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Punctuated Equilibria theories


bumab
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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:

 

...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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... 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.

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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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....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.

 

 

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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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.
I agree with that, I just keep getting the impression that Bio is saying 1) mutations do occur, but 2) they are always cancelled out and have *no* effect on speciation at all: that some other action causes genes to spontaneously rearrange themselves *only* when envronmental stresses occur. I think I'm arguing more along the same lines you are that there's mutations and they only express themselves under stress, probably due to other parts of the equation like proteins and hormones which do pretty bizarre things... Bio, you want to correct my impressions?

 

Cheers,

Buffy

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I agree with that, I just keep getting the impression that Bio is saying 1) mutations do occur, but 2) they are always cancelled out and have *no* effect on speciation at all: that some other action causes genes to spontaneously rearrange themselves *only* when envronmental stresses occur....
This is close. I suggest the following:

 

1) Mutations do occur, but they are not a significant driver of speciation. They are essentially unrelated to the discussion. Their relationship to speciation is not established in the fossil record, and that vast, vast, vast majority of viable "incremental" mutations would have been suppressed. The higher the life form, the more successful the suppression.

2) Sudden arrival of a new species (or phylum) cannot be via mutation in the sense that we usually use it. If a parent species is able to generate a daughter species that is both viable and yet different enough to preclude interbreeding in a small number of generations, it is probably because the DNA of the parent species provided for the DNA of the daughter species. DNA is remarkably stable over time (consider mitochondrial DNA). Dramatic changes in morphology are not accidental: they are part of the information load of the parent.

3) The probability of a life form producing a viable daughter species with significant morphological change is vanishingly small. This would include the examples (yours, Bumab?) about insects or frog progeny with additional legs. I contend this is not a mutation. It is an adaptive feature of the source DNA.

4) The implications are that the aggregate complexity of higher species (e.g., humans) is not a lot higher than the aggregate complexity of prokaryotes because the majority of the predispostiion for generation of higher life forms was already in the prokaryote.

5) This would turn the customary interpretation of natural selection a little bit sideways. It would suggest not that life forms adapt as environments change to enable survival. Rather, life forms are structured for adaptation, and environmental changes let the existing information features express themselves.

6) This is testable. There are many extant examples of viable offspring after dramatic morphological changes. Frogs with five legs. Insects with additional legs. If we check to see how many new functional genes there are after a single generation, it would be highly suggestive. If a single generation can produce even ten new funcitonal genes, it would be ludicrous to suggest that it was a random occurence in the progeny. The probabilistic numbers are easily less than 1 in 10^100. It would have to be intrinsic in the information load of the parent.

7) The examples in number 6 (above) are only noticed because the progeny look like the parents. If a single generation alteration can produce 10 functional genes, why not 100? Why not 1000? Within reason, the probability is essentially the same, as long as the feature was part of the parental information load.

8) If the number of new genes is high, the new species would not have to resemble the parent species. If it did not, we would not be able to find the link to the parent. Sound familiar?

9) This implies that a species could arrive without a morphologically similar precursor. Ergo, the links are missing in the fossil record because they are not there. Species arrive quickly because they are supposed to.

 

Have I seduced anyone toward the idea yet? If so, consider how complex that first prokayote really was. If it sounds ludicrous to put all that information load back on the prokaryote, consider the odds that the very,very first, most "simple" life form would use the very same nucliec acids and the very same amino acids as humans. There are an infinite number of possibilities (truly infinite) for amino acids but the same 20 lasted 4 billion years? Seem strange to anyone?

 

Strikes me as one of those things that makes you go "Hmmmmm".:hihi:

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Hmmmmm...... :hihi:

 

1) Mutations do occur, but they are not a significant driver of speciation. They are essentially unrelated to the discussion. Their relationship to speciation is not established in the fossil record, and that vast, vast, vast majority of viable "incremental" mutations would have been suppressed. The higher the life form, the more successful the suppression.

 

True, as far as the fossil record shows. I'd agree.

 

2) Sudden arrival of a new species (or phylum) cannot be via mutation in the sense that we usually use it. If a parent species is able to generate a daughter species that is both viable and yet different enough to preclude interbreeding in a small number of generations, it is probably because the DNA of the parent species provided for the DNA of the daughter species. DNA is remarkably stable over time (consider mitochondrial DNA). Dramatic changes in morphology are not accidental: they are part of the information load of the parent.

 

A logical step.

 

3) The probability of a life form producing a viable daughter species with significant morphological change is vanishingly small. This would include the examples (yours, Bumab?) about insects or frog progeny with additional legs. I contend this is not a mutation. It is an adaptive feature of the source DNA.

 

"Adaptive feature" sounds like my idea of a "mutative gene." DNA is not a mind, it can't "decide" to mutate. It's simply an information processing device. Input in, various protiens out. Something would need to be present to respond to the environmental change. You information load would simply be in the form of many genes, and then something to control them, right?

 

4) The implications are that the aggregate complexity of higher species (e.g., humans) is not a lot higher than the aggregate complexity of prokaryotes because the majority of the predispostiion for generation of higher life forms was already in the prokaryote.

5) This would turn the customary interpretation of natural selection a little bit sideways. It would suggest not that life forms adapt as environments change to enable survival. Rather, life forms are structured for adaptation, and environmental changes let the existing information features express themselves.

 

Life forms are structured for adaptation, you just don't think the existing theories account for the speed of adaptation accounted for in the fossil record. I certainly agree.

