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Topic: John A. Davison: An Evolutionary Manifesto: A New Hypothesis For Organic Change
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posted 22. June 2003 22:12
I feel like this thread is drawing to a close. Unless a case is made to keep the thread open, I'll close it in two days.
Final comments?
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nosivad
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posted 22. June 2003 22:30
charlie d. "Hypotheses have to be reasonable - facts don't". I'm sorry that you can't recognize satire when you see it. If the thread must be closed, there is nothing I can do about it. I've been rather enjoying myself. nosivad
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Nel
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posted 22. June 2003 22:35
Charlie, you can pretend to still think that Nup96 (not 76) is all that is needed for hybrid sterility, but we wouldn't be talking about it if it was. But you continually wrote that Nup96 alone is sufficient, when it isn't, throughout this thread:
quote:
Dr. Davison, what the paper shows is how reproductive isolation can be the result of relatively simple single gene changes, and how such changes may be due to selective pressures - which by the way may be entirely unrelated to the actual speciation event (so it's not like reproductive isolation is adaptive, but that adaptation can cause reproductive isolation).
(and you couldn't even get the name of the gene right) As you now realize, that's wrong. It was ironic how you continually challenged Davison to contradict your interpretation of the paper, when in fact, your interpretation was quite wrong (or just a half-truth).
But like I said, everyone is on the same page now and thats all that matters to me.
By the way, how do you figure that this:
"200 chromosomal regions that differ between the two fruit fly species to such an extent that they can cause death in hybrids"
is only in my imagination? Each one, as well as all of them, can cause death in hybrids. Or you don't still think that they only estimated 20 chromosome regions do you?
By the way you never responded to why I think that retinoblastoma is not monogenic, you simply assert that it still is, even though I showed how data suggests that it is not. It is irrelevant that something is "classic" in biology, life doesn't care what we think is "classic", it'll surprise us when we least expect it. Oh well, another thread perhaps.
[ 22. June 2003, 23:23: Message edited by: Nelson_Alonso ]
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charlie d.
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posted 22. June 2003 23:22
Call it quits, mod, before we have to start all over again. At some point I thought I had taken Nelson's claim down from 200 genes to 2, and had some hope he'd realize one was indeed sufficient in hybrids, but now he's back to 200. It feels like the "who's on first" routine.
Plus, I'll be busy asking all textbooks in cancer genetics to update their definition of retinoblastoma from a mendelian character to a nelsonian one - that may take a while.
EDIT: Actually I just realized you said this: quote:
Each one [of the "200 genes" - cd], as well as all of them, can cause death in hybrids.
Do you really mean that each gene individually can cause hybrid sterility? Or did you just mean the opposite of what you wrote, again?
[ 22. June 2003, 23:29: Message edited by: charlie d. ]
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Nel
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posted 22. June 2003 23:26
Charlie,
The thread doesn't close for two days. So feel free to show how I thought that 200 genes were essential for hybrid sterility, when in my first post about it, I specifically said that the minimum was 2, which even Rex has shown that that is the minimum. Go figure.
Also, when you update those textbooks, make sure that they include my comments on Rb-null retinoblasts. Good luck.
They estimated that there are roughly 200 chromosomal regions that differ between the two fruit fly species, each one can cause death in hybrids. In the first of these regions they identified Nup96 (not 76), wich causes death when its forced to interact with that second gene from the other species that seems to elude you.
[ 23. June 2003, 00:08: Message edited by: Nelson_Alonso ]
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peter borger
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posted 22. June 2003 23:59
That Davison's vision -'evolution' is probably (non randomly) draining from prexisting DNA elements present in the multipurpose genome- is very likely has recently been demonstrated in 'wing-evolution' in insects:
1) Nature. 2003 Jan 16;421(6920):264-7.
Loss and recovery of wings in stick insects.
Whiting MF, Bradler S, Maxwell T.
ABSTRACT: The evolution of wings was the central adaptation allowing insects to escape predators, exploit scattered resources, and disperse into new niches, resulting in radiations into vast numbers of species. Despite the presumed evolutionary advantages associated with full-sized wings (macroptery), nearly all pterygote (winged) orders have many partially winged (brachypterous) or wingless (apterous) lineages, and some entire orders are secondarily wingless (for example, fleas, lice, grylloblattids and mantophasmatids), with about 5% of extant pterygote species being flightless. Thousands of independent transitions from a winged form to winglessness have occurred during the course of insect evolution; however, an evolutionary reversal from a flightless to a volant form has never been demonstrated clearly for any pterygote lineage. Such a reversal is considered highly unlikely because complex interactions between nerves, muscles, sclerites and wing foils are required to accommodate flight. Here we show that stick insects (order Phasmatodea) diversified as wingless insects and that wings were derived secondarily, perhaps on many occasions. These results suggest that wing developmental pathways are conserved in wingless phasmids, and that 're-evolution' of wings has had an unrecognized role in insect diversification.
2) Curr Biol. 2003 May 27;13(11):R436-8. Related Articles, Links
Evolution: have wings come, gone and come again?
Stone G, French V.
ABSTRACT: Can complex traits be re-evolved by lineages that have lost them? Phylogenetic study now suggests that wings may indeed have reappeared several times within the ancestrally wingless stick insects.
And all this happened at random, I presume. Considering such data it should be VERY clear that evolutionary theory requires a bit of updating.
