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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 21. June 2003 21:04
Nelson still seems to be confused, not only do the authors of the paper contradict his claims but now he suggests that because there is an interaction between genes that it required two genes. All it required though was a change in one gene to become incompatible.
Simple as that.
I cannot understand why this is not obvious to Nelson?
Nelson the claims in his usual ad hominem fashion that
quote:
As far as Nup96, it's not sufficient to cause hybrid sterility and none of your quotes support that contention, which is why you didn't bother discussing them.
They speak for themselves which is perhaps why you did not really bother to discuss them?
That there may be more genes that can cause hybrid inviability is irrelevant for the discussion btw.
quote:
Complementation tests show that hybrid lethality is caused by the D. simulans (Ds) Nup96 protein and suggest (but do not prove) that hybrid lethality involves its amino terminus.
...
Our molecular and population genetic analyses ofNup96 allow us to address a number of issues in speciation genetics1,2. First, a single gene can explain the hybrid lethality of a small chromosomal region identified in our deficiency screen.
As far as your other 'claims' from nematoda to E. Coli, I fail to see how they are relevant and you have made not case as to their relevance as far as I am concerned.
When I point out that Nelson's tiresome accusations should perhaps be toned down he responds
quote:
That was not an accusation, that was an observation.
And yet history has shown us that your observation may be lacking in supporting evidence.
Rex has done also a great job addressing Nelson's puzzling claims.
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charlie d.
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Member # 159
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posted 21. June 2003 21:13
quote:
See, this is what I mean. What exactly is wrong with the term Rb-null fibroblasts? It's actually used quite commonly in the literature even in conjuction with retinoblastoma,
LOL. That's precisely what I mean, you use murky language and erroneous concepts, and then rather than admitting the problem, you change the subject. Here, you first said: "cell types that have Rb-null fibroblasts do not form tumors" which is biological nonsense: cell types don't have fibroblast, Rb-null or any other kind. Fibroblasts are a cell type.
But instead of saying "OOPS, sorry, I mistyped" , or "I didn't express myself properly", you go on some unrelated tangent: the fact that "fibroblast" and "retinoblastoma" appear often in the same sentence, which has nothing to do with your original mistake. And again, in doing this you dig yourself a deeper hole, mixing up levels of analysis again: what those quotes discuss about fibroblast is not retinoblastoma the trait (a tumor of retinal progenitors, which is what we were talking about), but retinoblastoma the protein (i.e. the product of retinoblastoma the gene), which is ubiquitous and also expressed in fibroblasts. Retinoblastoma-the-trait manifests itself in a monogenic dominant fashion in the retinal cells of carrier children. Thus, it is entirely irrelevant that to the sufficiency of retinoblastoma-the-gene mutations to determine retinoblastoma-the-trait whether or not retinoblastoma-the-protein-null fibroblasts display any phenotype at all, because that's not where the trait is expressed. Similarly, Nup96 is sufficient to cause sterility in hybrids, and it is entirely irrelevant whether it can or cannot cause sterility in non-hybrids, because that's not where the trait (hybrid sterility) is expressed.
But, again, whatever. You seem like you think you can interpret Orr's data better than he does, plus teach him and all of us some genetics, and new definition of the term "sufficient", which Orr himself uses in his own paper to describe how Nup96 determines hybrid sterility. I leave it to others to judge how preposterous that sounds.
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Nel
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Member # 614
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posted 21. June 2003 22:53
Rex, Charlie, and Pim,
The problem is that I don't regard hybrid sterility as a phenotypic trait. I think that those are two completely different things. Going back to my example, basically what you are saying is that mutation C that changes bbcc to bbCC alone is sufficient to cause hybrid sterility. But if specific incompatible interaction with a second specific gene is not needed, then that particular mutation wouldn't spread, because it would be incompatible with any gene. As I already stated, the Drosophila simulans copy of Nup96 only causes inviability when combined with genes from the Drosophila melanogaster X chromosome; it does not cause inviability when combined with genes from the Drosophila simulans X chromosome. So Nup96 alone is insufficient no matter which way you look at it.
If the sentence "cell-types with Rb-null fibroblasts" was unclear as written I can make it clearer, it does not detract from my main point. Retinoblastoma is derived from retinoblasts. Sarcoma is derived from fibroblasts. And RB is expressed in both. Rb null fibroblasts and Rb null retinoblasts suggest that inactivation of RB is not sufficient for tumorigenesis since the cell stays normal.
