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Author Topic:   What is the mechanism that prevents microevolution to become macroevolution?
Faith 
Suspended Member (Idle past 1444 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 166 of 301 (346797)
09-05-2006 6:41 PM
Reply to: Message 162 by EZscience
09-05-2006 12:22 PM


Re: mutation pressure
I had not heard the term used to imply asymmetry in forward/backward mutation rates. I was objecting to its use by Faith in the context of some sort of driving force in speciation.
I've never once used the term "mutation pressure." I have no idea what it means.
The only way I've used "driving force" I got off a definition of mutation at Wikipedia: mutation as the driving force of evolution.
{Edit: OK I see where you recognized your error, that you should have imputed it to Philip instead of me}
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.

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Faith 
Suspended Member (Idle past 1444 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 167 of 301 (346808)
09-05-2006 7:15 PM
Reply to: Message 165 by crashfrog
09-05-2006 4:52 PM


No, it's not just a matter of subtracting phenotypes
The cheetah is a NEW phenotype
I don't see how it is, or at least, I don't see how it's a "new phenotype" that arose through a reduction in allelic diversity.
The "cheetah body plan", or the traits that we recognize as the definitive morphological character of cheetahs, didn't arise because of the bottleneck event; they were already there in the population. The pre-bottlenect population of ur-cheetahs would have included individuals that looked like modern cheetahs, and individuals that looked differently.
Not necessarily at all. The particular alleles for the traits that characterize the cheetah were there in the population, but the particular combination of them that is the cheetah may not have been, and in fact probably wasn't, it took the bottleneck to isolate them and combine them.
All the alleles for the Great Dane or the poodle or the spaniel were already there in the dog population hundreds or thousands of years ago, but there is every reason to believe that neither a Great Dane nor a poodle nor a spaniel ever existed until recently. All the alleles for all the modern breeds were there even if the dogs all looked like wolves or mutts.
The bottleneck didn't give rise to anything new, it simply removed other phenotypes, so that the current cheetah "specification" was the only one left.
No, it removed alleles, and left those that put together the cheetah.
How is that a new phenotype? That's simply the loss of the old ones - a loss of phenotypic diversity, which is exactly what I've been telling you is the consequence of a loss of allelic diversity.
Well, others here seem to be disagreeing with you more than I am even. They tell me that I can't even talk on the level of the phenotype at all, that all the processes I'm talking about are about the genotype -- or something like that; I guess I'll eventually get around to those posts. I think that's wrong since the genotype codes for the phenotype and it's the phenotype we have in mind when we talk about evolution.
But in any case I disagree with your picture as I just explained. The cheetah phenotype did not exist until the bottleneck. It came about as the result of the alleles for it being isolated and recombined by inbreeding in the new population.
The phenotype is now completely defined for those particular traits by those single alleles. It is a NEW phenotype compared to the population it was bottlenecked from
No, it's not, because it was in the old population, too.
Not so, only the alleles for it were, and they were most likely mixed up among all the other alleles, and could only make the cheetah when they were isolated out. They could have been selected, for the special adaptive abilities of the fast cheetah for instance, but in this case they were bottlenecked. It's POSSIBLE that the cheetah in basic form did exist and the bottleneck merely streamlined it, but that's not necessarily the case, and the virture of the example of the bottleneck for my purposes is as a demonstration that dramatically new phenotypes can be put together by drastically reduced genetic diversity.
Let's say that we have a population of tall people and short people, and that that's determined, as it is in pea plants, by a single gene that is dominant for tall.
Now, imagine that aliens come down from space and because they hate tall people, they vaporize everybody who is tall. That leaves only the people who lack any tall alleles, who only possess the short allele. That's a loss of diversity, a loss of an allele (the tall one.)
Yes, if you focus on only one allele you can say the phenotype was already there, although it's even possible then that a recessive just never got expressed at all, or at least very very rarely in the population and it took a bottleneck for it to get expressed -- that would mean that the bottleneck just happened to isolate a pretty rare combination though, but it could happen. In any case, it's the combination of all the alleles of all the genes that make up the cheetah that wasn't there. Or probably wasn't.
So, all humans are now a lot shorter. But how is that "new"? All those short people where there in the old population, before the alien bottleneck. So there's no "new" phenotypes - only a loss of old ones. A loss of physical diversity that stemmed from something that reduced genetic diversity.
Well but even in that case you can talk of having an entirely new population even if the phenotype for that population did occur occasionally in the old. But again, it's a more complicated combination of many traits and their alleles that happens in reality, such that the new phenotype really has never been seen before.
{Edit: Not that it stops looking like its predecessors in any case, but that it is a new version of them, of course. All the new species that arise still have most things in common with all the others of their Kind. Whether this comes about as I am describing or by totally novel mutations, nothing newer than a variation on the theme happens phenotypically}
No, it's not. I've already referred to the direct experimental evidence that this is not the case. Alleles increase in diversity over time; that's the trend.
I don't know where you think you've proved this. The occasional mutation certainly wouldn't prove it.
Specific events might remove alleles, selection might do that (although for statistical reasons it's actually fairly hard to completely select out an allele, especially if it's recessive. The fewer number of individuals that possess an allele, the harder it is to select against.)
Yes.
But the overarching trend is always one of allelic increase, not decrease. That's been consistently borne out in observation and experiment, and mutations are known - known, Faith! Known like we know lightning is made of electricity! - to be the cause.
But Crash, you've said this many times and have NOT shown it to be the case in anything but the onecelled bacteria, and I'm not even certain in what sense the allele that pops up there is really "new." In multicelled creatures and sexually reproducing creatures, however, you are *assuming* that mutation brought about all the genetic material, but you haven't shown anything like that, not even the beginning of it.
and new phenotypes are certainly produced by this loss
If what you're saying is that they're "new" not because they're actually something different than has come before, but merely "new" because now they represent a greater fraction of individuals, that's pretty dumb.
I'm not. See above. Consider dog breeding.
Edited by Faith, : changed select to isolate
Edited by Faith, : No reason given.

