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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 121 of 301 (346137)
09-02-2006 10:15 PM
Reply to: Message 108 by Quetzal
09-02-2006 1:56 PM


Re: On predictions and tests.
I don't think this is what we are claiming. We are talking about alleles being lost, which wouldn't affect the size of the genome which contains the genes the alleles take turns occupying as it were.
I'm aware that this is your contention, but MJ was quite clear that he believes entire genes are lost during speciation.
OK, I guess I missed that. Perhaps he is right, perhaps whole genes are lost, at least in some speciation events.
I pointed out the differences between your stance and his in the post to which you are responding. Of course, you have yet to provide any example which indicates that what you are suggesting actually occurs. Now would be a good time. Find me an example in a living population where this has ocurred.
I'd love to but it's very hard in the same way it is hard for scientists to come up with examples of all the bazillion mutations they assume to be the driving force of evoluation, and even harder of course for us nonscientists because we have to depend on your data, and without the technical knowledge, galling though that is to all concerned. I hope you will forgive us but this is simply the reality of the EvC debate unless more scientifically knowledgeable creationists come along.
However, if our notion is true that a bigger original genome is implied to explain how all life could descend from an original pair, then this wouldn't happen with each "speciation" event but over greater swaths of time along the lines jar is suggesting -- something we would see over millennia, not generations. I don't know how this would work genetically of course but genes themselves would have to die, not just lose allelic contenders.
And you have an example of the genes dying or whatever?
It's all theory at this point.
I have given you examples of increasing genetic diversity in sister populations, which would tend to disconfirm your hypothesis. You need at this point to provide an actual counter-example. Otherwise, your argument stands refuted.
Well, I am still going to get back to that post and to the link to that article. I've done a little work on it but got distracted by these more recent posts.
However, as I recall, you gave no examples of increasing genetic diversity at all, of phenotypic divergence but not increasing genetic diversity. You merely asserted that it was there, the same way you asserted that mutations were behind phenotypic divergence, without proving it.
You have given lots of evidence in the form of references, but it doesn't answer what I'm claiming. I don't need a counter-example if it's all a matter of how we are to interpret the facts in the example you gave.
In Message 79 you really are only saying that you've proved me wrong by demonstrating "increasing divergence between the two populations" but this is a very odd thing to say if you get what I'm arguing, because that's the whole point I'm making -- we expect increasing divergence (in the phenotype) between the two populations over time simply as a result of the working through of the new allelic frequencies brought about by the split from the original population. So demonstrating increasing divergence between the two populations proves nothing since it isn't in dispute, to say the least -- we are simply accounting for this divergence in different ways, and to this point I have not seen a genuine case made for increasing genetic diversity as the explanation for this.
Quetzal in Message 79 writes:
Well, a lot of that's been done. The Ensatina article shows quite clearly increasing divergeance between the two populations.
See? As if "increasing divergence" is some kind of evidence against me, although this is exactly what I'm saying is to be expected from my own scenario. Your evidence simply does not prove your explanation of this divergence in terms of increasing genetic diversity.
If there's some kind of decrease in the genetics as the "strong claim" version of Faith and MJ's idea holds true (that genomes are reduced during speciation), then the genetics of the two salamander populations should show it. They don't.
If now you are changing the subject to decrease in genome size, how easy would it be to identify the death of a gene?
In fact, increased diversity is the case as different alleles exist in both populations with no apparent loss in genome size (MJ's claim), and insufficient gene flow/mixing for recombination to account for the novelty (Faith's claim).
Honestly, Quetzal, I don't see how you think you have shown this. You simply have NOT shown "increased diversity" if by that you mean GENETIC diversity which is what I mean. But I'll now go look at that link.
Edited by Faith, : No reason given.

This message is a reply to:
 Message 108 by Quetzal, posted 09-02-2006 1:56 PM Quetzal has replied

Replies to this message:
 Message 137 by Quetzal, posted 09-04-2006 9:40 AM Faith has replied

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


Message 122 of 301 (346140)
09-02-2006 11:00 PM
Reply to: Message 113 by Quetzal
09-02-2006 2:30 PM


Re: allozymes and other stuff
Quetzal (forgot which post) writes:
One of the really good examples of ring species that has been extensively studied in this context is the Ensatina salamander complex...
The interesting thing about this article, although the overall research was not directly related to my point, is that they were able to go back through 20 years of genetic data (as well as performing their own analyses), that showed divergeance between two subspecies populations (E. eschscholtzii xanthoptica and E. eschscholtzii platensis).
Why is showing divergence of relevance to our discussion?
The further apart geographically the populations of these two subspecies were, the greater the genetic divergeance.
Why is showing greater genetic divergence across greater distance of relevance to our discussion?
However, there was a well-defined hybrid zone between the closest populations. The researchers were able to show linkage disequilibrium due to differential selection pressures on either side of the zone. The selection pressures against the hybrids permitted the researchers to demonstrate a gradual increase in incompatibility between the two subspecies at the ends of the species' range.
Why would selection pressures against the hybrids have anything to do with demonstrating a gradual increase in incompatibility between the two subspecies?, question one, and question two, even if it does, how does the hybrid zone add anything to the ability to demonstrate this: it ought to be demonstrable simply by sampling the two subspecies. In other words, whatever role the hybrids play here, which is the whole point of this article, is completely lost on me.
Q writes:
In other words, we're looking at incipient speciation between E. eschscholtzii xanthoptica and E. eschscholtzii platensis - and where we draw the line is kind of arbitrary. A taxonomic "splitter" could conceivably declare the populations at the extreme ends of the range separate species.
I have no problem whatever with the idea that incipient speciation between the two subspecies is happening, or that speciation may already have happened for that matter. What we need is an explanation for the mechanism that is causing this and I'm arguing for mere change in allelic frequencies with probably a loss of some alleles.
I'm no longer at all clear what you are arguing for. I do not see how the hybrid population has anything to do with this speciation process for starters, although it may, but only in a way peculiar to this one example, and I certainly do not see any evidence in anything you said or the article itself says (below) for an "increase in genetic diversity" as an explanation for it. Can you point out where either you or the article, which follows, says this?
Q writes:
Making a long story short, there is sufficient genetic divergeance between the two "ends" of the E. eschscholtzii chain to indicate that a) the most distant populations do not simply represent a statistical assortment of existing alleles, and b) genetic diversity has not only not decreased, but has actually increased over the range of the species.
a) I believe this is begging the question. You seem to be saying that the mere fact of great divergence proves me wrong about how divergence is brought about.
b) And again, NONE OF THIS SHOWS THAT "genetic diversity is increased."
PLEASE point to where you or this abstract have shown how genetic diversity is increased.
Here is the abstract:
Strong selection against hybrids at a hybrid zone in the Ensatina ring species complex and its evolutionary implications.
Alexandrino J, Baird SJ, Lawson L, Macey JR, Moritz C, Wake DB.
Museum of Vertebrate Zoology, University of California, Berkeley, 3101 Valley Life Science Building 3160, Berkeley, California 94720-3160, USA. jalex@rc.unesp.br
The analysis of interactions between lineages at varying levels of genetic divergence can provide insights into the process of speciation through the accumulation of incompatible mutations.
Ring species, and especially the Ensatina eschscholtzii system exemplify this approach. The plethodontid salamanders E. eschscholtzii xanthoptica and E. eschscholtzii platensis hybridize in the central Sierran foothills of California. We compared the genetic structure across two transects (southern and northern Calaveras Co.), one of which was resampled over 20 years, and examined diagnostic molecular markers (eight allozyme loci and mitochondrial DNA) and a diagnostic quantitative trait (color pattern).
Key results across all studies were: (1) cline centers for all markers were coincident and the zones were narrow, with width estimates of 730 m to 2000 m; (2) cline centers at the northern Calaveras transect were coincident between 1981 and 2001, demonstrating repeatability over five generations; (3) there were very few if any putative F1s, but a relatively high number of backcrossed individuals in the central portion of transects; and (4) we found substantial linkage disequilibrium in all three studies and strong heterozygote deficit both in northern Calaveras, in 2001, and southern Calaveras. Both linkage disequilibrium and heterozygote deficit showed maximum values near the center of the zones.
Using estimates of cline [gradual change] width and dispersal, we infer strong selection against hybrids. This is sufficient to promote accumulation of differences at loci that are neutral or under divergent selection, but would still allow for introgression of adaptive alleles.
The evidence for strong but incomplete isolation across this centrally located contact is consistent with theory suggesting a gradual increase in postzygotic incompatibility between allopatric populations subject to divergent selection and reinforces the value of Ensatina as a system for the study of divergence and speciation at multiple stages.
Please show me in the above where either you or the article argue that increased genetic diversity explains the increasing phenotypic divergence of the two Ensatina subspecies with increasing distance from one another.
The mere existence of one identifiable mutation would not prove that increased genetic diversity caused the divergence, and nothing you have said shows that reduced genetic diversity which produces new phenotypes is not the explanation.
The abstract is too technical for me to read.

