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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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peter borger
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Member # 722
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posted 17. June 2003 23:50
Lonnig and Saedler indeed argue that in many cases phenotypic change could be a result of transposable-element induced rearrangements, and they provide a whole bunch of evidence for that.
So, it seems that shuffling of preexisting DNA equals what is coomonly regarded as evolution. However, it should than be noted that Darwin simply made an unwarranted extension from observation on non random DNA rearrangements. And this can be read in his book 'The Origin'.
In chapter V Darwin describes his ideas about the 'laws of variation', partly draining from what he knew about pigeon breeding and equine varieties:
"Distinct species present analogous variations; and a variety of one species often assumes some of the characters of an allied species, or reverts to some of the characters of an early progenitor. These propositions will be most readily understood by looking to our domestic races. The most distinct breeds of pigeons, in countries most widely apart, present sub-varieties with reversed feathers on the head and feathers on the feet, characters not possessed by the aboriginal rock-pigeon; these then are analogous variations in two or more distinct races." (The Origin, p195)
What Darwin observed here is that the same traits appear in distinct breeds of pigeons and these traits appear independent from each other. I wouldn't dare saying that both breeds arrived with the same characteristics through a random, chance-only driven mechanism. In fact, Darwin doesn't do that either. He is well aware of the profound lack of knowledge concerning laws of variation: "I HAVE hitherto sometimes spoken as if the variations so common and multiform in organic beings under domestication, and in a lesser degree in those in a state of nature had been due to chance. This, of course, is a wholly incorrect expression, but it serves to acknowledge plainly our ignorance of the cause of each particular variation. " (The Origin, p173).
Later the neo-Darwinian theoreticians chose randomness as the source of variation, since they were unable to find a mechanism to induce such variation. Therefore, the neo-Darwinian vision is not Darwinian, but a simplified (and atheistic) interpretation of his ideas.
Clearly, the mechanisms that lead to the characteristic of feathers on the feet and reversed feathered on the head are already present, pre-existing in the genome of the pigeon as DNA elements that affect gene programs in a non-random sense. In other words, Darwin's examples demonstrate the MPG in action. Through a pre-existing mechanism some pigeons get the same arrangement of DNA elements that induce the same characteristics independent from each other, and these traits are selected by the breeders. Darwin called this phenomenon of independent acquisition of the same traits 'analogous variation'. It is a common phenomenon well known to breeders. Darwin can easily find more examples of analogous variation:
"The frequent presence of fourteen or even sixteen tail-feathers in the pouter, may be considered as a variation representing the normal structure of another race, the fantail. I presume that no one will doubt that all such analogous variations are due to the several races of the pigeon having inherited from a common parent the same constitution and tendency to variation, when acted on by similar unknown influences. In the vegetable kingdom we have a case of analogous variation, in the enlarged stems, or roots as commonly called, of the Swedish turnip and Ruta baga, plants which several botanists rank as varieties produced by cultivation from a common parent: if this be not so, the case will then be one of analogous variation in two so-called distinct species; and to these a third may be added, namely, the common turnip. According to the ordinary view of each species having been independently created, we should have to attribute this similarity in the enlarged stems of these three plants, not to the vera causa of community of descent, and a consequent tendency to vary in a like manner, but to three separate yet closely related acts of creation." (The Origin, p195).
In conclusion, his ideas of evolution are based on non random rearrangements of DNA elements. Now we have finally an idea how genomes induce variation to rapidly adapt to different environments (through Non random mechanisms) is should be clear that Darwin made an unwarranted jump. The observations he describes do not justify the extrapolation from microbe to man, unless one assumes that all information has been present from the beginning.
I am not sure whether we can speak of evolution of genomes when all that happens is reshuffling of DNA elements. A shuffled genome simply has another meaning (phenotype). Like shuffled decks of cards could have a different meanings. Evolution from microbe to man requires novelties. And as I -and others- have shown it is highly doubtfull that they arise from random gene duplications and divergence. It is driven by as yet unknown mechanisms (maybe even external).
best wishes,
PB
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Rex Kerr
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posted 18. June 2003 00:38
Writing is merely shuffling of words. That doesn't make it any less interesting.