With respect to nematoda and E.Coli, I was referring to my specific examples,
Spudich, JL and Koshland, DE,
Jr (1976) Non-genetic individuality: chance in the single cell Nature.
Where related clones of E. Coli exhibited vastly different phenotypes.
With respect to nematoda I was referring to this:
quote:
We find a specific range of evolutionary variations at distinct developmental steps. (1) Unlike Caenorhabditis elegans and relatives, the vulva is formed from the four precursor cells P(5-8).p or, exceptionally, from P(6,7).p only. (2) The vulval competence group is restricted to these four cells or is larger. (3) The fates of more anterior and posterior Pn.p cells vary between closely related species (mostly cell death versus epidermal fate). (4) The mechanism of vulval cell fate patterning varies within a single genus, even between strains of the same species. (5) We describe the first example of a vulval cell lineage that is asymmetric between the anterior and the posterior sides of the vulva.
I can give much more examples. Changes to genes alone are not sufficient to cause phenotypic change. This is why I quoted Frank Harold, and he gives more examples:
quote:
Genes and gene products do, of course, retain a role in the evolutionary drama. Catalysts and structural molecules determine the numerical parameters that enter into the physical specification of each system, and they stabilize its organization. Much of that exploration of the range of possible forms is, in fact, carried out by mutation and recombination of genes. But it is system dynamics, not the genetic program, that gives rise to biological forms and function...selection has been ejected from its throne as the dominant creator of biological form.
In subsequent replies I will continue to give different examples, I don't have much more time tonight, but most likely Monday. I'm also considering starting a new thread on this. But the basic argument here is that genes alone are not sufficient, and as I said, the fact that we havn't found any genes that encode large amount of developmental information alone tells us that the gene is only part of the story.
[ 22. June 2003, 00:15: Message edited by: Nelson_Alonso ]
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Nel
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posted 22. June 2003 00:04
Pim,
What that quote is saying is simply that a single chromosome region out of the 200 that they estimitate is sufficient for hybrid sterility or inviability. But they write:
quote:
The D. simulans Nup96 protein is no longer compatible with an (unknown) interacting factor(s) encoded by the D. melanogaster X chromosome
Sometimes quotes don't speak for themselves, when you quote something, it's good to discuss the quote, because, to be quite frank, some of your quotes seem entirely irrelevant in general.
[ 22. June 2003, 00:04: Message edited by: Nelson_Alonso ]
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Rex Kerr
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Member # 632
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posted 22. June 2003 06:21
Nelson, I'm afraid the authors of the paper consider hybrid sterility a trait. Therefore, you'd best modify your language to make clear the distinction between what the paper shows and what you are claiming.
I do not believe that there were any statements that the Nup96 experiments showed that mutations in a single gene could lead to speciation. If you are arguing that their data doesn't show this, then I agree. They agree, as far as I can tell. Pim and charlie might agree (I certainly hope they do).
There is no point in attacking a straw man (once it is recognized as such), and even less point in defending it.
I can't really address E. coli references from 1976, but I don't see how the determination of vulval cell fate in C. elegans and other nematodes supports your claim in any substantive way. let-60, lin-15, and a bunch of other genes are required for cell fate determination; the pathway is fairly well understood. Loss of function and gain of function genes at the same step in the pathway have opposite phenotypes (e.g. underdifferentiation vs. overdifferentiation). In fact, this is part of the work that won Brenner, Sulston, and Horvitz the Nobel Prize. C. elegans vulval development is one of the best genetically explored developmental systems out there. To say that genes are "unimportant" in the face of an established pathway with literally dozens of known genes is just short of preposterous. And the passage you cite has essentially no bearing on whether genes are important or not.
I think there is a funtamental error in logic here, although I'm not sure what it is. Nelson says "changes in genes alone are not enough to cause phenotypic change". But as I describe above, changes in genes alone are enough. And his example of nematodes doesn't talk about genes at all--it just talks about different fates of vulval precursor cells. There is no information whatsoever as to whether genes are involved or not.
I agree, however, that this topic is probably best reserved for another thread.