This message is a reply to:
 Message 113 by Quetzal, posted 09-02-2006 2:30 PM Quetzal has replied

Replies to this message:
 Message 136 by Quetzal, posted 09-04-2006 9:11 AM Faith has replied

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


Message 123 of 301 (346183)
09-03-2006 8:09 AM
Reply to: Message 118 by Faith
09-02-2006 8:33 PM


Mutation and diversity
Faith writes:
You are apparently talking about diversity of phenotypes when you say "at the level of organisms"
Actually, genotypes. Phenotypes have no heritability. The genotype is the set of heritable units in the organism, although it is not heritable as a unit itself.
Faith writes:
I have been talking about diversity in terms of available alleles only.
Fine. I am just pointing out that genotypic diversity is more than a simple function of numbers of available alleles.
Faith writes:
Alleles don't HAVE to be reduced to produce new phenotypes, this can happen within a population with gene drift or unknown selection of some over others that changes the phenotype over time.
Actually, you can sometimes get a range of phenotypes from a single genotype, but the genotype is the set of genes underlying the organism so you are really talking about things affecting genotype. Genetic drift is a population-level phenomenon - the loss or fixation of some genes as opposed to others in particular populations purely be chance - so this can affect the range of genotypes observed in a population and their relative frequencies, but it doesn’t really ”produce new phenotypes’ or genotypes - that would require mutation.
Faith writes:
I am saying that phenotypic divergence, which means NEW phenotypes, is produced by reduced GENETIC diversity.
There are certainly cases where events reducing allelic diversity in a population can result in the subsequent appearance of novel genotypes, but to say that their emergence is invariably dependent on reductions in allelic diversity would be incorrect. Firstly, all genotypes (and the phenotypes they give rise to) in a population are novel (unless there is asexual reproduction) - they exist in one genration only and are never re-created - so population diversity is to some degree always a function of population size.
Faith writes:
I think you are confusing diversity of genetic possibilities with diversity of phenotypic expression. Again, I'm ONLY talking about diversity of genetic possibilities, which is determined by numbers of alleles or availablility of alleles within a population.
Not at all. I am refering specifically to genotypes. I think you are failing to recognize that the ”diversity of genetic possibilities’ (in genotypes) is determined by more than simply allelic diversity. Remember chimps have > 97 % of genes (alleles) in common with humans, and yet the organization and coordinated expression of these alleles is very different in the two species. You wouldn’t say we are 97% the same as a chimp would you? Allelic frequencies are just one of the things we can measure to compare divergence between populations, but they are not the sole determinant of genetic diversity.
Faith writes:
And I don't know what you mean by "on a statistical level."
Simply allele frequencies. Higher order structure on the genome is another important component of genotypic diversity that transcends simple allele frequencies. Non-transcribed regions may have unrecognized importance here.
Faith writes:
what changes genetically when populations split is allele frequencies and this is all it takes to produce the new organismal forms.
Allele frequencies are one thing that will change inevitably with population subdivision and the range of genotypes will be affected, but it is not the only way new genotypes emerge. Let’s not forget about mutation. Even if mutation rates are similar across the genome in disparate populations, different alternative alelles may become fixed in the two by chance. So we might have a number of loci in which a single allele is fixed in the 2 populations (no alternative alleles floating around), so their allelic diversity at those loci is quantitatively equivalent, and yet their genotypes are qualitatively very different.
Faith writes:
And back we go to mutation, and again it's only a hypothetical and not a known.
But it IS a known. Mutations are observed and have been proven to occur. Crash gave the example a way back of the bacterial experiment where only mutation in the culture could account for the results. Yes, we cannot observe directly or predict exactly where or when a mutation will occur, but the evidence for their occurrence is overwhelming and undeniable.
Faith writes:
I'd love to see that this is really possible, that mutation, or at least some form of mutation, really does do this, really does recreate viable alleles that have been lost through such things as a bottleneck event.
I am not a molecular biologist, so someone like WK could probably provide you with better specifics, but there are recurrent mutations - changes between bases that tend to happen in particular sequences with higher probabilities than elsewhere on the genome. Alleles that are lost in a population can ocassionally reappear through recurrent mutation, although their fate in one population may be very different than their fate in another, even with similar rates of reversion. If we accept that errors during replication can occur, then they inevitably will occur - with some statistical probability. What is difficult to accept here? It seems to me that the alternative hypothesis - that all the chemical complexities of genetic replication must occur perfectly every time - is by far a more contrived and unlikely scenario.
Faith writes:
And there again is the cheetah, still getting along on one allele per locus over many loci without the benefits such a re-creation process would bestow on it.
Your mistaken inference is that mutations are not occurring simply because so many loci are fixed for a single allele. There likely are occuring, but rates are very low because effective population size is very low, or the sequences of the alleles in question are highly conserved.
Faith writes:
And again, the usual processes of allelic sorting and recombining are enough in themselves to produce new phenotypes; mutation is simply not needed.
Substituting ”genotype’ for phenotype, yes, you are correct. New genotypes can evolve without novel alleles, but that does not exclude the contribution of allelic diversity (created by mutation) to evolution. Novel alleles are required in order to produce novel proteins. There may be many situations where mutations are ”not needed’, but they happen anyway and they often contribute important changes to population structure. That changes in genotypic profiles in populations can occur without mutation is not evidence that mutations are not an important source of genetic diversity.

This message is a reply to:
 Message 118 by Faith, posted 09-02-2006 8:33 PM Faith has replied

Replies to this message:
 Message 124 by Faith, posted 09-03-2006 9:49 AM EZscience has replied
 Message 144 by Philip, posted 09-04-2006 2:45 PM EZscience has replied

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


Message 124 of 301 (346199)
09-03-2006 9:49 AM
Reply to: Message 123 by EZscience
09-03-2006 8:09 AM