This message is a reply to:
 Message 165 by crashfrog, posted 09-05-2006 4:52 PM crashfrog has replied

Replies to this message:
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NosyNed
Member
Posts: 8996
From: Canada
Joined: 04-04-2003


Message 168 of 301 (346812)
09-05-2006 7:39 PM
Reply to: Message 165 by crashfrog
09-05-2006 4:52 PM


New alleles
Crash, I have read about a mutation in some Italian village (IIRC) that conveys particular resistance to heart disease. It (IIRC again) is supposed to have appeared about 200 or 300 years ago. (Maybe they even have a name of the 'common ancestor'.
However, since we don't have the genetic maps of the parents of that individual (and cohort) how do we know, other than assumption that it was a mutation?

This message is a reply to:
 Message 165 by crashfrog, posted 09-05-2006 4:52 PM crashfrog has replied

Replies to this message:
 Message 170 by crashfrog, posted 09-05-2006 8:08 PM NosyNed has replied

crashfrog
Member (Idle past 1467 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 169 of 301 (346820)
09-05-2006 8:04 PM
Reply to: Message 167 by Faith
09-05-2006 7:15 PM


Re: No, it's not just a matter of subtracting phenotypes
The particular alleles for the traits that characterize the cheetah were there in the population, but the particular combination of them that is the cheetah may not have been, and in fact probably wasn't, it took the bottleneck to isolate them and combine them.
What's your evidence for that assertion? Basic statistics tells us that we should expect to find that combination, at random, over and over again before the bottleneck. That's why sex evolved in animals, after all - to increase the chances of those combinations occuring.
No, it removed alleles, and left those that put together the cheetah.
Cheetahs were already in the population - they were the population. The phenotype had to predate the bottleneck, because they were all the bottleneck left. If they hadn't been present, what cheetahs would have survived to pass on those alleles?
The cheetah phenotype did not exist until the bottleneck.
What's your evidence for that assertion?
Not so, only the alleles for it were, and they were most likely mixed up among all the other alleles, and could only make the cheetah when they were isolated out
You can't isolate alleles, Faith. You can only isolate individuals. The bottleneck was a reduction in the number of individuals, not just of alleles. In fact, it's a reduction in alleles because it was a reduction in individuals.
So the only individuals who survived were the ones who had those alleles. So they had that combination of alleles. So they had that phenotype. And they must have been in the population, because where else did they come from?
You can't just pick and choose alleles from around the population - a few out of this guy, a few out of that guy. Individuals are the unit of selection in this example.
and the virture of the example of the bottleneck for my purposes is as a demonstration that dramatically new phenotypes can be put together by drastically reduced genetic diversity.
They can't. The reduction doesn't give you anything new. That's the problem with your example - the reduction was a loss of phenotypes, not a gain of new ones.
Well but even in that case you can talk of having an entirely new population even if the phenotype for that population did occur occasionally in the old.
It's not a new population. It's a remnant of the old one. Nothing about it is new, just as nothing about your child's old toy is new simply because you've thrown all the other toys away.
I don't know where you think you've proved this.
Christ, Faith, this discussion isn't going to get very far if you can't understand that you need to remember what I've said in my posts. Once again, I'm referring to experiments where an entire population is grown from a single individual - who can hold at most one allele per gene, remember - and then the number of alleles in the population is sampled after many generations.
The number of alleles always goes up. Always! There's always more in the end than you started with. Mutation is the cause of that.
How many times do we have to go over that?
But Crash, you've said this many times and have NOT shown it to be the case in anything but the onecelled bacteria, and I'm not even certain in what sense the allele that pops up there is really "new."
Where else are they coming from, Faith? Every other explanation you've attempted has been specifically contradicted by the structure of the experiment. The experiments are designed to eliminate all the alternate alleles but one. Any subsequent alternate alleles have to be new. There's no other way for them to get into the population!
Your example proves my point, Faith, it doesn't prove yours. Reducing alleleic diversity reduces diversity in phenotypes. It doesn't produce new ones, because alleles determine phenotype. It's like saying that deleting half the files on your harddrive can produce a book report you haven't written yet. You would find this logic idiotic in any other circumstance. Do you really think that this is what it's going to take to disprove evolution? Logic that even a child would reject?