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nosivad
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Member # 767
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posted 22. June 2003 07:44
I agree with Nelson that hybrid sterility is not a phenotypic trait. It has nothing to do with appearance since it actually prevents that appearance. I disagree with Nelson when he says: "Changes in genes alone are not sufficient to cause phenotypic change." Heidi, my Dachshund, has short legs because of a single dominant gene that causes the premature cessation of the growth of the long bones. That same gene produces the achondroplastic human dwarf. In both cases the hind limbs are straight and the forelimbs are somewhat twisted, probably for the same developmental reasons. Phenomen, from the Greek, meaning that which is seen. nosivad
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nosivad
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Member # 767
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posted 22. June 2003 08:09
While looking up the meaning of phenotype I came across the following derivation of the word evolution. It comes from the Latin evolutionis meaning an unrolling or opening of a book. Needless to say, a book has been written. That is what I have been trying to say, but no one seems to be listening! nosivad
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charlie d.
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Member # 159
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posted 22. June 2003 09:33
I of course agree that - evolutionarily - reproductive isolation between melanogaster and simulans involved the evolution of incompatibility between Nup96 alleles and other genetic factors. However, because all those factors are by definition represented in hybrids, Nup 96 is sufficient to cause hybrid sterility in melanogaster x simulans hybrids. Indeed, all 20 of the loci identified by Orr and colleagues are individually sufficient to cause hybrid sterility. If they weren't, they wouldn't have been identified by their screening system. Simple as that.
If one looks at the big picture, this suggests that simple, straightforward changes at the level of individual genes, like those that we observe daily in any genetics and molecular biology lab, are able to cause reproductive isolation and speciation. No need for major karyotypic changes, invisible hands, unfolding books, and so on. This does not mean that genomic rearrangements are not involved in speciation - there sure is plenty of evidence that they were in many cases. However, as usual, evolution has no preferred paths or favored mechanisms.
As for the definition of phenotype, any aspect of an organism that is detectable is a phenotype. Hybrid sterility is no less a phenotype than blue eyes or my cat's calico fur. Heck, death is a phenotype.
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nosivad
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posted 22. June 2003 10:08
charlie d. You define phenotype your way. I'll define phenotype as the word roots mean. I also don't see anything magical about the interpretation that the information for evolution was preformed. You are simply rejecting ideas because you don't like them. Physicists have made great progress because they accept what seem to be crazy ideas. There is a story about Niels Bohr and Wolfgang Pauli that goes this way. Pauli had just presented a paper and Bohr commented as follows: Dr Pauli, your ideas are very interesting but they aren't crazy enough to be right. Darwinian gradualism is altogether too reasonable to be even remotely correct. nosivad
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charlie d.
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Member # 159
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posted 22. June 2003 12:15
Dr. Davison:
that's not my definition of phenotype. That's any genetics or biology textbook's definition. That's the definition that anyone in the profession uses(you should know). As for the root, you are right that it's from the greek "to show" or "to manifest"; thus, any observable trait of an organism is part of its phenotype, including the objectively observable trait of sterility.
Regarding modern evolutionary theory being "too reasonable", you seem to be in disagreement with most ID advocates, who claim instead that darwinian mechanisms are patently unable to generate the diversity we see in life, while the evidence of design is manifest and obvious. Go figure.
As for crazy ideas, some indeed turn out to be right. The vast majority, unfortunately, are just plain loony.
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Pim van Meurs
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Member # 541
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posted 22. June 2003 12:21
Nelson: Sometimes quotes don't speak for themselves, when you quote something, it's good to discuss the quote, because, to be quite frank, some of your quotes seem entirely irrelevant in general.
Perhaps because I assumed that the recipient would comprehend its relevance.
Speaking of irrelevant quotes, have you spent some time expanding on your quotes of nematodes et al?
As far as NUP96 is concerned, your comments and claims seem to be quite at odds with the original paper as well as common biological knowledge.
NUP96 alone is sufficient to cause hybrid inviability.
Simple.
Davison: Darwinian gradualism is altogether too reasonable to be even remotely correct.
And yet it seems to be. Remarkable.
As far as 'crazy ideas and progress, may I remind you that cold fusion seems to be a good counterexample. :-)
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nosivad
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posted 22. June 2003 15:03
charlie d, I regard Intelligent Design as obvious in both the animate and inanimate world. I am certainly not at odds with the ID camp. If you think I am it can only mean that you have not read my papers. What I cannot understand is how anyone can adhere to a model for which there is not a shred of experimental, paleontological or cytological evidence. The neoDarwinians are chasing a phantom. nosivad
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Nel
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posted 22. June 2003 15:42
Rex,
First of all, the paper doesn't "show" that hybrid sterility is a trait. I also disagree that the authors of the paper consider hybrid sterility or inviability a trait but thats really irrelevant, I never claimed that the authors think a trait and hybrid inviability/sterility were either the same or different, so there is no reason to modify anything. Because if they did think it was the same then I would disagree with them, what matters is our interpretation of the data , there is no reason to make an argument from authority. The data is right here in front of us, and when an attempt was made to treat hybrid sterility as a monogenic trait, the definition of "monogenic trait" imploded. It's not a trait at all. It's two genes that are incompatible. Thats the best way to describe that paper. However, the question of whether hybrid inviability is a trait is one of semantics. I don't really care if two individuals from two seperate species can't form a viable hybrid. I'm interested in phenotypic origination.
