BiologyLife in all varieties. What is it, and how does it evolve?
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While many evolutionists argue for PE, and many against it, I'm not sure there's been a satisfactory mechanism proposed for causing such rapid speciations. In another thread we were talking about why PE might be lacking, as well as gradualism. Well, I've been thinking:
After a major extinction (local, reigional, or global), a lot of niches are open. Basically anything that's born could conceivably find a place to prosper, as long as it's not competing with anything. So in that case, a gene that causes mutations to occur would be selected for, providing there's a means to turn that gene on and off. Could a "mutation gene" in fact exist, and only be expressed after some extreme stress when many neighbors have been killed off? If that's possible, it seems entirly possible that such a gene would be selected for, as all the decendents in their various niches would carry it. In the selfish gene sense, it's perfectly conceivable.
This would allow for rapid speciation of higher order animals, and provide a possible explanation for the apparent PE that has been observed, especially after mass extinctions, but could also conceivably argue for local extinction events as well.
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I am going to cut in my post from the Intelligent design thread here, because it is applicable:
Quote:
Originally Posted by Buffy
...I'm just trying to get you to do some weight lifting! Sure, love to hear how speciation occurs without mutation and selection... Got a theory? I won't lose my respect for you if you don't of course...
As you might expect, I am not enthusiastic about introducing heretical ideas into a forum of antagonists. Further, I am not a researcher, so I am not likely to be in a position to advance any particular theory by producing serial evidences, or even serial reviews of such. But what the heck.
I do think that Gould and Eldridge were being careful. They were not in a position to rule out speciation through mutation. They had to maintain professional decorum (not to mention get more grants). But they certainly did nothing to confirm speciation by mutation. Even in the Sci Am article you linked, there was NO evidence that the morphological changes were driven by mutation, but that was the proffered mechanism in the article. Based on what? The triumph of hope over data?
Emperor? clothes? Maybe we can be kind and call it group think.
Let me offer the heresy. I am too far away to hear you laugh anyway.
I think that production of daughter species is not caused by serial mutation, gradual or otherwise. The intracellular biochemical strictures that keep us in stasis are far too complex and far too successful for a large number of serial mutations to survive long enough to effect a significant morphological change. Therefore, one would have to conclude the that capacity for dramatic change in genotype (reflecting itself in significant change in phenotype) is part of the information load in the parent species. That is, viable genotypical change that is dramatic enough to preclude interbreeding of the daughter species with the parent is maintained in the parental genotype. This sudden expression of genotypical shift tends to express itself when a small isolated population is under environmental stress. I do not believe this is a mutation. It is a feature of the information load in the parent species.
This would suggest that the majority of animal and plant kingdom information content was reflected in the first prokaryote. Go figure. But I think this model better reflects our current state of biochemical understanding and our current state of paleontological knowledge than any mutation-based model. Mutations actually might occur, but they have nearly nothing to do with speciation.
Doesn't stike me as a whole lot more difficult to swallow that the entire mass of the universe being squashed into a space the size of a Planck length.
Feel free to name my theory. I think I like "Biological Big Bang". Do keep in mind that if my heretical theory is true, then the IDers would have to prove an incredible level of CSI in the first prokaryote. Everyting after that would be a natural consequence of that information load, and a fundamentally "natural" process.
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Last edited by Biochemist; 05-25-2005 at 02:22 PM.
... This would allow for rapid speciation of higher order animals, and provide a possible explanation for the apparent PE that has been observed, especially after mass extinctions, but could also conceivably argue for local extinction events as well.
This is the essence of the PE model proposed by Gould and Eldredge, but it does not really describe the mechanism, just the circumstances of the speciation event.
I wrote above that I think our reliance on speciation by mutation is unfounded.
__________________ Few problems are so complex that they cannot be substantially clarified by one more cup of coffee (or a nice cabernet if it is after 5:00)
Moderator in absentia. Return anticipated. Timing somewhat vague.
That is, viable genotypical change that is dramatic enough to preclude interbreeding of the daughter species with the parent is maintained in the parental genotype. This sudden expression of genotypical shift tends to express itself when a small isolated population is under environmental stress. I do not believe this is a mutation. It is a feature of the information load in the parent species.