Re: Mutation and diversity - no demonstrated relation
You are apparently talking about diversity of phenotypes when you say "at the level of organisms"
Actually, genotypes. Phenotypes have no heritability. The genotype is the set of heritable units in the organism, although it is not heritable as a unit itself.
For my purposes this is getting too technical. When we talk about the organismal changes that differentiate one population from another in a ring species, for instance, we are talking about phenotype, and it seems to do well enough for my purposes to keep the focus there. I'm aware that genotype is the coding FOR phenotype, but since it's a more complex level I'd rather stick to phenotype, and I don't see how that's a problem for this discussion.
Faith writes:
I have been talking about diversity in terms of available alleles only.
Fine. I am just pointing out that genotypic diversity is more than a simple function of numbers of available alleles.
As I answered you, I believe that numbers of available alleles is the basis on which that "more" is built, and it is best to keep the discussion simple if we can.
Faith writes:
Alleles don't HAVE to be reduced to produce new phenotypes, this can happen within a population with gene drift or unknown selection of some over others that changes the phenotype over time.
Actually, you can sometimes get a range of phenotypes from a single genotype, but the genotype is the set of genes underlying the organism so you are really talking about things affecting genotype.
Yes, but this is not necessary to the discussion.
Genetic drift is a population-level phenomenon - the loss or fixation of some genes as opposed to others in particular populations purely be chance - so this can affect the range of genotypes observed in a population and their relative frequencies, but it doesn’t really ”produce new phenotypes’ or genotypes - that would require mutation.
All it takes to produce new phenotypes OR genotypes is a new combination of alleles, which can arise even through genetic drift, although this is definitely more likely to happen in the case of a population split. A new combination arises within a population which produces a new phenotype which for some reason is favored and passed on. Note I'm saying this CAN happen. It could be a combination already present in the population that simply becomes favored and then becomes a more frequent type until perhaps eventually it comes to characterize the population as a whole. Gene drift CAN lead to a new population-wide phenotype, perhaps even speciation, and I see no reason to think this requires any more than the usual combinations and frequencies of alleles in the population from generation to generation. This is the only one of all the evolutionary processes of population genetics that I've read about that does not involve a form of population reduction or isolation to bring about phenotypic change or even speciation.
This continuing assertion of the need for mutation is simply not demonstrated, it is merely assumed. You underestimate the effect of the mere shuffling of alleles in the normal course of sexual recombination.
Faith writes:
I am saying that phenotypic divergence, which means NEW phenotypes, is produced by reduced GENETIC diversity.
There are certainly cases where events reducing allelic diversity in a population can result in the subsequent appearance of novel genotypes, but to say that their emergence is invariably dependent on reductions in allelic diversity would be incorrect.
I have very carefully said this is NOT invariable and the discussion above is a case in point. From the beginning my point has been that this is an overall trend of the processes that bring about speciation, and it may take generations to begin to show allele loss. Even in the case of population splits such as the ring species, alleles are not necessarily lost, at least not in the first split, but they MAY be. All that NEEDS to happen to bring about a new phenotype is a change in the frequencies of the alleles and the split will most likely bring that about as individuals with different alleles sort into the two populations. New traits then arise and over time spread in the new populations until a new phenotype comes to characterize each.
Firstly, all genotypes (and the phenotypes they give rise to) in a population are novel (unless there is asexual reproduction) - they exist in one genration only and are never re-created - so population diversity is to some degree always a function of population size.
Excellent point. Yes, they are ALL novel. In this basic constant production of novelty, one or a few individuals may have a set of traits that becomes favored for some reason or another and spread throughout the population and come to characterize it even to the point of speciation. IN the case of population splits which may eliminate some alleles the new phenotype may be rather dramatically different from the old population.
Faith writes:
I think you are confusing diversity of genetic possibilities with diversity of phenotypic expression. Again, I'm ONLY talking about diversity of genetic possibilities, which is determined by numbers of alleles or availablility of alleles within a population.
Not at all. I am refering specifically to genotypes.
Fine, but genotypes are on the same level as phenotypes in relation to what I'm talking about, since they are the INDIVIDUAL coding for the phenotype.
I think you are failing to recognize that the ”diversity of genetic possibilities’ (in genotypes) is determined by more than simply allelic diversity.
I think you are confusing this subject by bringing in extraneous considerations. I am focusing on allelic diversity which is ALWAYS there and it can be discussed exactly as I'm discussing it. It doesn't take anything more than a change in frequencies of alleles to bring about dramatic phenotypic AND genotypic changes in a population.
Remember chimps have > 97 % of genes (alleles) in common with humans, and yet the organization and coordinated expression of these alleles is very different in the two species. You wouldn’t say we are 97% the same as a chimp would you? Allelic frequencies are just one of the things we can measure to compare divergence between populations, but they are not the sole determinant of genetic diversity.
This is irrelevant to the point I'm trying to make. Please try to keep this simple. We are talking about the processes of speciation that can be observed, and allelic frequencies underlie it all, including the "organization and coordinated expression" thereof as I said in my previous post.
Faith writes:
And I don't know what you mean by "on a statistical level."
Simply allele frequencies. Higher order structure on the genome is another important component of genotypic diversity that transcends simple allele frequencies. Non-transcribed regions may have unrecognized importance here.
Please stick to allele frequencies. Other factors do not have to be brought into this. Allele frequencies alone can accomplish what I'm talking about.
Faith writes:
what changes genetically when populations split is allele frequencies and this is all it takes to produce the new organismal forms.
Allele frequencies are one thing that will change inevitably with population subdivision and the range of genotypes will be affected, but it is not the only way new genotypes emerge.
It is the only way that is under discussion, and it is sufficient by itself to bring about all the changes in both genotype and phenotype that come to characterize a new population to the point even of speciation.
Let’s not forget about mutation. Even if mutation rates are similar across the genome in disparate populations, different alternative alelles may become fixed in the two by chance.
Since the normal processes of allelic shuffling are enough all by themselves to bring about speciation, mutation becomes redundant, and truly, it has NOT been shown to have any role in the production of new phenotypes at any rate that would bring about speciation. It is assumed but it has not been demonstrated.
So we might have a number of loci in which a single allele is fixed in the 2 populations (no alternative alleles floating around), so their allelic diversity at those loci is quantitatively equivalent, and yet their genotypes are qualitatively very different.
This is adding unnecessary technicalities to this discussion.
Faith writes:
And back we go to mutation, and again it's only a hypothetical and not a known.
But it IS a known. Mutations are observed and have been proven to occur.
Yes, of course they are OBSERVED, of course they OCCUR, but their role in speciation is merely assumed, it has not been shown. Most of them don't do anything; others produce diseases, even diseases that survive in the population, and very very very few SEEM to have anything beneficial to confer on a population. And meanwhile there are thousands of other genetic factors that are constantly in operation that DO make a difference in the processes that lead to speciation, all this shuffling of already-present alleles that I've been talking about.
Crash gave the example a way back of the bacterial experiment where only mutation in the culture could account for the results. Yes, we cannot observe directly or predict exactly where or when a mutation will occur, but the evidence for their occurrence is overwhelming and undeniable.
I have NOWHERE denied this. I was not talking about their mere occurrence, which is not in doubt, but their character and their function in speciation and their effect on the population at all.
Faith writes:
I'd love to see that this is really possible, that mutation, or at least some form of mutation, really does do this, really does recreate viable alleles that have been lost through such things as a bottleneck event.
I am not a molecular biologist, so someone like WK could probably provide you with better specifics, but there are recurrent mutations - changes between bases that tend to happen in particular sequences with higher probabilities than elsewhere on the genome. Alleles that are lost in a population can ocassionally reappear through recurrent mutation, although their fate in one population may be very different than their fate in another, even with similar rates of reversion. If we accept that errors during replication can occur, then they inevitably will occur - with some statistical probability. What is difficult to accept here? It seems to me that the alternative hypothesis - that all the chemical complexities of genetic replication must occur perfectly every time - is by far a more contrived and unlikely scenario.
Even if it does occur it is apparently a very occasional thing and in actual observed reality hasn't been shown to contribute anything to the actual plight of species on the verge of extinction.
And there again is the cheetah, still getting along on one allele per locus over many loci without the benefits such a re-creation process would bestow on it.
Your mistaken inference is that mutations are not occurring simply because so many loci are fixed for a single allele. There likely are occuring, but rates are very low because effective population size is very low, or the sequences of the alleles in question are highly conserved.
Fine, they occur, which I haven't denied, but then the upshot of this is that mutations are useless even if they are in fact occurring, so why do you all make so much of them? However it happens, mutations simply are not having this hugely necessary influence that is so often imputed to them.
And again, the usual processes of allelic sorting and recombining are enough in themselves to produce new phenotypes; mutation is simply not needed.
Substituting ”genotype’ for phenotype, yes, you are correct.
THANK YOU. That's ALL I'm talking about. If you agree that the usual processes are sufficient, and that mutation is not needed, then we are on the same page. Please let's stay there.
I guess I can keep on saying "genotype OR phenotype" since you insist. I guess in the end it really does not make an important difference.
New genotypes can evolve without novel alleles,
Thank you.
but that does not exclude the contribution of allelic diversity (created by mutation) to evolution.
Theoretically it does not, but in actuality it has not been shown, and everything everybody has said about the actuality of mutations continues to add up to a big lack of contribution of anything of any value to the processes that are said to bring about evolution. Meanwhile the normal processes of allelic shuffling are ongoing and potent in their production of genotypic/phenotypic variations.
Novel alleles are required in order to produce novel proteins.
Is there such a thing as a truly novel protein or a truly novel allele for that matter? And what would guarantee that such novelty would be of any real use? Aren't there enough proteins and alleles already in circulation to float the whole boat of what is actually observed in species variation?
There may be many situations where mutations are ”not needed’, but they happen anyway and they often contribute important changes to population structure.
So it has been said many times, but when it comes down to discussion of the actual observed occurrences and effects of mutations they simply do not cut the mustard. How could they possibly "contribute important changes to population structure" considering their rarity of occurrence, their usual lack of effect at all, their frequent effect in disease processes and their extremely rare supposedly beneficial effect? Please. This is constantly asserted, but it has not been demonstrated at all.
That changes in genotypic profiles in populations can occur without mutation is not evidence that mutations are not an important source of genetic diversity.
I haven't presented it as evidence against mutations. (Mutations are evidence enough against themselves from what has been said about them.) All I have been saying is that allelic sorting is sufficient to drive all the changes that lead to speciation. If mutation enters into this somewhere, sobeit, but it doesn't change this basic fact.
Edited by Faith, : No reason given.

This message is a reply to:
 Message 123 by EZscience, posted 09-03-2006 8:09 AM EZscience has replied

Replies to this message:
 Message 161 by EZscience, posted 09-05-2006 12:16 PM Faith has not replied

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


Message 125 of 301 (346214)
09-03-2006 10:56 AM
Reply to: Message 119 by Faith
09-02-2006 8:47 PM


Re: On predictions and tests.
Dang, Crash, I may love you after all, mutation notwithstanding.
I don't see your point as wrong, but akin to Nosyned, I don't see it as terribly significant, either. Assuming that speciation is a discreet "event" that you can point to, and it usually isn't - it's more akin to the question "when does it start raining?" - we would expect a certain statistical loss of genetic diversity right then.
Almost immediately, though, the diversity is going to rise in both populations, because it's always rising.
So, while I see the merit in your position - I always have - your position is predicated on a certain simplification of speciation, and certainly represents no obstacle to evolution due to the constant rising diversity seen in populations.
I'm just saying. I think you deserve credit for the things that you are right about, and it's these kinds of insights that convince everybody you're far more intelligent than generally given credit for, but you haven't overturned evolution just yet.

This message is a reply to:
 Message 119 by Faith, posted 09-02-2006 8:47 PM Faith has replied

Replies to this message:
 Message 127 by Faith, posted 09-03-2006 11:57 AM crashfrog has replied

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


Message 126 of 301 (346220)
09-03-2006 11:28 AM
Reply to: Message 105 by crashfrog
09-02-2006 1:01 PM