Secondly, you really ought to keep track of the context of conversations if you are going to comment on them. The reason why this whole thing got started was precisely because the claim was made that "Nup96 experiments showed that mutations in a single gene could lead to speciation."
In a post dated 13. June 2003 09:06. charlie d. wrote:
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
What are you talking about when you bring up the "straw man" fallacy? ![[Confused]](confused.gif) There is no straw man.
Of course thats false. As you now realize, changes to a single gene being sufficient for hybrid sterility or inviability would result in the mutation being weeded out and wouldn't cause anything, much less reproductive isolation(because it would be incompatible with any gene).
I'll let this go now, since we all seem to be on the same page (except for Pim) regarding Nup96, I'm satisfied. I'll move on.
With respect to E. Coli and vulval cell fate, the C. elegans paper and the 1976 paper I referenced supports my claim substantively (the date is irrelevant, the experiment is still valid). You say that phenotype are the result of genes alone, and and yet with this paper Dev. Biol., 221, 68-86. we see that the genotype changes and morphology stays the same, "We find a specific range of evolutionary variations at distinct developmental steps."
It doesn't seem like you even looked at the paper. It's irrelevant whether the paper talks about whether genes are involved or not, because my argument is not that genes aren't involved, the paper shows different developmental steps forming the same phenotype which suggests genes aren't the whole story.
In fact, vulval development in nematoda is just about the worst example you could possibility use to make the case that changes to genes alone are sufficient to cause phenotypic change. It is so different even within the same species and yet the phenotype remains constant.
Furthermore, I agree that to say that genes are "unimportant" is just short of preposterous. But that wasn't my claim, that statement exists only in your imagination. Be careful in the future with your use of quotation marks. I'm not saying that genes are unimportant, just that they are only part of the story. This is a good topic for a new thread though and I am satisified with letting this one go as well.
[ 22. June 2003, 17:44: Message edited by: Nelson_Alonso ]
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charlie d.
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posted 22. June 2003 20:38
Nelson:
You are right that quote of mine was improperly phrased. However, the entire sentence said: 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, which was shown to be sufficient for hybrid sterility in melanogaster x simulans crosses.
and it was in response of this erroneous claim 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.
So, what I was pointing out to you that the "200 chromosomal regions that differ between the two fruit fly species to such an extent that they can cause death in hybrids" were entirely the product of your imagination, and that Nup76 was in fact sufficient for hybrid sterility. Altogether, I thought it was quite clear that I was referring to hybrid sterility between current species, and not the evolutionary history of reproductive isolation. Nevertheless, saying "reproductive isolation was achieved" gives the erroneous impression of an evolutionary process, while I was referring to the gene transfer experiments in the paper.
Oh, and the definition of "monogenic"
has not "imploded", rather by using it incorrectly it has exploded in your hands, leading you to absurdly deny the monogenicity of a classic monogenic trait, familial dominant retinoblastoma, as well as of any other monogenic trait with incomplete penetrance or variable expressivityn (which are almost the rule, rather than the exception, for monogenic traits). Similarly, you are still incorrectly using the terms trait and phenotype, but you seem blissfully unaware of it.
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charlie d.
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posted 22. June 2003 20:44
quote:
charlie d, I regard Intelligent Design as obvious in both the animate and inanimate world. I am certainly not at odds with the ID camp. If you think I am it can only mean that you have not read my papers. What I cannot understand is how anyone can adhere to a model for which there is not a shred of experimental, paleontological or cytological evidence. The neoDarwinians are chasing a phantom. nosivad
Well, just a post ago you said instead that darwinian evolution was obvious ("too reasonable"), while ID was the "crazy idea". Now, like most other IDist, you're saying that ID is obvious and anyone who is convinced by darwinian evolutionary models is following a crazy idea. Pardon me if this is just confusing. Maybe I'm too reasonable to debate you.
[ 22. June 2003, 20:45: Message edited by: charlie d. ]
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