quote which is why I have quoted them. The gradualist Darwinian model has proven to be a dismal failure. There is still no clear demonstration of natural selection producing new kinds of living creatures. The very notion of natural selection as a creative force is highly questionable. How can that which has been created, Nature, become the creator? More and more of what we learn about various gene families supports the view that all the genetic information for evolution, just as in ontogeny, has been present all along. There is nothing in molecular biology that is in conflict with my suggestions. I have simply offered an alternative to the gradualist, sexual Darwinian model. One might think I had committed a crime against humanity! I still maintain that a primary function for sex is to stabilize a successful evolutionary product and at the same time to allow a limited capacity for change. Major evolutionary changes could not conceivably have been produced through such a conservative device as sexual reproduction. If it could be done we would be doing it right now. If there ever was a time in the history of the earth when the environment was undergoing the most drastic changes it is now. Yet all we see is rampant extinction. I remain convinced that macroevolution is finished and obligatory sexual reproduction has brought it to an end.
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Rex Kerr
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posted 13. June 2003 06:30
Since there was something of substance to respond to, I will happily repsond.
While it is true that small inbreeding populations speed homozygosity (necessary for the selection of recessive traits), it is also true that there are very many of these small inbreeding populations. Look up the Drosophila papers on Evolution Canyon, for example. So I don't really see how Darwinism 'fails' here. If there were no small reproductively isolated populations, then there might be a problem (although dominant and semidominant mutations would still be selectable).
There's a difference between sexual reproduction being the means for macroevolution and sexual reproduction being compatible with macroevolution. The claim in the article was that sexual reproduction was not even compatible with macroevolution. I've provided references to speciation events, including those observed in the lab; maybe that doesn't count as "macroevolution" or "any significant evolutionary change". Perhaps before saying more, I should ask what does count.
I don't have any good explanations for the varied mechanisms of sex determination in various taxa. Sex determination is not all that well understood, though, so I'm hesitant to extrapolate from it too much. I'm happy to grant that a semimeiotic process could have been functioning historically at some point--although it's not clear to me that it was necessary. However, evolution in many recent lineages (e.g. all mammals) is not parsimoniously explained by semi-meiosis since these organisms appear to be obligate sexual reproducers, and since as mentioned above, evidence does not support the claim that sexual reproduction precludes macroevolution.
Finally, regardless of what Michael J.D. White thinks, there are a huge number of Drosophila strains with chromosomal rearrangements generated in the lab under sexual reproduction, all conveniently listed in FlyBase. I was only providing evidence that chromosomal rearrangements are compatible with sexual reproduction, which is exactly what this shows.
Unfortunately, I'm unable to figure out what Nelson's point to me was supposed to be. As near as I can tell, I made a claim of the form, "changing X can be sufficient to change Y", and he countered with an example of the form, "X1 and X2 both cause Y". But since this doesn't contradict my statement (I didn't claim "any change in X necessarily causes a change in Y"), I'm unclear on what the point was--especially since Nelson used the word "refutes". If he hadn't used that word, I'd have thought the first paper supported my claim. I'm not proposing a grand unified model of genotype-to-phenotype mapping; I'm simply noting that mutational changes in single genes can have profound phenotypic consequences, and thus there is little reason to assume that macroevolution must involve mechanisms beyond mutations in single genes. (It may and probably does involve additional mechanisms, given that chromosomal structure, chromatin condensation patterns, and so on, can change.)
[ 13. June 2003, 06:33: Message edited by: Rex Kerr ]
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nosivad
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Member # 767
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posted 13. June 2003 07:29
Rex, what Michael J.D. White thinks is very is mportant because it is based on reality. Of course one can generate paired rearrangements in the laboratory. I never claimed that they would necessarily cause speciation. I am willing to bet that most of them lead to reduced fitness. The Darwinian, gradualist, sexualist model for evolution simply has not resulted in speciation. Darwin's finches would seem to be all the same species. The bill modifications are phasic and reversible. No real evolutionary event has been reversed to my knowledge. Base pair substitutions (point mutations) are reversible and that fact alone indicates they have had a negligible role in evolution. Demonstrably beneficient mutations are so rare that one may reasonably conclude that the only truly beneficial mutations are the ones that return the mutant allele to the original wild type. I have said as much in the Manifesto because the evidence supports it.
Finally, let me say that it may be impossible to create new true species or higher categories. That was apparently Schindewolf's position. I sincerely hope that is not so. Of one thing I remain confident. It will never be achieved through sexual reproduction. I know this sounds terribly corny, but if Luther Burbank couldn't do it nobody can. The prospect of speciation never crossed his mind. So much for natural or unnatural selection! nosivad
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Rex Kerr
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Member # 632
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posted 13. June 2003 09:03
And one can isolate rearrangements from outside the laboratory, so one wonders why the need for an elaborate semi-meiotic hypothesis that in addition to its advantages has the dramatic disadvantage of being at odds with the mode of reproduction of organisms whose origin it is supposed to explain. You can get all the chromosomal rearrangement you need without semi-meiosis, albeit not as efficiently.