This message is a reply to:
 Message 167 by Faith, posted 09-05-2006 7:15 PM Faith has not replied

crashfrog
Member (Idle past 1467 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 170 of 301 (346822)
09-05-2006 8:08 PM
Reply to: Message 168 by NosyNed
09-05-2006 7:39 PM


Re: New alleles
However, since we don't have the genetic maps of the parents of that individual (and cohort) how do we know, other than assumption that it was a mutation?
Mutation is the origin of all alleles. If it's not a mutation, where else did it come from? Mind beams from Alpha Centarui? If it was "created", why isn't it in more people?

This message is a reply to:
 Message 168 by NosyNed, posted 09-05-2006 7:39 PM NosyNed has replied

Replies to this message:
 Message 171 by NosyNed, posted 09-05-2006 8:20 PM crashfrog has replied

NosyNed
Member
Posts: 8996
From: Canada
Joined: 04-04-2003


Message 171 of 301 (346828)
09-05-2006 8:20 PM
Reply to: Message 170 by crashfrog
09-05-2006 8:08 PM


From alpha centari?
No, maybe it was already in the gene pool but unexpressed. Maybe it was expressed but not noticed. (It wasn't until the last decade or less).
How do we know?

This message is a reply to:
 Message 170 by crashfrog, posted 09-05-2006 8:08 PM crashfrog has replied

Replies to this message:
 Message 172 by crashfrog, posted 09-06-2006 1:15 PM NosyNed has replied

crashfrog
Member (Idle past 1467 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 172 of 301 (346978)
09-06-2006 1:15 PM
Reply to: Message 171 by NosyNed
09-05-2006 8:20 PM


Re: From alpha centari?
No, maybe it was already in the gene pool but unexpressed.
What kept it from being expressed? What turned it on only in this one Italian village?
If we sequence the gene and find no evidence of it in anybody else - random members of other populations - is that sufficient to conclude that this is recent, rather than an ancient, mutation?
Maybe it was expressed but not noticed. (It wasn't until the last decade or less).
Why wouldn't we notice it if it were in other populations besides the one in Italy?

This message is a reply to:
 Message 171 by NosyNed, posted 09-05-2006 8:20 PM NosyNed has replied

Replies to this message:
 Message 177 by Faith, posted 09-06-2006 3:44 PM crashfrog has replied
 Message 204 by NosyNed, posted 09-06-2006 8:07 PM crashfrog has replied
 Message 210 by Faith, posted 09-07-2006 2:09 AM crashfrog has replied

Philip
Member (Idle past 4722 days)
Posts: 656
From: Albertville, AL, USA
Joined: 03-10-2002


Message 173 of 301 (346979)
09-06-2006 1:19 PM
Reply to: Message 156 by EZscience
09-05-2006 7:01 AM