Evolution NEEDS mutations but they aren't up to the job
Finally I get to this post.
What I'm asking is whether it is a mistake, a disease process, an attack on the integrity of the organism, or really can be relied upon to produce something useful.
Well, from experiments that we've performed, we believe that there's ample reason to conclude that the answer to this question is "yes."
Yes it's all of those things I guess you are saying. I guess there's no way to tell from the kind of mutation it is which effect it is going to have? I mean whether it reverses the order of the bases, or jumps a chromosome or whatever?
One interesting thing about bacteria -- I suspected this or at least wondered so I looked it up and sure enough, bacteria don't have any junk DNA.
This is true. The proper name for the sequences you're referring to are called "introns", and they are sequences within genes that are replicated from generation to generation, but spliced out from the RNA product after transcription.
The amount of introns in the genome varies from species to species, and even from individual to individual, and the origins of this material is probably quite varied. Some of these sequences appear to be accumulated duplications and reduplications that occur via mutations. Some of them appear to be endogenous retroviral sequences that the host has deactivated for its own protection. Some of them appear to be a mechanism to encode multiple protein products into the same gene; a kind of "genetic compression."
But whatever they are specifically, junk DNA overall appears to be some sort of genetic graveyard, yes?
But, it's true that they are only found in eukaryotic organisms, and not in prokaryotes like bacteria. It may very well be that the fact that a eukaryote has a membrane-bound nucleus to cram all it's DNA into, while the prokaryote does not, means that the prokaryote simply doesn't have the room to store an enormous amount of introns.
Well, another question is how much actual coding DNA does bacteria have? Some worm or other small organisms have more than human beings do, correct?
But all this is really a side issue. On to the meat of the discussion:
Chipmunks do not need mutations. None of us need mutations. All the diversity of traits / phenotypes imaginable is possible with merely the given allotment of alleles.
But where would those alleles come from, if not mutation?
Finally, this is the crux of the matter of mutation I believe. It's not that mutations have been OBSERVED to do all the work ascribed to them, it is simply ASSUMED that they do because without them evolution can't explain the ORIGIN of all the alleles already present. Am I reading this right?
The creationist answer to your question is that all the alleles and genes in existence have been present since the Creation (and we figure LOTS of them have died, and I think possibly ended up in that junk DNA graveyard).
And what about if an environment required a trait that nobody had an allele for?
Happens, doesn't it? Either there is an adaptation possible from the assortment of alleles available in the population, or the population goes extinct.
But this raises the question how on earth this random unpredictable rare occurrence of useful mutations could possibly be expected to provide the necessary adaptive allele in such a circumstance. You mean as soon as an inhospitable environment is encountered, presto chango abracadabra The Mighty Mutation comes along right on cue and supplies the necessary protection against the environment before it kills off our victim species? Where is there any evidence that such a thing is possible, let alone that it actually occurs? Doesn't this expectation that such a useful thing could be counted on amount to a teleology?
It seems to me that every living thing needs mutations, simply because without mutation, the number of different alleles and therefore the number of possible phenotypes is finite and limited by what you already have.
That is true. But this is only a problem for evolutionists; it doesn't bother creationists. We know they are sufficient for all the variations we see coming about all the time, all kinds of new breeds. We also figure they are very gradually being reduced in all species as well.
Only mutation allows for potentially limitless variation, and the introduction of new alleles into the population.
Yes, this is exactly what evolution requires, isn't it? For there to be potentially limitless variation, mutation HAS to occur, doesn't it?
I believe you are implicitly acknowledging here that even if there isn't actual proof of mutations bringing about the limitless variation evolution requires, it is assumed that they do, because without them evolution is a dead duck.
Mm but exactly how certain are you that no ancestory had it, and that it's not just an extremely rare one that happened to pop up?
How could it be that rare? Think back to the mendelian genetics that you're familiar with. Surely, at the time you learned that, you did some simple problems in inheritance? If you inherited the gene from your ancestors, they surely must have expressed it then, too. You only get genes from your mother and father. You don't get any genes from your great-great-granduncle twice removed unless that gene was in one of your parents, too.
Yes, but that's focusing on an individual. My mistake I guess since of course if an individual has it then it was passed down. But if you focus on the population at large, it is possible for there to be a rare or recessive allele out there somewhere that gets expressed, especially if the population is greatly reduced, and if there are favorable circumstances, it could even increase in frequency and come to spread in the population, that trait eventually characterizing the majority.
If an organism has a gene, and we want to know where that gene came from, it's sufficient to examine the genome of both parents. If neither of them have the gene, then we know it arose through mutation. You don't get genes from anybody except your parents.
Got it. But still, a gene could be rare in a population as a whole, no?
But ruling out the possibility of rare alleles coming to expression can't be a sure thing.
Sure it can. If we grow a population of bacteria from a single individual, who at most can only have one allele per every gene, then we know that there's only one allele that organism can pass on to its decendants - that, indeed, the whole population should have no more than one allele per every gene. If there are more alleles than that we know that mutation is the origin, because there's no other source. The original founder of the population didn't have any "room" for any other alleles, rare or not.
But what about complex organisms? There it is not all that easy to rule out the possibility of a rare allele -- Quetzal's orange sock, remember? -- in the population. Rare meaning very low frequency.
And again, if they are mutations, are these really viable alleles mutation is bringing about?
They must be, if we're detecing them in these experiments. Nonviable alleles would lead to the immediate death of the organism before we could possibly hope to detect it in one of our samples.
In complex organisms at least, it appears possible that all kinds of less-than-desirable mutations may spread in the population and not lead to immediate death.
Do they look like normal alleles? Do they code the same way? And what effects do they cause?
Well, they "code the same way" in the sense that the mutation results in DNA that's made of the four nucleotide bases, just like "normal" DNA. That doesn't ever change.
What effects do they cause? That's random, and it depends obviously on what the mutation did to the gene, what the gene does, what it's protein does, the shape of its protein, etc.
This being the case, Crash, isn't it a fair inference from these facts that mutation couldn't possibly be relied upon to supply an adaptive allele to deal with environmental threats? I suppose you are assuming very gradual changes in long time frames here, but even then the rate of mutation of any kind whatever, let alone possibly useful ones, seems astronomically unlikely to turn up one that might provide precisely the adaptive value needed in a particular environmental pinch. In fact if anything borders on "God did it," or sheer magic, this does. It is far easier to assume that the allele(s) for the needed adaptation is already present among the allelic possibilities in the population, having been there all along, and gets selected by the environmental threat itself. If you want to say that mutation put it there in the first place, and it's been there since then, well, then we're back to assuming this because evolution needs it anyway, since it can't be proved to be the case. Far more likely all the genetic possibilities were built in back in Eden. Oh I suppose there could be some mutational effects in here somewhere, for repairing broken genes maybe, restoring lost alleles maybe, but not of a degree that would fuel evolution.
Then the questions about what the change actually does are the main thing.
Yes. That's the focus of the ongoing research into genetics and proteinomics.
And I guess we know so far that the effects are mostly neutral, a far number deleterious, even some that aren't lethal at least right away, and very very few are possibly useful.
And what does that work out to in a human time frame? How many viable new alleles per unit of time?
Your genome is about 6 billion base pairs long, and that gets replicated a lot. Obviously, it was replicated enough to take you from a single-celled zygote to a human being with literally billions of cells.
It's replicated every time natural cell division occurs, as you generate new hair, new skin, new blood cells, a new intestinal lining, every part of your body that grows, or regenerates, or is replenished. It was replicated to create every one of your ova cells. It's replicated every time I generate a sperm.
Every single one of those replications introduces about 2 point substitutions, plus other kinds of mutations, into the resulting cells. The genome is large enough and redundant enough that most of those changes do nothing. Sometimes they result in a cell that our bodies destroy immediately. Very, very rarely they may result in a cell that begins to divide uncontrollably, and that's a very dangerous situation indeed. Sometimes they result in a cell with some minor improved fuction, but amongst the billions of cells in my body that doesn't really matter.
Sometimes they result in a mutation to one of my sperm cells, and then the offspring that results from that sperm carries the mutation in every one of its cells. If the mutation signals tissues to develop in a different way than normal, those effects could be very profound indeed, and result in the development of what you might call a different "body plan."
I guess the point here is that mutations do a lot, and to try to summarize every effect that a mutation could have would be impossible. The effects of mutations are limitless because what genes do is limitless. Every physical property of every single organism (barring a few exceptions) is governed by the interaction of genes.
I find it a bit scary myself that there is so much of it since the vast majority of the changes are not clearly desirable. The neutral ones are a wild card it seems. Nothing in all that shows anything that could be relied on for useful or adaptive changes.
Genes are the blueprint of life, as they say. So what you're asking me is essentially "what can you design on a blueprint?" Obviously, the answer there is "almost anything."
But what evolution needs is mutations that contribute alleles that can form viable useful variations, and nothing in any of that whole process you just outlined, which tosses up mostly unknowns and undesirables, suggests such a possibility in reality, except at such an astronomically low probability it's as good as nothing at all.
This plus the fact that I'm convinced that normal allelic shuffling and transmission is all that's needed to account for all the processes of phenotype divergence, which makes mutations inexplicable.
Well, I can point out how you're wrong with simple math. Any finite population of individuals holds a finite number of alleles. Any finite number of things can only combine in a finite number of ways.
That is true. But this number is still large enough for the number of possible combinations to produce very striking variations.
So clearly, allele recombination can't be expected to result in limitless numbers of phenotypes, but only in a limited number of different combinations, even if that number is very large.
That is quite true, but it is evolution that demands the limitless variations, not creationism. The existing stash of alleles is quite sufficient for enormous variations, even after millennia of attrition due to the Fall. It won't ever produce anything beyond the Kind though.
And obviously that's kind of your point; that the evolutionary history of life is false because there's no way to get that kind of limitless variation - goo to you, or whatever - from nothing but alleleic recombination.
Yay, Crash, that is absolutely correct.
Well, you're right about that. That's why mutation exists, and persists in every organism - because it's a source of variation that has no limit. And that's why the evolutionary history of life is possible, because there's no limit to phenotypic variation, thanks to mutation.
Absolutely. Evolution absolutely depends upon mutation. Unfortunately what is actually known of mutations does not bode well for their capacity to work the miracles needed by evolution.
Edited by Faith, : No reason given.