Best Wishes
Peter
[ 23. June 2003, 00:00: Message edited by: peter borger ]
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nosivad
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posted 23. June 2003 00:14
I am confident that even if the parents were identical at the gene level, one could still have hybrid sterility. All that would be required would be a few translocations or pericentric inversions. This would create problems when crossovers took place prior to meiosis I, resulting in unbalanced gametes. Isn't this the primary reason the mule is sterile? In other words, position effects tend to produce sterility in heterozygous form. Also, note that it is unecessary to postulate any additional genetic information. I still don't see any mechanism whereby meaningful genetic information can be inserted into the genome. That is the primary, but not the only reason, that I have suggested that the information was already there. Berg, Grasse and Goldschmidt have all subscribed to preadaptation in evolution. I have simply extended and amplified the idea. What has been called convergent evolution is not that at all but simply the independent reading of the same blueprint. The best evidence in support of this notion is provided by the parallels between marsupial and placental mammals. We had marsupial moles, rodents, insectivores, predators even to include marsupial saber toothed cats. Maybe there were marsupial bats. It wouldn't surprise me. Schindewolf has some great pictures of these forms in his book Basic Questions in Biology. nosivad
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nosivad
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posted 23. June 2003 00:22
Woops. It is Basic Questions in Paleontology. I can't believe someone (Peter Borger) is taking my heresy seriously. God bless you Peter! nosivad
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Moderator
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posted 23. June 2003 07:57
Both charlie d. and Nelson A.
Please stop the bickering. I've had to do a lot of forceful moderating lately, and would not like to have to do it in this case. Think of this as a Double Technical foul. If the childish posts continue I'll have to ban both of you.
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gordon
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posted 23. June 2003 08:07
Dr.Davison:
quote:
You define phenotype your way. I'll define phenotype as the word roots mean.
Just a minor point. Charlie D. is right. Regardless of the exact definitions of the word roots, it makes more sense to use terms the way that they are used by those in the appropriate fields use them, even if that meaning is at odds with 'strict definitions.'
I pulled a genetics textbook - Genetics, From Genes to Genomes. Hartwell et al., 2000.
The glossay lists phenotype as "an observable characteristic." One can 'observe' sterility, just as one can observe eye color. I have heard the term phenotype used to describe cellular processes and physiological traits.
So lets not try to re-define terms to suit our needs, shall we?
I will respond to your posts when I have more time.
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gordon
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posted 23. June 2003 08:10
If this thread closes, I should like ot follow up on this discussion, elsewhere if necessary.
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Moderator
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posted 23. June 2003 08:16
Regarding this thread: some people have written to me requesting that I leave it open. My main concern is the level of dialogue that is occurring.
For example:
quote:
"And ever since, there has been a flood of half-truths and outright deceit comming from your direction. I don't mind though, as you can see, I had no problem filling in the blanks."
quote:
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.
Conversations of these types (accusations of deceit and blank assertions) do nothing to move the discussion forward. If I see an improvement in the level of discussion over the next two days, the thread will stay open...especially since there seems to be a lot of interest in continuing it.
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Nel
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posted 23. June 2003 16:56
Davison,
I was wondering if you had any thoughts on bluehead wrasse, Thalassoma bifasciatum. It's an interesting organism, if the larva enters a reef where there are no males, it becomes male, and if there is a male already present, it becomes a female. Most of the time, there is only 1 male for 12 females. If the male dies, a female develops testes in only 24 hours and can make sperm in two weeks. There is also Armadillidium vulgare whose sex can be determined by bacterial infection.
[ 23. June 2003, 17:03: Message edited by: Nelson_Alonso ]
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nosivad
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posted 23. June 2003 19:46
There is no question that the vertebrate gonad is bipotential. Like the kidney and the adrenal gland the embryonic gonad has an outer cortex and an inner medulla. Normally, the cortex becomes the ovary and the medulla the testis. The sex of the animal can be modified during development by the influence of hormones, testosterone promoting the testis, estradiol the ovary. Once differentiated the hormones inhibit the differentiation of the opposite sex. This is demonstrated in chickens which like all birds have only one ovary. If it is removed or destroyed by disease the opposite undifferentiated gonad can become a testis. It was known in medieval times that hens could transform into crowing roosters, although the mechanism was not known then. The bipotential capacity of the vertebrate gonad is an essential feature of the semi-meiotic hypothesis. Such a simple thing as a delay in fertilization can lead to an excess of males in frogs to include those with a genetic female (XX) constitution. XX male frogs are fertile and when mated with normal XX females produce mostly daughters but about one in 20 is a male like his father. Both sexes can be produced experimentally semi-meiotically by inhibition of the second meiotic division. I discuss this in some detail in the Manifesto
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Rex Kerr
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posted 23. June 2003 21:46
Nelson, I'd missed Charlie's quote, leading to my straw man claim. If I'd seen it, I'd have said that it was probably a simple mis-statement on Charlie's part. People make errors in their posts. Luckily, this seems resolved now.
I have not read the nematode paper that you refer to because I never actually saw the reference, just the quote. However, I'm familiar with the work in Pristionchus pacificus as well as C. elegans.
In any case, your argument is illogical. There are about five convenient ways to drive from where I work to where I live. Therefore, which roads I take are obviously just a minor part of the story of where I end up!
Do you see how nonsensical this is?
As with roads and destinations, there's nothing that says that you can't have multiple genotypes that give the same phenotype.
Finally, with respect to definitions: even if we don't call hybrid sterility a trait--let's call it a zawarin instead--and even if we don't say a gene is sufficient if adding it leads to the development of a trait (or zawarin)--we'll call it enablizing--we end up with the same biological point. Nup96 is enablizing for the zawarin of hybrid sterility, and hybrid sterility can thus be a uniactivated zawarin.
But to keep things simple, let's use the standard, well-established terminology for such things, okay? I.e., Nup96 is sufficient for the trait of hybrid sterility. And hybrid sterility can therefore be a monogenic trait.
Added in edit: the phenotype of lethality is epistatic to most other phenotypes, since death in early development tends to preclude e.g. an assessment of hair color.
[ 23. June 2003, 21:47: Message edited by: Rex Kerr ]
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