I dont' think that idea is a mutation either, it's just a cumulative effect that's reached some "breaking point" or "tipping point." It's an interesting idea, but the mechanism (or a possible one) elludes me. How would an environmental stress suddenly tip over a gradual process like this?
The mutations in gradualism don't have to be overly dramatic to induce a possible speciation event. They can be relativally simple, like a coloration change that makes them less desirable as mates, but no less fit. If that happens, they may either move to another habitat, or only interbreed with their own new color. This produces two breeding populatiosn which can undergo speciation.
Or it could be a behavioral change, as well. That's a non-morphological change that can easily cause a speciation event.
But anyway, your theory- how an environmental stress cause the scales to tip, as it were?
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This is the essence of the PE model proposed by Gould and Eldredge, but it does not really describe the mechanism, just the circumstances of the speciation event.
Yes, but did they propose a gene (or gene set) that promoted mutation? If they did, I missed it. They simply promoted the idea that all offspring were fit, but that doesn't really provide enough variation for me. I understand your objection to mutation, so I was attempting to address it in a more conventional sense.
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But anyway, your theory- how an environmental stress cause the scales to tip, as it were?
I, of course, only have guesses. But the empirical evidence that the paleontologists have offered is that phyla tend to crop up after cataclysms.
You could argue that the population thinning after a cataclysm tends to force a small number of families to interbreed, and this drives the kind of macro "anomalies" that are typical of interbreeding. Most are tragically lethal but perhaps some are wonderfully beneficial. If this is a feature that is endemic in most species, it is hard to imagine that it is "random" in benefit. A complex gene change resulting in a viable offspring should be a vanishingly small probability. But it apparently is not. Not with humans, anyway.
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I think I'm getting a good sense of what you're talking about the more you do. I don't get the sense from my reading of Gould that he has in fact done anything to discount mutation as a key factor, although he clearly states that environmental pressures actually cause the spurt in changes, and the data clearly shows that these changes in many cases correspond to catastrophic events. What I don't get the sense of at all from my reading of contemporary evolutionary biology is the sense that mutation plays no significant role at all (not that it doesn't *happen*. I understand you're not saying that...). It seems to me that mutations that survive--and its *clear* that many do not get backed out--can remain dormant *until* stress causes them to express themselves. I don't really understand how changes--that must *eventually* be recorded in changes in DNA--just spontaneously happen, but its clear that mutations that happen all the time can get turned on and off once the they *exist*.
I need to go do some more reading as its been awhile since I've thought about this much. Continue guys!
Cheers,
Buffy
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By the way Bumab, thanks for opening this thread! I'm sure gubba will be thrilled when he logs in this morning...
Cheers,
Buffy
__________________ "If you do not agree with anything I say, I'll not only retract it, but deny under oath that I ever said it!" __________________________________________________ ______________-- Tom Lehrer
"What, you guys couldn’t even wear one of your tuxedo t-shirts? I mean, I know each one of you have one."
....cause the spurt in changes, and the data clearly shows that these changes in many cases correspond to catastrophic events.
Yes, those changes are preceeded by a catastrophic event many times, however the actual causal agent is unknown, to my knowledge.
Quote:
Originally Posted by Buffy
It seems to me that mutations that survive--and its *clear* that many do not get backed out--can remain dormant *until* stress causes them to express themselves. I don't really understand how changes--that must *eventually* be recorded in changes in DNA--just spontaneously happen, but its clear that mutations that happen all the time can get turned on and off once the they *exist*.
If the mutation does happen to cause a new, functional gene, then as long as that gene is recessive, it will survive until interbreeding brings it out (or some other cause), since a truely recessive gene does not affect fitness. So perhaps, any catastophic event that killed off a lot of members of a breeding population would "bring the recessive genes to the surface" through interbreeding with carriers. That's the heart of punctuated equlibrum, last I looked at it.
But a gene that specificly caused it's "host" (in the selfish gene sense, again) to mutate rapidly would certainly be selected for in a post-catastrophy environment, as most offspring would be likely to survive. I am just speculating, of course, but I am not completely satisfied (like Bio) that mutation rates alone can explain punctuated eq., since in most organisms mutatitve propensities are selected against- witness the sharks, a constant evironment has made them very resistant to mutations. Why screw with something that's already about perfect?
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