There is no evidence that the nonrandomness has any purpose associated with it. Lightning bolts do not strike at random; tall, conductive objects in areas of where thunderstorms are common are preferentially hit. However, that does not mean that lightning bolts strike with purpose.
Even if there weren't massive amounts of evidence from genetic screens that changes are not simply a result of shuffling, shuffling is neither trivial nor indicative of a non-Darwinian process.
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peter borger
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posted 18. June 2003 00:49
Writing may be shuffling of words but it requires intelligence to give it some meaning.
pb
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nosivad
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Member # 767
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posted 18. June 2003 07:42
Evolution was a reality. I don't care for the term reshuffling as it does not get to the heart of the matter. I believe there is evidence showing that whole blueprints were in existence specifying particular morphologies. One of the best examples is given by the marsupial and placental saber toothed cats. These occurred in the fossil record separated both spatially and temporally. The idea that they arrived at that state through some kind of gradual transformation is in my view absurd, especially since they all became extinct! Accordingly, the Darwinian idea of convergent evolution becomes a myth. Many other examples could and have been drawn (Berg 1969, Davison, "Ontogeny, Phylogeny and the Origin of Biological Information" and the Manifesto which is under discussion here). The evidence for preformed blueprints is there. Since evolution has been largely irreversible, the question becomes what happened to the blueprints once they were expressed. Maybe they became junk DNA!
nosivad
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charlie d.
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posted 18. June 2003 08:19
quote:
The portion of my quote that you posted has nothing to do with what you asked. That portion states that D. simulans Nup96 does not cause inviability when combined with genes from the D. simulans X chromosome. This is very different from what your Rb example showed.
Why? Only 90% of the individuals with heterozygous Rb mutation actually get retinoblastoma. Moreover, only very few of their millions of retinal cells bearing the same mutation actually transform into actual retinoblatomas. Furthermore, mice with the same mutation don't get retinoblastoma at all (though they get other kinds of cancer). What more evidence do you need that dominant hereditary retinoblastoma needs other factors (at least in part genetic) to express itself?
As for your quote, here it is in its entirety: quote:
D. simulans Nup96 + D. melanogaster X chromosome = hybrid inviability
D. simulans Nup96 + D. simulans X chromosome = diddly squat
It's not monogenic, plain and simple. Whereas, your Rb example is more like what would be described as monogenic. If you are unforutnate enough to inherit the mutated Rb, you'll get retinoblastoma as a consequence and it has absolutely nothing to do with simultaneously inheriting another variant at a second gene.
And again my objection stands: if you think that Nup96 is not sufficient to cause hybrid sterility because it doesn't cause sterility in non-hybrids, you have to conclude that Rb is not sufficient to cause retinoblastoma either. Your problem is, you are hung up on this "monogenic" term, and lose sight of the biology in the process. Retinoblastoma is a monogenic disease, though the Rb mutation is not sufficient to cause transformation, either at the organismal or cellular level. Things are just that way - biology doesn't always conform to neat mental schemes. quote:
I don't understand what you mean by "mystery of speciation", there may be, however, the main point is that this is certainly not the result of changes to a single gene. How exactly is this semantics?
If it's not semantics, it's arithmetics. As I said, whatever: even if reproductiuve isolation is the result of changes in two genes, or three, or five, that's certainly not the kind of overwhelming, ultra-complex, genomic-level, almost biologically incomprehensible (and irreproducible) process that Dr. Davison claims it to be. In fact, it can occur through well-known, simple genetic changes. How is that for a biological concept? Do you find it objectionable? quote:
As far as incomplete penetrance and Darwinian dogma go, the fact of the matter is that various phenotypes can arise from the same genotype. Population genetics assumes that the phenotype is determined from the genotype and enviornment. Now, it does matter, and matter very much, if examples such as different phenotypes arising from the same genotype or vice versa (and other examples) is not the result of genes only, as my quote from the Way of the Cell and my discussion of the various references showed. The problem is that we can no longer talk in terms of natural selection acting on changes to genes. If you notice, no genes found to date encode huge amounts of information for development. We see gene products in molecular machines, and other constructs, and we see them throw switches but thats about
That's a non-sequitur. Again, as far as a trait's variation is at least partially heritable, it's partially subject to evolutionary mechanisms. This affects evolutionary mechanisms quantitatively, but makes no theretical difference to them.