This message is a reply to:
 Message 105 by crashfrog, posted 09-02-2006 1:01 PM crashfrog has replied

Replies to this message:
 Message 128 by crashfrog, posted 09-03-2006 1:53 PM Faith has replied

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


Message 127 of 301 (346222)
09-03-2006 11:57 AM
Reply to: Message 125 by crashfrog
09-03-2006 10:56 AM


Rise in which kind of diversity?
I don't see your point as wrong, but akin to Nosyned, I don't see it as terribly significant, either. Assuming that speciation is a discreet "event" that you can point to, and it usually isn't - it's more akin to the question "when does it start raining?" - we would expect a certain statistical loss of genetic diversity right then.
I'm not so much pointing to the speciation "event" as to the allelic circumstances that bring it about. Back to the example of the ring species, which is a series of populations that migrated each from the former, in other words sticking to the example that best shows what I'm trying to say, the processes that lead to speciation START with the population split. I'm focusing on the situation of a reduced number of individuals being isolated, so that they stop interbreeding with the former population, or at least mostly stop, and inbreed among themselves. This is what happens in various forms of "evolutionary processes" including selection processes. While some processes such as bottleneck will severely alter allele frequencies, in fact eliminate most of them, in most other circumstances the process is slower, but over time you still get to the point where you have fewer alleles, reduced genetic diversity AND strikingly new phenotypes. In the ring species, the reduction in allelic diversity may not be apparent until the last population in the series. The new species doesn't really emerge until the new allelic situation has worked itself through the new population, and I agree there is no absolute identifiable point when this can be said to have occurred.
Almost immediately, though, the diversity is going to rise in both populations, because it's always rising.
I note you say "diversity" rather than "genetic diversity" and this makes all the difference, and this ambiguity I think is responsible for much confusion on this subject as people have been using it in different senses and thereby missing my whole point.
Diversity at the level of phenotype (or genotype) or at the "organismal" level WILL rise. But this is BECAUSE of
1) change in allele frequencies, which may include, and does include in severely reduced populations or after many population splits,
2) actual loss of alleles.
In other words, an increase in one kind of diversity is the product of either a change in frequencies or a decrease in the other kind of diversity. Not an increase, which only happens in the case of hybridization.
{EDIT: The use of "diversity" in relation to phenotype is a mistake that confuses the discussion. I allowed myself to accept the term "diversity" against my better judgment. I'm trying to talk about phenotypic divergence or genotypic divergence from the original population, not diversity. New traits do emerge which is a sort of diversity, but all that I want to focus on is the new phenotypes themselves as divergent from the old. This is brought about by new frequencies of alleles which often involves a loss of alleles which is a reduction in genetic diversity. }
New phenotypes emerge when new alleles are expressed at the expense of alleles that defined the old phenotype. This happens most dramatically when the old alleles are completely eliminated from the population.
BUT, if you DO mean GENETIC diversity "is going to rise" no. Only diversity of phenotypes will rise. And this is BECAUSE there is less genetic diversity.
If you are claiming a rise in numbers of alleles, and therefore genetic diversity, has been OBSERVED, nobody has shown this to be the case. It has merely been assumed and asserted. The occasional mutation has been observed, but its role in the processes under discussion could only be negligible.
So, while I see the merit in your position - I always have - your position is predicated on a certain simplification of speciation, and certainly represents no obstacle to evolution due to the constant rising diversity seen in populations.
True, you appreciated it early on, thank you.
Again that ambiguous use of "diversity." Again, of course we see PHENOTYPIC/GENOTYPIC diversity rising. What I am doing is EXPLAINING this rise in phenotypic diversity by the reduction of ALLELIC diversity.
And again, if you mean allelic diversity is rising, this has not been shown to be the case.
I'm just saying. I think you deserve credit for the things that you are right about, and it's these kinds of insights that convince everybody you're far more intelligent than generally given credit for, but you haven't overturned evolution just yet.
Odd way to put it but I know what you're trying to say, so thanks. In any case, I think the creationists overturned evolution years ago myself, but anyway.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.
Edited by Faith, : bunch of edits to provide indents, signature, various grammatical improvements.
Edited by Faith, : Added Edit section in middle.

1Corinthians 1:25-29: Because the foolishness of God is wiser than men; and the weakness of God is stronger than men. For ye see your calling, brethren, how that not many wise men after the flesh, not many mighty, not many noble, [are called]: But God hath chosen the foolish things of the world to confound the wise; and God hath chosen the weak things of the world to confound the things which are mighty; And base things of the world, and things which are despised, hath God chosen, [yea], and things which are not, to bring to nought things that are: That no flesh should glory in his presence.

This message is a reply to:
 Message 125 by crashfrog, posted 09-03-2006 10:56 AM crashfrog has replied

Replies to this message:
 Message 129 by crashfrog, posted 09-03-2006 2:08 PM Faith has replied

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


Message 128 of 301 (346243)
09-03-2006 1:53 PM
Reply to: Message 126 by Faith
09-03-2006 11:28 AM


Mutation - The Creative Force
I guess there's no way to tell from the kind of mutation it is which effect it is going to have? I mean whether it reverses the order of the bases, or jumps a chromosome or whatever?
We can say what kinds of mutations are statistically more likely, what kinds of results are more likely than others, but no, when we introduce mutagens, there's no way to predict what kind of effect they'll have. That's what we mean when we say mutation is random.
But whatever they are specifically, junk DNA overall appears to be some sort of genetic graveyard, yes?
I guess I wouldn't say that, no. The term "junk DNA" isn't even a scientific term, really. In eukaryotes, genes contain sequences that are transcribed onto mRNA but are spliced out before protein translation. I don't think it's fair to call that stuff a "genetic graveyard", in fact sometimes those sequences form a kind of genetic "nursery". They're not where genes always go to die; sometimes, they're where genes are born, too.
Well, another question is how much actual coding DNA does bacteria have?
It varies by species. If you're curious, I'd just Google it.
It's not that mutations have been OBSERVED to do all the work ascribed to them, it is simply ASSUMED that they do because without them evolution can't explain the ORIGIN of all the alleles already present. Am I reading this right?
No, you're not. Mutations are observed to do all the work ascribed to them, because experiments are set up where nothing is avaliable to do the work but mutation, and the result of these experiments is that the work is done.
Look, I don't know how it gets any clearer than that - a simple experiment to test the results of a known process in isolation. It's exactly what you would do to see if a known process or actor had the capability to do what was claimed - you'd test that process or actor in isolation, and if the work was done, you'd know that process or actor was responsible.
Isn't that clear? How is that not clear proof of the creative power of mutation?
The creationist answer to your question is that all the alleles and genes in existence have been present since the Creation
If that's true, then where are all the new alleles coming from? You seem to think that you can just dismiss that question and say that there aren't any new alleles, but I've told you already how we know that's not true. We can set up experiments where any additional alleles we observe have to be new ones, not ones that were already there but "hidden." So we know that new alleles are showing up.
Where are they coming from, if not mutation?
You mean as soon as an inhospitable environment is encountered, presto chango abracadabra The Mighty Mutation comes along right on cue and supplies the necessary protection against the environment before it kills off our victim species?
No. The required mutation is already there, somewhere in the population, or else the whole population goes extinct. It arose at random before it was needed. (Or else it didn't, and the population goes extinct.)
Again, this is something that we have proven experimentally. A sample of bacteria taken out of the bioreactor shows that some of them, just at random, usually have an adaptive resistance to an antibiotic that hasn't yet been introduced into the population. It's not magic, it's not seeing into the future - it just happens at random.
Doesn't this expectation that such a useful thing could be counted on amount to a teleology?
I don't see it as telological, since 99.9% of all species that have ever lived are now extinct. Clearly, eventually, an environment always comes along for which no mutative adaptation exists in the population, yet. Hence, extinction.
But if you focus on the population at large, it is possible for there to be a rare or recessive allele out there somewhere that gets expressed
In an individual. And that rare allele is only rare to the population at large. If the individual has it, inherited it, it has to be common among his ancestors. Otherwise it's only rare because he's the first one to have it, because it's a mutation.
There it is not all that easy to rule out the possibility of a rare allele -- Quetzal's orange sock, remember? -- in the population. Rare meaning very low frequency.
If an individual inherited it, it has to have high frequency within his ancestry. 1/2 of his parents, at least, have to have the gene. That's a pretty high frequency right there.
In complex organisms at least, it appears possible that all kinds of less-than-desirable mutations may spread in the population and not lead to immediate death.
Sure. But, again, the experiments to which I'm referring have been conducted on bacteria and other fast-growing organisms.
This being the case, Crash, isn't it a fair inference from these facts that mutation couldn't possibly be relied upon to supply an adaptive allele to deal with environmental threats?
Most species go extinct when the environment changes. The vast, vast majority of all species that have ever lived are now extinct. This is something very important to keep in mind.
I don't know that it can be "relied on," in other words. If you're sitting around waiting to mutate in order to have some specific advantage, you're probably going to die waiting (literally.)
But that's totally the wrong perspective to look at it. Look at it the other way - every species that didn't die waiting, didn't die because it mutated. The amazing variety of life you observe on planet Earth in this day is but a very small fraction of all the variety that has existed over time. They're the sole survivors of a hostile universe. The lottery winners, if you will. We few, we lucky few, we band of brothers.
I suppose you are assuming very gradual changes in long time frames here, but even then the rate of mutation of any kind whatever, let alone possibly useful ones, seems astronomically unlikely to turn up one that might provide precisely the adaptive value needed in a particular environmental pinch.
99.9% unlikely, we might say.
I find it a bit scary myself that there is so much of it since the vast majority of the changes are not clearly desirable.
Well, wear sunscreen and eat less red meat. Eat vegetables rich in anti-oxidants. All that stuff people say "fights cancer"? What they really mean is that those things reduce your exposure to, or mitigate the effects of, mutagens in your environment.
But, hey. Did you really expect to live forever? Almost everybody who lives long enough gets cancer, unless you die of something else first. (That might be a tautology, I hope you'll accept it as a joking one.)
But what evolution needs is mutations that contribute alleles that can form viable useful variations, and nothing in any of that whole process you just outlined, which tosses up mostly unknowns and undesirables, suggests such a possibility in reality, except at such an astronomically low probability it's as good as nothing at all.
"Low" isn't the same as "None." That's your big mistake. An astronomically low probabilaty isn't the same as nothing at all - it's much, much greater than that.
The astronomically low probability is more than enough to account for the variation among the Earth's countless individual living things, all those today, all those who have ever lived. Try to think how many individual living things that would be over 3 billion years, and then come back and tell me that 2-3, or 50-500 mutations per individual is the same as no mutations at all. Even if only 1 in 100 of those individuals had a beneficial mutation, can you imagine how many that would be? How can that be the same as none at all?
But this number is still large enough for the number of possible combinations to produce very striking variations.
Sure. But remember that Mendel figured out discreet genetic inheritance from nothing but examining pea plants. He had no knowledge of the actual mechanisms of molecular genetics. So clearly, in a lot of cases, the range in variation isn't that great.
The existing stash of alleles is quite sufficient for enormous variations, even after millennia of attrition due to the Fall.
I simply don't see alleleic recombination as supportive of enough diversity to account for the diversity of living things we see today and in the fossil record.
Evolution absolutely depends upon mutation. Unfortunately what is actually known of mutations does not bode well for their capacity to work the miracles needed by evolution.
Well, let me assure you that the science proves the exact opposite - that mutation is the source of more than enough genetic novelty to account for the origin of all alleles. No miracles needed, just successive changes adding up over countless generations.