You continually repeat that no speciation has been observed. Numerous counterexamples have been offered--that is, examples of directly or indirectly observed recent speciation--and you've provided no explanation for them. Among those that have been mentioned are triticale, the greenish warbler (a ring species), cichlids of e.g. Lake Malawi, incipient speciation in Drosophila in "Evolution Canyon" in Israel, recent speciation of a variety of Drosophila species/subspecies in various places, and so on.
Claiming that speciation is not occuring seems tantamount to claiming that comets do not exist. Neither are something you see every day, but there are abundant records of both.
[ 13. June 2003, 09:04: Message edited by: Rex Kerr ]
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charlie d.
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Member # 159
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posted 13. June 2003 09:06
Nelson:
I think Pim was expressing skepticism that either of your references supported your statements:
"... the same genotype does not cause the same phenotypes..."
and
"In one case the genotype changes and morphology stays the same..."
You may want to elaborate how exactly those works support those claims and counter Rex's contention that
"developmental studies are consistent with changes in genes alone causing phenotypic change."
As for this other statememt of yours: quote:
Charlie, this paper is just an extension of an initial paper which demonstrates that there are 200 chromosomal regions that differ between the two fruit fly species to such an extent that they can cause death in hybrids. The Nature article you reference by Dembksi's good friend is simply the first of these regions in which they identified the gene Nup96. I guess that was pretty good timing.
I am not sure what you are trying to say, but my point was that reproductive isolation can be achieved on the basis of changes in a single gene, in this case Nup76, which was shown to be sufficient for hybrid sterility in melanogaster x simulans crosses. The fact there there are a total of 20 loci involved in hybrid inviability in these crosses is not very relevant, since each and every one is sufficient for isolation to occur (and that's how they were identified). I guess once a species becomes isolated, it diverges (I wonder why they'd do that! ![[Wink]](wink.gif) )
Anyway, I thought it was an interesting piece of empirical evidence regarding the actual mechanisms of speciation, alas in this thread textual exegesis seems to take preeminence over experimental observation.
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nosivad
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Member # 767
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posted 13. June 2003 11:37
Dear Rex. I require a physiological definition which means an identification of the source and the proof that the hybrid is sterile. The instances you cite do not meet that criterion. I would also demand that the so-called evolution was mediated through sexual reproduction. I find "incipient speciation" meaningless. Dobzhansky claimed as much but later recanted when he tried to evolve Drosophila through intensive artificial selection. A rare semi-meiotic event can theoretically be of great significance because the new form is by definition in a balanced chromosome configuration. Chromosome heterozygotes typically suffer from varying degrees of sterility. I also refer you to White's claims that the many rearrangements in Drosophila were not mediated through sexual reproduction. It was precisely those observations that led me to the semi-meiotic hypothesis. White was no "straw man" in my estimation. Neither were Grasse, Broom, Berg, Goldschmidt, Bateson, Punnett or Schindewolf, all of whom cast doubt on the gradualist Darwinian model as well as the role of natural selection as an instrument of evolutionary change. The simple truth is that no one has the foggiest notion of what has driven evolution. It remains a mystery except to the neoDarwinians.
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Nel
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Member # 614
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posted 13. June 2003 20:49
Charlie wrote:
quote:
I think Pim was expressing skepticism that either of your references supported your statements:
You mean by questioning why genes actually should cause genetic changes?
I already elaborated on how those references do not support Rex's gene-only statement. That development can be rewired without causing much phenotypic change was one example. I guess that scheme of yours works both ways.
Charlie writes:
quote:
I am not sure what you are trying to say, but my point was that reproductive isolation can be achieved on the basis of changes in a single gene, in this case Nup76,
No. The gene they've identified not only shows many genetic changes, but Nup96 causes death when its forced to interact with another (still unidentified) gene from the other species. So the amount of genes required for this type of isolation to occur is at least two. It is by far not the result of changes to a "single gene".
But the fact that this paper is just elaborating on the first of 200 chromosome regions that was discussed much earlier was what made your statement about timing kind of funny.
[ 13. June 2003, 21:14: Message edited by: Nelson_Alonso ]
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Rex Kerr
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Member # 632
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posted 14. June 2003 06:42
I'll get back to John Davidson's points when I have a chance to take a look at White's book.
But I may have figured out what Nelson was getting at. In response, I say:
The genotype-to-phenotype mapping is not 1-1. Multiple genotypes can give the same phenotype.
It does not follow that genotype does not affect phenotype.