But maybe the better question is: how many biologically relevant traits (such as adaptations) that are entirely non-heritable can you think of, compared to similar traits that are at least partially, if not completely, heritable?
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gordon
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posted 18. June 2003 11:58
Dr.Davison,
You had written:
quote:
Gordon, I have no idea where you got the idea that Grasse was at odds with Goldschmidt. Here is what Grasse has to say on page 97 of his book :
"Gene variations are not the only ones which modify the cell structure. Mutations due to chromosomal rearrangements (translocations, inversions of segments, exchange of segments between chromosomes, breaking and reunion of chromosomes) are hereditary and play a part in the differentiation and separation of races, of subspecies, and even of species. They produce new genetic arrangements without alteration of the genes."
and later:
quote:
Gordon, in the Manifesto I clearly indicated that we know that many chromosome rerrangements have not resulted in speciation.
Here is where I got the idea that Grasse did not believe that chromosomal rearrangements resulted in speciation:
quote:
”A fact such as this [intraspecific chromosome aberrations] confirms that neither the number nor the arrangement of the chromosomes affects the characteristics determined by the genes, and only the presence of the latter has any importance (except in the handful of cases of position effect reported by geneticists)."
which is from p. 188 of the same book you cited. It would seem that Grasse believed that chromosome rearrangements caused speciation, except when they do not (for if chromosomal rearrangements did not affect the "characteristics" of an organism, it seems that, by definition, it would be the same species).
Which is what you have essentially stated here and in the manifesto.
As such, it appears that your hypothesis is rather Darwinian in nature – changes in chromosome number/arrangement have random effects, some of which initiate speciation, some of which do not. I fail to see, then, why you are so at odds with randomness – which you clearly endorse as an “alternative” to neoDarwinism.
Additionally, I am still bothered by your intimation that the speed of a (point) mutations’ occurrence dictates that they cannot be involved in “gradualism.” I do not believe you have addressed this. Since a translocation or similar chromosomal rearrangement would also be “instantaneous”, does that imply that this mode of evolution is also instantaneous? I presume you would agree with this, based on the title of your latest paper.
If this is so, how is it that this new species can actually be a species? Is a single “mutant” a new species, in your view? Would not this aberration have to leave offspring, that is, produce a population with similar genotypes, in order to be considered a species?
Thanks.
[ 18. June 2003, 12:03: Message edited by: gordon ]
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nosivad
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posted 18. June 2003 14:16
As I have indicated in a recent post, the question as to whether two forms are different species is functionally defined as follows. If their hybrid is sterile they are different species. This, by the way, is a definition proposed by a Darwinist, Theodosius Dobzhansky. I think it makes very good sense and am perfectly content with it. Even if there were no point genetic differences between the parents, extensive chromosomal structural differences will lead to sterility due to the problems of synaptic pairing during meiosis. It is unfortunate that we cannot have the karyotype of Neanderthal to compare with our own. nosivad
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nosivad
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posted 18. June 2003 14:25
Gordon, I am not at all certain that chromosomal restructurings are random events. In fact, I agree with Leo Berg that chance has little to do with either ontogeny or phylogeny. As you probably are aware, I even asked the question -Has evolution been guided? Of course that question is unanswerable at the present time. nosivad
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peter borger
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posted 18. June 2003 20:57
I agree with Davison that chromosomal restructurings are most likely non-random events. This becomes evident from acareful look at primate chromose 10(12). Both human and orangutan have the same topolgy but not human and chimp or gorilla and orang. And at least one break point is identical. Pure evidence for NRM.