This message is a reply to:
 Message 126 by Faith, posted 09-03-2006 11:28 AM Faith has replied

Replies to this message:
 Message 130 by Faith, posted 09-03-2006 8:30 PM crashfrog has replied

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


Message 129 of 301 (346245)
09-03-2006 2:08 PM
Reply to: Message 127 by Faith
09-03-2006 11:57 AM


Re: Rise in which kind of diversity?
I'm not so much pointing to the speciation "event" as to the allelic circumstances that bring it about.
Well, speciation is not driven by alleles, it's driven by environment. So I don't know what circumstances you're referring to.
Diversity at the level of phenotype (or genotype) or at the "organismal" level WILL rise. But this is BECAUSE of
1) change in allele frequencies, which may include, and does include in severely reduced populations or after many population splits,
2) actual loss of alleles.
1 I think you're right about. 2 I don't understand. How could a loss of alleles be an increase in diversity?
Did I do the paint shop analogy once? Paint shops mix paint by adding color concentrates ("primaries") to white bases. So if you can imagine a paint shop with, say, four colors (cyan, magenta, yellow, and black), they can mix a certain range of colors (we call this range a "gamut".) If we use 5 or 6 colors instead of 4, we can mix a larger gamut of colors. So, the different primary colors we choose to use are the alleles in this example.
But if we take some of those alleles away, how can we possibly wind up with a larger gamut? If we only have cyan, yellow, and black, how can we possibly have a wider gamut than if we had magenta as well?
You've long asserted that the loss of alleles can mean a greater diversity, but diversity is determined by the number of alleles at a given locus, so I simply don't see how that can be true. I don't recall you explaining it very well, so I guess I have to ask you once more to attempt to do so for my benefit, if you wish.
Again, of course we see PHENOTYPIC/GENOTYPIC diversity rising. What I am doing is EXPLAINING this rise in phenotypic diversity by the reduction of ALLELIC diversity.
That doesn't make any sense to me.
And again, if you mean allelic diversity is rising, this has not been shown to be the case.
I understand you to mean, by "allelic diversity", what scientists refer to as "genetic diversity", that is, the number of different alleles within a population for a given gene. If that's the case, I don't understand how less alleles can result in more diversity of either phenotype or genotype. Less alleles would mean that every individual was more similar to its conspecifics, and that's the exact opposite of diversity.
If that's not what you mean, I have no idea what you mean. Maybe you mean something else by "diversity"? I assume that word to mean "the degree to which individuals tend to be different than each other." The least possible diversity in a population would be a population of clones, and such a population would by definition have the least possible alleles.

This message is a reply to:
 Message 127 by Faith, posted 09-03-2006 11:57 AM Faith has replied

Replies to this message:
 Message 131 by Faith, posted 09-03-2006 9:30 PM crashfrog has replied

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


Message 130 of 301 (346292)
09-03-2006 8:30 PM
Reply to: Message 128 by crashfrog
09-03-2006 1:53 PM