For example, one of the first developmental regulatory pathways was worked out in C. elegans based on mutations in genes that affected the development of egg-laying structures. Changes in genes can and do cause changes in morphology.
(Analogy: multiple roads can lead from where you are to your destination; it does not follow that which roads you take does not affect where you end up.)
I do agree that Nup96 alone can't cause reproductive isolation; alone it causes death or nondeath, depending on context. It will be interesting to see what the difference in contexts is.
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nosivad
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Member # 767
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posted 14. June 2003 08:13
Dear Rex, when you are in the library be sure to check out Grasse's book. I particularly recommend chapter 5 - Evolution and Natural Selection. This chapter ends with the following:
"The genic differences noted between separate populations of the same species that are so often presented as proof of ongoing evolution are, above all, a case of the adjustment of a population to its habitat and of the effects of genetic drift. The fruitfly (Drosophila melanogaster), the favorite pet insect of the geneticists, whose geographical biotropical, urban and rural genotypes are now known inside out, seems not to have changed since the remotest times." nosivad is davison, not davidson, spelled in reverse.
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Itzpapalotl
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Member # 623
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posted 14. June 2003 08:30
Rex Kerr wrote:
quote:
I don't have any good explanations for the varied mechanisms of sex determination in various taxa. Sex determination is not all that well understood,
Although there is still much to learn about sex determination systems in the last few years there have been substantial progress. One of the key discoveries was that of the conserved role of DMRT1 in sex determination, homologs of this gene have been found to be part of the sex determination pathway in Drosophila C. elegans and vertebrates indicating that the sex determination pathway has been conserved in part throughout metazoan evolution.
Sex related genes have been found to evolve extremely rapidly in many different organisms, for example the sex determination pathway gene FEM-3 is the most diverged protein yet discovered in Caenorhabditis. After longer periods of time no homology might be recognisable even though two genes share a common origin.
It is also possible for several sex determination systems to coexist within a single species. An example of this is the housefly (Musca domestica) in which at least 8 different sex determination systems have been found in the wild and generated in the lab. The most common system is XY/XX but XX/XX also occurs and strains with male determining genes on all five autosomes have also been found. Different genes are not necessarily involved in the different systems for example the same gene traslocated from the Y to the X and various autosomes could account for all this variety.
It is also possible for the genes at the 'top' of the pathway to change but the basic developmental pathway and the other regulatory genes to remain. An example is found in flies, in Drosophila the pathway is sxl->tra->dsx->(developmental genes) but in Ceratitis capitata it is just tra->dsx->(developmental genes), sxl has taken over the master regulatory role of tra in Drosophila. The system could at first sight appear to be very different but is in fact substantially conserved.
Rapid evolution of sex determining genes combined with the possibility to change the appearance of the system without necessarily changing the genes and the possilbility of adding upstream regulators to the system would give rise to an extreme diversity of mechanisms that was consistant with the evolution of sexually reproducing species.
Raymond, C.S., Murphy, M.W., O¹Sullivan, M.G., Bardwell, V.J., and Zarkower, D. (2000). Dmrt1, a gene related to worm and fly sexual regulators, is required for mammalian testis differentiation. Genes Dev. 14:2587-2595.
Zarkower, D. (2001). Establishing sexual dimorphism: conservation amidst diversity? Nature Reviews Genetics 2:175-185.
A. DÜBENDORFER, M. HEDIGER, G. BURGHARDT and D. BOPP. Musca domestica, a window on the evolution of sex-determining mechanisms in insects. Int. J. Dev. Biol. 46: 75-79 (2002).
E. S. Haag, S. Wang, and Judith Kimble, Rapid Coevolution of the Nematode
Sex-Determining Genes fem-3 and tra-2. Current Biology, Vol. 12, 2035–2041, December 10, 2002.
P. Graham, J. K. M. Penn, and P. Schedl. Masters change, slaves remain. BioEssays 25:1–4 2002.
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nosivad
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posted 14. June 2003 20:32
Itzpapalotl (sounds Aztec like axolotl). I take it from your comments that you assume all of evolution took place through one form or other of sexual reproduction. That of course is exactly what I have questioned. It also seems to be tacitly assumed that protein divegence implies rapid evolution. I don't have that much confidence in the molecular clock or am I missing something? I fully expect there to be a great deal of gene homology in all organisms because I feel, like Berg and Grasse that much of evolution has resulted from the expression of preformed elements. The fact remains however that the cells destined to become the eggs and sperm in mammals and birds arise in totally different portions of the embryonic body and reach the gonad by drastically different means. The germ cells of anuran and urodele amphibians don't even come from the same germ layer, arising from the endoderm and mesoderm respectively. These fundamental differences do not indicate, to me at least, a sexually mediated evolutionary continuum.
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