Re: Mutation Fallacies in Macro-ToE
Thankyou for responding.
Albeit, you just bashingly-handwaved off my questions with nonsensical off-topic evasions, like: "Mutational pressures ... no such thing", "Where did you learn biology?" (BTW, Rockhurst College, Kansas City), "Do you even know what a plasmid is?", etc. (EZ, I can bash much of what you state (in conscience), but that's neither science, good-will, nor on-topic). I'll simplify best I can as a stupid 'Dorothy-like' podiatrist (with my 4 non-AL science degrees, MSBS (Barry Univ, Miami), AASEET (Craven Cmpty College, NC), BS-Psychology (Univ of DE), and DPM (Barry Univ, Miami) ... If I explained to my cat the fallacy...
Beneficial Mutation *occurs* in
(1) Non-highly conservative portions? ... and/or
(2) Highly-conserved portions (of DNA)?
Which is it EZ?
EZ writes:
The AIDS virus has a protein capsid that recognizes a particular protein structure specific to the surface of human T-cells. A mutation occurs in a single base pair that changes one amino acid in this protein leaving its function as a membrane protein unaffected, but rendering it un-recognizable to the AIDS virus.
I (presently) perceive that your classic AIDS virus *ontogeny* is NO *raw mutation*, just another genetic adaptation within a "highly-conserved" viral gene pool (1)...
... a biological-misnomer for *raw mutation* ... in your case, genetic adaptation only, within the HIV gene pool.
(Note, I invite any of you biologists and laymen to invalidate my logic)

DISCLAIMER: No representation is made that the quality of scientific and metaphysical statements written is greater than the quality of those statements written by anyone else.

This message is a reply to:
 Message 156 by EZscience, posted 09-05-2006 7:01 AM EZscience has replied

Replies to this message:
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EZscience
Member (Idle past 5154 days)
Posts: 961
From: A wheatfield in Kansas
Joined: 04-14-2005


Message 174 of 301 (346991)
09-06-2006 2:30 PM
Reply to: Message 173 by Philip
09-06-2006 1:19 PM


Re: Mutation Fallacies in Macro-ToE
Philip writes:
Beneficial Mutation *occurs* in
(1) Non-highly conservative portions? ... and/or
(2) Highly-conserved portions (of DNA)?
Which is it EZ?
The answer is that a mutation can occur in either conserved or unconserved regions - it's just a difference in the *probability* of mutation that distinguishes the two. By definiton, a conserved region is a region where mutations either rarely occur, or if they do, they are not tolerable and invariably result in an inviable genotype that fails to develop (or reproduce) successfully. Similarly, there are unconserved regions where the reverese is true, usually because these are sequences that are not transcribed and therefore do not code for proteins with exacting structural requirements.
There seems to be a desire on your part to view 'beneficial mutations' as some sort of special case. A mutation is just a mutation. Whether it is deleterious, neutral, or beneficial is CONTEXT-DEPENDENT and depends on 1) the environmental context in which the individual lives, and sometimes 2) the genotype (genetic context) in which the mutation occurs. So the same mutation may be deleterious in one context, but beneficial in another. I can give you a nice example if you like.
Philip writes:
I (presently) perceive that your classic AIDS virus *ontogeny* is NO *raw mutation*, just another genetic adaptation within a "highly-conserved" viral gene pool
Of course it is a 'raw' mutation.
Check back in whatever biology text they gave you at Rockhurst.
Heritable mutations comprise additions, deletions and substitutions of bases in germ cell DNA. I posited a base substitution that generated a change in one amino acid following transcription.
..and viral gene pools are notoriously unconserved.
Viruses can evolve faster than almost any other living thing.
How do you think bird flu is starting to infect humans suddenly after being restricted to birds up till now?
It has to be a 'beneficial' mutation (beneficial for the virus, not for us).

This message is a reply to:
 Message 173 by Philip, posted 09-06-2006 1:19 PM Philip has not replied

crashfrog
Member (Idle past 1467 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 175 of 301 (346996)
09-06-2006 2:42 PM
Reply to: Message 173 by Philip
09-06-2006 1:19 PM


Re: Mutation Fallacies in Macro-ToE
Note, I invite any of you biologists and laymen to invalidate my logic
Ok, well, I'm a layperson. Here I go:
You say "genetic adaptation" like it's a different thing than a mutation. What is the adaptive mechanism operating on genetics if it isn't selection operating on random mutations?

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 Message 176 by Faith, posted 09-06-2006 3:34 PM crashfrog has replied

Faith 
Suspended Member (Idle past 1444 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 176 of 301 (347010)
09-06-2006 3:34 PM
Reply to: Message 175 by crashfrog
09-06-2006 2:42 PM


Re: Mutation Fallacies in Macro-ToE
You say "genetic adaptation" like it's a different thing than a mutation. What is the adaptive mechanism operating on genetics if it isn't selection operating on random mutations?
Here's my answer. It's selection operating on the pre-existing alleles in a population. "Selection" in the broad sense. It can mean natural selection, or sexual selection, or the random selection processes of geographic isolation, migration etc etc etc. But it all operates on pre-existing genetic potentials, that is, the variety of alleles available.