Re: Mutation - The Creative Force
Mutations are observed to do all the work ascribed to them, because experiments are set up where nothing is avaliable to do the work but mutation, and the result of these experiments is that the work is done.
Crash, great claims are made for mutations, very great claims. Mutations are evoked to explain speciation in all creatures. They are evoked to explain the formation of new phenotypes /genotypes /organismal diversity in ring species or in any species.
From what I've been arguing here, it is not needed to produce new phenotypes at all, shuffling of pre-existing alleles alone can explain absolutely everything that has occurred in this process, all the way out to frank speciation.
And so far the only experiment you've actually referenced is this one with the bacteria. By the way, is that experiment performed frequently and always with the same results? And I assume you examine the genome of the bacteria before and after the mutation event, so what exactly are you seeing there in the basic genetic stuff? Is it possible to pinpoint the mutation, identify what it did to the DNA, and the protein it codes for and all that?
Anyway, I have no problem with the fact that mutation occurs, but I continue to maintain that so far nothing has been shown that comes anywhere near supporting the great claims that are made for it, and quite a bit of evidence that suggests otherwise.
I do wonder about the occasional beneficial mutation. EZ suggested that one kind may restore or replace a lost allele. He didn't have evidence, merely hypothesized it, saying that mathematically it is likely. In any case, this is interesting to think about. But even if it occurs, that is not enough beneficial mutation to power evolution, and not even the right kind since it's more like a healing process.
And again, what DOES power evolution, microevolution I mean -- meaning the development of new phenotypes -- is the normal processes of gene drift, population splitting, migration, allelic shuffling and often allele loss and so on. Mutation is simply being mentally substituted in the role of these normal processes, being assumed to perform the functions these normal processes perform.
Please show me that mutations occur often enough even to make a difference in the development of a new phenotype in a ring species.
Look, I don't know how it gets any clearer than that - a simple experiment to test the results of a known process in isolation. It's exactly what you would do to see if a known process or actor had the capability to do what was claimed - you'd test that process or actor in isolation, and if the work was done, you'd know that process or actor was responsible.
Isn't that clear? How is that not clear proof of the creative power of mutation?
Well, I know you get mutations. I know sometimes they spread in populations. I don't know what the relevance of getting them in bacteria is to chipmunks. For all I know this is simply an expectable natural form of reproduction and not a mutation of the mistake kind.
You've claimed you can do the same sort of experiment in other species, so could you give me a reference to such experiments?
The creationist answer to your question is that all the alleles and genes in existence have been present since the Creation
If that's true, then where are all the new alleles coming from?
What new alleles? I think you are mostly assuming new alleles rather than proving they exist. I mean truly novel chemical coding stuff that codes for something the cell can actually use. You have claimed this happens but all I've seen is processes that would bring up previously suppressed alleles, recessive alleles and so on.
You seem to think that you can just dismiss that question and say that there aren't any new alleles, but I've told you already how we know that's not true. We can set up experiments where any additional alleles we observe have to be new ones, not ones that were already there but "hidden." So we know that new alleles are showing up.
Where are they coming from, if not mutation?
Please again reference these experiments. I haven't been impressed with what you've shown so far.
You mean as soon as an inhospitable environment is encountered, presto chango abracadabra The Mighty Mutation comes along right on cue and supplies the necessary protection against the environment before it kills off our victim species?
No. The required mutation is already there, somewhere in the population, or else the whole population goes extinct. It arose at random before it was needed. (Or else it didn't, and the population goes extinct.)
OK, big hypothetical there. You say all the pre-existing stuff mutated there. You are merely ASSUMING that it mutated there. I assume it was created there in the very beginning.
Again, this is something that we have proven experimentally. A sample of bacteria taken out of the bioreactor shows that some of them, just at random, usually have an adaptive resistance to an antibiotic that hasn't yet been introduced into the population. It's not magic, it's not seeing into the future - it just happens at random.
Well, drat, Crash, this is what I assumed was the case way back, that the adaptive potential was already present in the population and merely selected out in the presence of the antibiotic. Its already being there fits MY model. YOU have to show that it APPEARED in response to the antibiotic or you have not proved anything about mutations having anything to do with it.
Doesn't this expectation that such a useful thing could be counted on amount to a teleology?
I don't see it as telological, since 99.9% of all species that have ever lived are now extinct. Clearly, eventually, an environment always comes along for which no mutative adaptation exists in the population, yet. Hence, extinction.
But the odds against a mutation happening along EVER that can protect against a completely unpredictable environmental change is just beyond calculation in the real world.
But if you focus on the population at large, it is possible for there to be a rare or recessive allele out there somewhere that gets expressed
In an individual. And that rare allele is only rare to the population at large. If the individual has it, inherited it, it has to be common among his ancestors. Otherwise it's only rare because he's the first one to have it, because it's a mutation.
Yes, it has to be common among his ancestors, most of whom are back in the first population that the new population split from if we're talking about a new ring species population for instance, and where this trait of his ancestors may have occurred at a relatively low frequency or been recessive or that sort of thing.
There it is not all that easy to rule out the possibility of a rare allele -- Quetzal's orange sock, remember? -- in the population. Rare meaning very low frequency.
If an individual inherited it, it has to have high frequency within his ancestry. 1/2 of his parents, at least, have to have the gene. That's a pretty high frequency right there.
But we are talking about population level changes.
In complex organisms at least, it appears possible that all kinds of less-than-desirable mutations may spread in the population and not lead to immediate death.
Sure. But, again, the experiments to which I'm referring have been conducted on bacteria and other fast-growing organisms.
Again, the role you claim that mutations play in the whole process of evolution of all species is not going to be proved by your ability to create a culture of mutated bacteria. And if what you said above is the case, that the different bacteria were already in the population, then scrap the whole show because that fits MY model.
This being the case, Crash, isn't it a fair inference from these facts that mutation couldn't possibly be relied upon to supply an adaptive allele to deal with environmental threats?
Most species go extinct when the environment changes. The vast, vast majority of all species that have ever lived are now extinct. This is something very important to keep in mind.
*I* have no problem keeping this in mind. It's the tragic consequence of the Fall. And what I've been arguing is that it is very likely to occur at the far edge of the evolutionary processes, at the extremity of allele depletion, because it is this depletion which is the overall trend of all these processes, and ultimately powers the formation of new phenotypes to the point of speciation. Allelically depleted species simply do not have the capacity to produce an adaptive variety. So in my model extinction is the natural ultimate end of all the evolutionary processes. Were it not for the Fall, even the most extremely allelically-depleted species would exist without threat of extinction.
I don't know that it can be "relied on," in other words. If you're sitting around waiting to mutate in order to have some specific advantage, you're probably going to die waiting (literally.)
My point exactly.
But that's totally the wrong perspective to look at it. Look at it the other way - every species that didn't die waiting, didn't die because it mutated. The amazing variety of life you observe on planet Earth in this day is but a very small fraction of all the variety that has existed over time. They're the sole survivors of a hostile universe. The lottery winners, if you will. We few, we lucky few, we band of brothers.
Well, that's the evolutionary model for sure. In my model those that didn't die waiting, didn't die because those normal adaptive variations that had been provided them back at the Creation, happened to be still available to them despite horrific losses over the millennia. Not mutation, original creation.
I suppose you are assuming very gradual changes in long time frames here, but even then the rate of mutation of any kind whatever, let alone possibly useful ones, seems astronomically unlikely to turn up one that might provide precisely the adaptive value needed in a particular environmental pinch.
99.9% unlikely, we might say.
More like .0000000000000000001 likely. But anyway, how can you expect mutation to be anywhere near the kind of influence you are all claiming given its rarity, its high proportion of uselessness which may in fact be destructive in the end, and so on?
I find it a bit scary myself that there is so much of it since the vast majority of the changes are not clearly desirable.
Well, wear sunscreen and eat less red meat. Eat vegetables rich in anti-oxidants. All that stuff people say "fights cancer"? What they really mean is that those things reduce your exposure to, or mitigate the effects of, mutagens in your environment.
But, hey. Did you really expect to live forever? Almost everybody who lives long enough gets cancer, unless you die of something else first. (That might be a tautology, I hope you'll accept it as a joking one.)
Oh I'm not thinking of myself, just the plight of the creation. I expect all the death and ultimate exinction. It fits my model. But you guys are pursuing this fantasy of its all being normal, and that's far scarier than facing the facts of what is really happening.
But what evolution needs is mutations that contribute alleles that can form viable useful variations, and nothing in any of that whole process you just outlined, which tosses up mostly unknowns and undesirables, suggests such a possibility in reality, except at such an astronomically low probability it's as good as nothing at all.
"Low" isn't the same as "None." That's your big mistake. An astronomically low probabilaty isn't the same as nothing at all - it's much, much greater than that.
It isn't enough to do what you all claim it must do. It just isn't. Astronomically far from it.
The astronomically low probability is more than enough to account for the variation among the Earth's countless individual living things, all those today, all those who have ever lived.
Here comes the Credo, the Statement of Faith.
Try to think how many individual living things that would be over 3 billion years, and then come back and tell me that 2-3, or 50-500 mutations per individual is the same as no mutations at all. Even if only 1 in 100 of those individuals had a beneficial mutation, can you imagine how many that would be? How can that be the same as none at all?
I guess you believe that.
But this number is still large enough for the number of possible combinations to produce very striking variations.
Sure. But remember that Mendel figured out discreet genetic inheritance from nothing but examining pea plants. He had no knowledge of the actual mechanisms of molecular genetics. So clearly, in a lot of cases, the range in variation isn't that great.
But that's only for one trait that has one gene for it, and there can be many genes for the same trait in some cases.
The existing stash of alleles is quite sufficient for enormous variations, even after millennia of attrition due to the Fall.
I simply don't see alleleic recombination as supportive of enough diversity to account for the diversity of living things we see today and in the fossil record.
Depends on how big the original genome was.
Also could be that this mutation EZ was hypothesizing about, that simply reproduces a known allele where one has been lost, is simply part of the normal way DNA works. But then I do have to wonder why the cheetah hasn't experienced this.
Evolution absolutely depends upon mutation. Unfortunately what is actually known of mutations does not bode well for their capacity to work the miracles needed by evolution.
Well, let me assure you that the science proves the exact opposite - that mutation is the source of more than enough genetic novelty to account for the origin of all alleles. No miracles needed, just successive changes adding up over countless generations.
Faith, Crash, nothing but blind faith.

This message is a reply to:
 Message 128 by crashfrog, posted 09-03-2006 1:53 PM crashfrog has replied

Replies to this message:
 Message 133 by crashfrog, posted 09-03-2006 11:15 PM Faith has not replied

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


Message 131 of 301 (346299)
09-03-2006 9:30 PM
Reply to: Message 129 by crashfrog
09-03-2006 2:08 PM