 

6) This is testable. There are many extant examples of viable offspring after dramatic morphological changes. Frogs with five legs. Insects with additional legs. If we check to see how many new functional genes there are after a single generation, it would be highly suggestive.

 

The extra legs are a single gene which doesn't get turned off in growth, so that's one strike. I'm not sure about the frogs, I'll look when I get home. Regardless, genetic mapping is coming up with a lot of dramatic morphological changes that can result from single gene mutations.

 

If a single generation can produce even ten new funcitonal genes, it would be ludicrous to suggest that it was a random occurence in the progeny. The probabilistic numbers are easily less than 1 in 10^100. It would have to be intrinsic in the information load of the parent.

 

8) If the number of new genes is high, the new species would not have to resemble the parent species. If it did not, we would not be able to find the link to the parent. Sound familiar?

9) This implies that a species could arrive without a morphologically similar precursor. Ergo, the links are missing in the fossil record because they are not there. Species arrive quickly because they are supposed to.

 

Possible, although that would make a lot of species where the parents are raising strange, strange offspring. I don't know how many animals will raise offspring that look nothing like them. But perhaps. Still- what turns this on? If the information load is present (which I'll grant could be, we've got all sorts of wierd genes in us), how does it become expressed?

 

 

There are an infinite number of possibilities (truly infinite) for amino acids but the same 20 lasted 4 billion years? Seem strange to anyone?

 

Yes and no- could be that any (ANY) change to the amino acid structure proved deleterious, because the whole DNA would need to change AT THE SAME TIME in order for all the genes and protiens to be expressed in any consistent way. That's a pretty big roadblock of amino acids changing over time.

 

 

Interesting ideas!

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...If it sounds ludicrous to put all that information load back on the prokaryote, consider the odds that the very,very first, most "simple" life form would use the very same nucliec acids and the very same amino acids as humans. There are an infinite number of possibilities (truly infinite) for amino acids but the same 20 lasted 4 billion years? Seem strange to anyone?....
I cannot think of any way to calculate the probability of the above this state of nature without the answer coming out essentially zero, unless you assume that the entire information load for development of life was already in the prokaryote.

 

An interesting probklem.

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"Adaptive feature" sounds like my idea of a "mutative gene." DNA is not a mind, it can't "decide" to mutate. It's simply an information processing device. Input in, various protiens out. Something would need to be present to respond to the environmental change. You information load would simply be in the form of many genes, and then something to control them, right?
At the risk of raising semantic arguments, folks that discuss "mutation" usually are presuming that some random occurence resulted in a morphological change. I am suggesting that the source DNA already had the "pre-genes" (if you will) to allow for significant rapid adaptation. This does NOT mean that the "new" genes were preexisting and already functional. It suggests that there is MUCH more information in the nucleic acid sequence than the genes that are expressed. It suggests that many as-yet-unexpressed permutations of the extant genes are already in the information load. Imagine a 100 number combination lock that requires 5 dials for the combination. There are 100^5 "dialable" combinations, but you could design the lock with 50 valid unlock combinations. I am suggesting that the adaptive combinations of "new" genes are already present in the parent species, like one of the 50 valid combinations. This is not random, so it is not a mutation.
The extra legs are a single gene which doesn't get turned off in growth, so that's one strike. I'm not sure about the frogs, I'll look when I get home. Regardless, genetic mapping is coming up with a lot of dramatic morphological changes that can result from single gene mutations.
I would argue that a sigificant morphological change pursuant to a singe gene change supports my case.
...that would make a lot of species where the parents are raising strange, strange offspring. I don't know how many animals will raise offspring that look nothing like them.
This assumes the offspring need raising, but this is a good point.
... what turns this on? If the information load is present (which I'll grant could be, we've got all sorts of wierd genes in us), how does it become expressed?
Well, since I am hypothesizing an inexplicable quantity of information load into the prokaryote, it isn't a much larger step to hypothesize that the trigger recognition is there as well. What the heck.
... could be that any (ANY) change to the amino acid structure proved deleterious, because the whole DNA would need to change AT THE SAME TIME in order for all the genes and protiens to be expressed in any consistent way....
Sure. But doesn't that support the case that the probability of the first prokaryote was even smaller than one might have imagined previously? Exactly one set of 20 amino acids out of an infinite set of possibilities???
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I am suggesting that the source DNA already had the "pre-genes" (if you will) to allow for significant rapid adaptation.

 

Sounds good, I was just looking for clarification.

 

This does NOT mean that the "new" genes were preexisting and already functional. It suggests that there is MUCH more information in the nucleic acid sequence than the genes that are expressed. It suggests that many as-yet-unexpressed permutations of the extant genes are already in the information load.

 

Seems that emerging molecular biology more then supports that idea. Our understanding of just how many protiens can come from a single gene through alternate splicing and other methods is continually growing.

 

But doesn't that support the case that the probability of the first prokaryote was even smaller than one might have imagined previously? Exactly one set of 20 amino acids out of an infinite set of possibilities???

 

Well, perhaps there were many possible sets of amino acids taht would work, however those 20 were simply the chosen one. Once that is established, however, it would be nearly set in stone. During the establishment period, however, your point is valid. Why aren't there seperate lines of organisms with seperate amino acid sequences? Possible fitness variances, or interbreeding, or whatever...

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Well, perhaps there were many possible sets of amino acids taht would work, however those 20 were simply the chosen one. Once that is established, however, it would be nearly set in stone. During the establishment period, however, your point is valid. Why aren't there seperate lines of organisms with seperate amino acid sequences? Possible fitness variances, or interbreeding, or whatever...
Good points, both.
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