PB
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Nel
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Member # 614
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posted 18. June 2003 23:51
charlie d. writes:
quote:
Only 90% of the individuals with heterozygous Rb mutation actually get retinoblastoma.
Yes, and the reason why shows how different the situation with hybrid sterility is and why hybrids sterility cannot be monogenic.
Two things have to happen for retinoblastoma to occur, loss of both maternal and paternal alleles of the Rb gene. The deal with heterozygous Rb mutation is genetic predisposition. In other words, every cell in the body is heterozygous at the Rb locus. The second is the change from RB+/rb- to rb-/rb- and is a mistake at mitosis most commonly from the total loss of the 13 chromosome carring the RB+ allele. That second event is thought to occur at a rate of about 1 in a million cells. That event will happen about 3 times in most eyes where all retinoblastoma precursors are RB+/rb- but about 10% of eyes will not have that event happen (and thus will not have a tumor develop) , and a similar small number of eyes will have 6-10 tumors, all of this by by chance alone. A second gene is not required.
Whereas with hybrid sterility in the context of the fly paper, a second gene is required.
If a second gene was necessary in your Rb example, it would not be monogenic and therefore your example would be irrelevant in the first place.
Charlie writes:
quote:
Moreover, only very few of their millions of retinal cells bearing the same mutation actually transform into actual retinoblatomas.
Yes, and the reason why shows how different the situation with hybrid sterility is and why hybrid sterility cannot be monogenic.
As I already discussed, the reason that only very few of their millions of retinal cells bearing the same mutation actually transform into actual retinoblastomas is because it is mostly influenced by the rate of loss of the second allele of Rb. In other words, those that inherited the mutant are born with one bad copy in all cells so they still need to lose the second copy since growth suppression is dominant on an individual cell basis. Nothing at all to do with interaction with a variant at a second gene.
charlie writes:
quote:
Furthermore, mice with the same mutation don't get retinoblastoma at all (though they get other kinds of cancer).
Mice have Rb related proteins that can substitute for Rb in the retina, thats why they don't get it.
Charlie writes:
quote:
And again my objection stands: if you think that Nup96 is not sufficient to cause hybrid sterility because it doesn't cause sterility in non-hybrids, you have to conclude that Rb is not sufficient to cause retinoblastoma either.
I submit that your objection has been fully rebutted. Nup96 is not sufficient to cause sterility because it must combine with a second gene. Rb, as I show above, does not require a second gene, and the factors you cite can be explained by without the requirement of having to combine with a second gene. And if it had to interact with another gene, it wouldn't be monogenic, it would be polygenic, and therefore your example is irrelevant anyway.
Note, you don't have to invoke the impreciseness of biological definitions to explain this. All you have to do is count the genes involved in the situation with retinoblastoma, even considering other factors and events, it only takes one gene. With hybrid sterility, it takes at least two to tango. It conforms with the mental scheme that 1 + 0 = 1 is monogenic and 1 + 1 = 2 is polygenic.
charlie writes:
quote:
As I said, whatever: even if reproductiuve isolation is the result of changes in two genes, or three, or five, that's certainly not the kind of overwhelming, ultra-complex, genomic-level, almost biologically incomprehensible (and irreproducible) process that Dr. Davison claims it to be.
Actually I think that your error was significant. Reductionists can't help but treat things like a black box, they see simplicity everywhere, and they have jumped the gun many times (most notably with the cell, they used to think it was like a bag of goo). You thought this was a simple change to a single gene, but further examination revealed a bit more complexity to it, and no doubt, going even further will reveal much more to the story. Thats a predictable trend in science, predictable especially from an ID standpoint, the more we look into things, the more complex it actually turns out to be.
For example, I don't really think that retinoblastoma is reducible to a single gene. AFAIK, no cancer is really reducible to a single gene. For example, the cell is actually pretty normal in Rb-null fibroblasts.