This message is a reply to:
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Replies to this message:
 Message 178 by crashfrog, posted 09-06-2006 3:50 PM Faith has replied
 Message 181 by RickJB, posted 09-06-2006 4:07 PM Faith has replied

Faith 
Suspended Member (Idle past 1444 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 177 of 301 (347013)
09-06-2006 3:44 PM
Reply to: Message 172 by crashfrog
09-06-2006 1:15 PM


Re: From alpha centari?
No, maybe it was already in the gene pool but unexpressed.
What kept it from being expressed? What turned it on only in this one Italian village?
It was probably not very numerous in the population at large, and to be expressed probably had to get paired up with another of the same, a low probability occurrence. Other people could be carriers of it without expressing it, if this is how it operates.
If we sequence the gene and find no evidence of it in anybody else - random members of other populations - is that sufficient to conclude that this is recent, rather than an ancient, mutation?
No. It could be an allele that used to be very numerous but has been destroyed by deleterious mutations {Edit: or by one of those "neutral" mutations that "don't do anything" because their effect isn't detectable unless you know what the allele that got destroyed was supposed to do}. So this allele in its original form only survives in small numbers here and there. A random sample could all too easily fail to pick it up.
Maybe it was expressed but not noticed. (It wasn't until the last decade or less).
Why wouldn't we notice it if it were in other populations besides the one in Italy?
What's to notice? Are you checking everybody's DNA? Some people live longer than others. Are you checking the DNA of all of those? You can't even identify them UNTIL they've lived longer. Maybe they live longer because they have this allele but there could be other factors. How are you going to identify who has this allele if it's rare?
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.

This message is a reply to:
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crashfrog
Member (Idle past 1467 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 178 of 301 (347016)
09-06-2006 3:50 PM
Reply to: Message 176 by Faith
09-06-2006 3:34 PM


Re: Mutation Fallacies in Macro-ToE
How does that apply to this case? The trait is dominant. You can't hide a dominant trait, you can only lack it by being homozygous recessive.
If an individual has a trait that is dominant, but neither of the parents have the trait, then either the gene came about through mutation or the parents aren't who you think they are.
Genetics 101. How can your mechanism of "pre-existing alleles" possibly apply in this case?

This message is a reply to:
 Message 176 by Faith, posted 09-06-2006 3:34 PM Faith has replied

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 Message 179 by Faith, posted 09-06-2006 3:55 PM crashfrog has not replied

Faith 
Suspended Member (Idle past 1444 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 179 of 301 (347017)
09-06-2006 3:55 PM
Reply to: Message 178 by crashfrog
09-06-2006 3:50 PM


Re: Mutation Fallacies in Macro-ToE
How does that apply to this case? The trait is dominant. You can't hide a dominant trait, you can only lack it by being homozygous recessive.
If an individual has a trait that is dominant, but neither of the parents have the trait, then either the gene came about through mutation or the parents aren't who you think they are.
Do you have a link to a discussion of these factors in this case?
Edited by Faith, : No reason given.

This message is a reply to:
 Message 178 by crashfrog, posted 09-06-2006 3:50 PM crashfrog has not replied

crashfrog
Member (Idle past 1467 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 180 of 301 (347022)
09-06-2006 4:07 PM
Reply to: Message 177 by Faith
09-06-2006 3:44 PM


Re: From alpha centari?
It was probably not very numerous in the population at large, and to be expressed probably had to get paired up with another of the same, a low probability occurrence.
A brief discussion of the mutation which you can read here:
Apolipoprotein AI Mutations and Information
shows that this is not the case. All known carriers of the mutation are heterozygous for it - they only have one copy of the gene, and the trait is dominant.
No. It could be an allele that used to be very numerous but has been destroyed by deleterious mutations
We would be able to detect evidence of that - the "pieces" of the gene, if you will, much as we detect the vitamin C pseudogene. It would take millions upon millions of generations for a gene to be rendered completely unrecognizable by mutations, and in that amount of time, it would be impossible for anyone to have the gene.
What's to notice?
The near-immunity to arteriosclerosis regardless of lifestyle? I would think that would be something fairly easy to notice in a society where people eat fatty food and smoke - like the US and Europe - and heart diseases are some of the leading causes of death.

This message is a reply to:
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