Or it may turn out that this is all there is to hybrid sterility. But so what? What are we really interested in? Origination of biological form, organic change, like we see in the Cambrian explosion, and that is what Davison's paper is about, and he can correct me if I'm wrong (although he does get into discussing humans). It's not really, in my opinion, whether two flies can get it on. Semi-meiotic theory seems to indicate that speciation is simply not a gradual process, it is a fast process, almost instantaneous.
Putting that theory aside,for now, my main purpose in this thread is to put the spotlight back on what matters, phenotypic origination. And hybrid sterility, as I have already stated, is very different from phenotypic traits. And it may be completely seperate from the reason why Davison and others are attempting to show why the Darwinian mechanism cannot account for organic change. So far, what I have seen, development is horribly complex . And various new hypothesis concerning phenotypic change involves processes that are just as horribly complex. Whats more, it has very little to do with small incremental changes to genes that are selected for. In fact,
quote:
Evolution is possible only because selection collaborates with that spatial order intrinsic to living systems; and this order may persist ("shine through") even in the face of contrary pressure from natural selection.
Way of the Cell
charlie writes:
quote:
That's a non-sequitur. Again, as far as a trait's variation is at least partially heritable, it's partially subject to evolutionary mechanisms. This affects evolutionary mechanisms quantitatively, but makes no theretical difference to them.
I'm not talking about whether traits are heritable, I'm asking where that inherited variation came from. Neo-Darwinists claim it came from changes to genes that are selected for. But none of this leads to new organs, heads, eyes, tissues, etc.
[ 20. June 2003, 20:59: Message edited by: Nelson_Alonso ]
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Pim van Meurs
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posted 18. June 2003 23:55
Dear Peter,
I am still mystified why you continue to make your claims about NRM's and human and orangutan genomes. We have gone through this before and have established that mutations indeed are non-random with respect to location, time etc but that mutations as far as we know are random wrt fitness.
Furthermore I was hoping that you would be presenting an example of NRM's in humans and orangutans to support the various claims you have made about NRM's. For instance the suggestion that NRM's would create a false common descent pattern.
Btw if these mutations were non random how come that humans and orangutans have them but not chimps and gorilla's? So far I have seen some vague references to terms like non-random without much of an effort to define the term randomness. So far NRM seems to be describing Neo-Darwinism quite well.
To come back to your support of Davison, could you help me understand how you use the term non-random here? Purposeful changes?
It's easy to get confused by the use of definitions of randomness or non-randomness which are highly equivocal.
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peter borger
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posted 19. June 2003 01:12
dear Pim,
I recommend you to read Annual reviews of genetics 2002 from cover to cover. You will find out about: 1) Phenotypes are determined by DNA element topology, 2) the specificity of spontaneous mutations (NRM), and 3) a new and better evolutionary hypothesis than the current one.
Furthermore, I have already adressed your comments: NRM is with respect to positions (see above refered journal for mechanisms). Commonly with respect to nucleotides, and sometimes (as we know of now) with respect to impoved fitness
as a response to the environment (the constantly ignored conesnail toxins, parasite-host interaction, immunogenes, etc (read: Caporale's book for a nice overview).
The discussion on chromosome 10(12) can be found on the EvC forum. The reference that shows the data: Nickerson & Nelson. Genomics 1998, 50:368-372.
The authors say: "First, the cytogenetic bands associated with evolutionary pericentromeric inversion breakpoints are overrepresented among chromosome rearrangement in humans, suggesting that these sites are hot spots for chromsome breakage."
In other words NRM. The mechanism? Read above mentioned new hypothesis and pay attention to what Davison says.
Added by edit:
In addition it should be clear that each individual cytogenetic rearrangent is frequently associated with cancer and thus would have been selected against.As a whole the cytogenetic rearrangements in human are stable and thus it is likely that they have to be rearrangent in one single event. It neatly explains the gaps in the fossil record.
Best wishes,
Peter
Best wishes,
Peter
[ 19. June 2003, 01:56: Message edited by: peter borger ]
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charlie d.
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posted 19. June 2003 08:33
quote:
Nelson:
- [In Retinoblastoma] A second gene is not required.
- If a second gene was necessary in your Rb example, it would not be monogenic...
- [Retinoblatoma development has] Absolutely nothing to do with interaction with a variant at a second gene.
- For example, I don't really think that retinoblastoma is reducible to a single gene. AFAIK, no cancer is really reducible to a single gene. For example, the cell is actually pretty normal in Rb-null fibroblasts.
So, is it or isn't it? You seem to be a little confused. Does a monogenic hereditary cancer syndrome like retinoblastoma need other gene mutations, beside Rb, or not?
In fact, retinoblatoma is a monogenic trait, which however, like many other incompletely penetrant monogenic traits, requires other (genetic, environmental, stochastic) factors to be expressed.
But again, this is increasingly irrelevant. I think as far as hybrid sterility goes, your expectation that hybrid sterility be expressed in non-hybrids in order for Nup96 to be called sufficient is rather silly, but I am tired of beating that dead horse. I am however glad that you concede that speciation may indeed turn out to be a simple process, at least in some instances. That's exactly my point. As for your other claim: quote:
Putting that theory aside,for now, my main purpose in this thread is to put the spotlight back on what matters, phenotypic origination. And hybrid sterility, as I have already stated, is very different from phenotypic traits. And it may be completely seperate from the reason why Davison and others are attempting to show why the Darwinian mechanism cannot account for organic change. So far, what I have seen, development is horribly complex. And various new hypothesis concerning phenotypic change involves processes that are just as horribly complex.
I can assure you that some people have fun figuring out "horribly complex" things, and don't give up just as easily. Others, on the other hand, just like to whine about how difficult it all seems. That's why some become scientists and others don't.
Finally: quote:
I'm not talking about whether traits are heritable, I'm asking where that inherited variation came from. Neo-Darwinists claim it came from changes to genes that are selected for. But none of this leads to new organs, heads, eyes, tissues, etc.
It doesn't really matter to darwinian theory whether the changes are in the genes or somewhere else (remember, Darwin didn't even know what genes were). As long as heritable changes are present, they are subject to evolutionary mechanisms. We just happen to know now, thanks to the progress of genetics and molecular biology in the past half century, that most heritable information resides in genes.
But again, where do you think heritable traits come from, if not genes? How does it work according to you? Or is is just too "horribly complex" to figure out?
[ 19. June 2003, 08:35: Message edited by: charlie d. ]
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nosivad
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posted 19. June 2003 11:40
Charlie d, you seem to be confident that evolution is in progress now. Robert Broom and Julian Huxley and John A. Davison feel that it is not. Primarily what we see today is the substitution of alleles. The vast majority of such substitutions would seem to be either deleterious or neutral. Furthermore. unlike evolution, gene mutations are reversible. For that reason and others I have suggested that point genetic changes have had little or nothing to do with evolution. By way of contrast chromosome restructurings require two breaks. The probability of such an alteration being reversed is very small. nosivad
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gordon
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posted 19. June 2003 12:36
Dr.Davison,
I did not write that chromosomal rearrangements are random, I wrote that, according to you and one of your sources, the effect of such rearrangements are random. And with this I agree, as it is in evidence in the literature.
As such, again, there seems to be no quarrel with standard 'Darwinism' as far as chromosomal changes go - some cause speciation, some do not.
Random effect.
I find it troubling that you will not address your implication about the timing of mutation events as they regard speciation and my queries regarding what a species is.
If you have no intention of 'brainstorming' this issue, say so and I will draw my own conclusions.
Mr.Borger,
Please read my reply to Dr.Davison. Whether or not chromosomal rearrangements or insertion/deletion events are mediated by enzymes and occur at certain loci is irrelevant as to whether or not the events cause/influence speciation. It is obsevred that not all such events correlate to speciation events, so it should be obvious that, as far as speciation goes, the effects of such phenomena are random.
I fail to see how any of that has anything to do with your vision of a multi-purpose genome.
[ 19. June 2003, 12:39: Message edited by: gordon ]
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