Re: Rise in which kind of diversity?
I'm not so much pointing to the speciation "event" as to the allelic circumstances that bring it about.
Well, speciation is not driven by alleles, it's driven by environment. So I don't know what circumstances you're referring to.
In saying it is driven by environment you seem to be claiming that natural selection is the only method that can bring about speciation? But a bottleneck can bring it about, and that can be caused by accidental factors that happen to isolate a tiny remnant of a population. Gene drift can bring it about. And migration alone can bring it about. There need be no selection pressures involved at all. Ring species may form simply by migration and isolation of a part of a population.
These are all the processes that create new phenotypes, and you get speciation at a certain extremity of phenotype change. There is no reason to assume that the alleles that bring about these changes were not always present in all previous populations. There is no reason to assume mutation at any point and there is no reason to assume selection pressure, although selection pressure MAY certainly be part of it.
Diversity at the level of phenotype (or genotype) or at the "organismal" level WILL rise. But this is BECAUSE of
1) change in allele frequencies, which may include, and does include in severely reduced populations or after many population splits,
2) actual loss of alleles.
1 I think you're right about. 2 I don't understand. How could a loss of alleles be an increase in diversity?
This has been my argument from the very beginning. {EDIT: But I only recently started using "diversity" at the level of the phenotype by mistake. This confuses things. I merely mean that new phenotypes are brought about by the shuffling of alleles which may include loss of alleles}.
In fact I used to overemphasize it to the slighting of the role of frequency changes without loss of alleles. It's simply a more extreme version of frequency changes, though: instead of one allele's becoming very rare in the new population it simply is nonexistent, because the individuals that possess it didn't happen to be in the migrating population at all. In the original population they might have been fairly numerous, but are simply not part of the new one at all.
The cheetah, again, is an example of a population that has lost all but one of the alleles for many genes, in this case because of a bottleneck. But a series of population splits by migration can over time also eliminate alleles completely. Obviously this must be a common occurrence given that population splits in the wild are common.
Did I do the paint shop analogy once? Paint shops mix paint by adding color concentrates ("primaries") to white bases. So if you can imagine a paint shop with, say, four colors (cyan, magenta, yellow, and black), they can mix a certain range of colors (we call this range a "gamut".) If we use 5 or 6 colors instead of 4, we can mix a larger gamut of colors. So, the different primary colors we choose to use are the alleles in this example.
But if we take some of those alleles away, how can we possibly wind up with a larger gamut? If we only have cyan, yellow, and black, how can we possibly have a wider gamut than if we had magenta as well?
Paint doesn't make a useful analogy here. The removal of alleles allows others previously less frequent in the population, perhaps suppressed by being recessive, to be expressed and come to characterize the new population that is without the competing alleles. Usually it's a matter of change in frequencies and the previously dominant alleles are not completely eliminated but merely now far less frequent; but total loss can occur and in fact is pretty much guaranteed to occur over many population splits. In some domestic breeds you can be sure that you will NEVER get certain traits if you keep inbreeding them. They simply do not have the alleles for those traits any more.
You've long asserted that the loss of alleles can mean a greater diversity, but diversity is determined by the number of alleles at a given locus, so I simply don't see how that can be true.
I don't recall you explaining it very well, so I guess I have to ask you once more to attempt to do so for my benefit, if you wish.
This is the problem with allowing the term "diversity" into this discussion. I finally allowed it, but I didn't like it at first at all. EZ brought it in and I didn't do a very good job of dealing with it at that point. I had been only saying that "phenotypic change" or "new phenotypes" is brought about by a reduction in allelic diversity, NOT "phenotypic diversity." Perhaps I should go back to that after all. I decided at one point that diversity might not be as big a problem as I'd thought, since what happens when frequencies change is that a bunch of new traits come out, and that IS diversity, and it IS caused by the increase in some alleles along with decrease in others; and if some alleles are totally lost, the new traits based on the remaining alleles that now come to the fore, that were previously less frequent in the population, STILL amount to an increase in diversity -- of traits, of phenotypes. This is all in the context of population splits.
It's not a larger RANGE, it's simply the greater expression of previously unexpressed traits, or previously less frequently expressed traits.
This is a semantic problem. I may have to throw out "diversity of phenotypes" after all. It just makes it more confusing as I feared. Get back to "new phenotypes" and "phenotypic change."
Again, of course we see PHENOTYPIC/GENOTYPIC diversity rising. What I am doing is EXPLAINING this rise in phenotypic diversity by the reduction of ALLELIC diversity.
That doesn't make any sense to me.
OK, let me go back to my original way of saying it:
We see new PHENOTYPES/GENOTYPES. What I am doing is EXPLAINING these new phenotypes by the reduction of ALLELIC diversity.
And again, if you mean allelic diversity is rising, this has not been shown to be the case.
I understand you to mean, by "allelic diversity", what scientists refer to as "genetic diversity", that is, the number of different alleles within a population for a given gene.
Yes, and again I decided to change the terminology, thinking "allelic" might be clearer than "genetic" since EZ for one seemed to be getting confused by it.
If that's the case, I don't understand how less alleles can result in more diversity of either phenotype or genotype. Less alleles would mean that every individual was more similar to its conspecifics, and that's the exact opposite of diversity.
Fewer choices of alleles means that the fewer now bring about new traits that were not in the former population, at least not in such numbers. There is less competition from the lost or reduced alleles so that the greater frequency of the others comes to characterize the new population overall. This is a new phenotype brought about by the favoring of a smaller set of alleles than formerly existed.
{EDIT: If a new population has fewer of some alleles than were present in the former population, then they will come to expression in greater numbers than they did in teh former population. So they are fewer with respect to the former population but greater in the new. These formerly few now get to proliferate and come to characterize the new population.
It's sort of like, to ridiculously oversimply, say the former population had equal numbers of alleles for purple fur, green fur, orange fur and silver fur. Forget dominant-recessive and other sensible considerations. Say a portion of the population gets isolated, which is made up of 50% individuals with the purple allele, 30% with the green, 19% with the orange and 1% with the silver.
Then say this population further splits and the new isolated population is made up of 40% individuals with the purple, 10% with the green, 30% with the orange and 20% with the silver.
Say it further splits and this time only orange and silver migrate, with maybe one purple individual, no greens.
And so on. I'm too tired to work out the implications. Maybe later.
If that's not what you mean, I have no idea what you mean. Maybe you mean something else by "diversity"? I assume that word to mean "the degree to which individuals tend to be different than each other."
Exactly. But in this case I mean mostly different from the main type in the previous population. I'm sorry I gave into the pressure to use "diversity." I think there IS a new diversity of traits in a split-off population, certainly in the first generation or so, but what I'm really trying to say is merely that you get a new phenotype that characterizes that new population over time.
The least possible diversity in a population would be a population of clones, and such a population would by definition have the least possible alleles.
Yes, but I'm talking about the point at which this population split off from the previous population. This new allelically depleted creature is a new phenotype in contrast to the old. But the usual example is when there are still plenty of alleles, only fewer than before the split.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.

This message is a reply to:
 Message 129 by crashfrog, posted 09-03-2006 2:08 PM crashfrog has replied

Replies to this message:
 Message 132 by crashfrog, posted 09-03-2006 10:34 PM Faith has replied

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


Message 132 of 301 (346308)
09-03-2006 10:34 PM
Reply to: Message 131 by Faith
09-03-2006 9:30 PM


Re: Rise in which kind of diversity?
But a bottleneck can bring it about, and that can be caused by accidental factors that happen to isolate a tiny remnant of a population. Gene drift can bring it about. And migration alone can bring it about. There need be no selection pressures involved at all. Ring species may form simply by migration and isolation of a part of a population.
Those things are what I was referring to by "environment." Not just selection. A mudslide could seperate one population into two. Some finches are blown off their migratory course to some distant tropical island.
The cheetah, again, is an example of a population that has lost all but one of the alleles for many genes, in this case because of a bottleneck.
Sure. Cheetahs, though, have so little phenotypic diversity that you can skin graft from one unrelated individual to another without rejection. So I don't see how this is an example of increased diversity through a reduction in alleles.
The removal of alleles allows others previously less frequent in the population, perhaps suppressed by being recessive, to be expressed and come to characterize the new population that is without the competing alleles.
If these alleles couldn't compete with their alternates, how is it that they're not the first alleles removed?
I had been only saying that "phenotypic change" or "new phenotypes" is brought about by a reduction in allelic diversity, NOT "phenotypic diversity."
That still doesn't make any sense, because phenotype is determined by genetics.
Look, the population with the least genetic diversity, the least number of alleles per gene, is the population of clones. Aka the "monoculture." And a population of clones has the least possible diversity, because everybody has the same phenotype.
We see new PHENOTYPES/GENOTYPES. What I am doing is EXPLAINING these new phenotypes by the reduction of ALLELIC diversity.
Still not making any sense. If a phenotype is truly new, how can it be the result of having less alleles? New phenotypes come from either new alleles, or pre-existing alleles combining in new ways. How can reducing the number of alleles lead to either one of those outcomes? If you have less alleles, that's less ways they can combine, not more. That's just basic combinatorics. 6th grade math.
Fewer choices of alleles means that the fewer now bring about new traits that were not in the former population, at least not in such numbers.
How? How would less other alleles change the traits that the existing alleles encode?
If all you're saying is that, in a static population, when the frequency of allele A decreases, the frequency of other alleles increases, sure. That's not a contentious statement. But it doesn't make sense to describe that as diversity, or "new phenotypes", or anything like that. If that's what you're talking about, talk about it in terms of allele frequencies. Anything else is just too confusing.
This is a new phenotype brought about by the favoring of a smaller set of alleles than formerly existed.
It can't be knew if it was there all along. If you're saying it's frequency within the population increases, ok, I'll accept that - it's obvious - but how does that make the phenotype new? "More of something" is not at all the same as "new something."
It's sort of like, to ridiculously oversimply, say the former population had equal numbers of alleles for purple fur, green fur, orange fur and silver fur. Forget dominant-recessive and other sensible considerations. Say a portion of the population gets isolated, which is made up of 50% individuals with the purple allele, 30% with the green, 19% with the orange and 1% with the silver.
Then say this population further splits and the new isolated population is made up of 40% individuals with the purple, 10% with the green, 30% with the orange and 20% with the silver.
Say it further splits and this time only orange and silver migrate, with maybe one purple individual, no greens.
There's no new phenotypes in any of that. There's a loss of alleles leading to a loss of phenotypes. That's less phenotypes, not more. The situation you've described is a decline in diversity, not an increase.
But in this case I mean mostly different from the main type in the previous population.
I don't see the idea of the "main type" as meaningful. Species don't have a "main type." It's like saying "the average American family." It doesn't exist. There's no family in America you can go to that has 2.5 children. How could a real family have half a child?
Things like "main type" or "average family" aren't real things. They're statistical constructs, not realities. The degree to which an individual differs from that construct is only so interesting. It's certainly not really relevant to that individual's existance as an individual.
This new allelically depleted creature is a new phenotype in contrast to the old.
Now I'm really confused. Are you genuinely thinking about this in terms of allelic diversity rising and falling within an individual? Because that's a completely inaccurate portrayal of the biological reality. As diplod organisms we have 2 of every chromosome. So, we have two alleles for every gene. No more, no less, unless one happens to have two copies of the same allele at both genes, on both chromosomes.

This message is a reply to:
 Message 131 by Faith, posted 09-03-2006 9:30 PM Faith has replied

Replies to this message:
 Message 134 by Faith, posted 09-04-2006 2:11 AM crashfrog has replied

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


Message 133 of 301 (346314)
09-03-2006 11:15 PM
Reply to: Message 130 by Faith
09-03-2006 8:30 PM


Re: Mutation - The Creative Force
And so far the only experiment you've actually referenced is this one with the bacteria. By the way, is that experiment performed frequently and always with the same results?
It's not exactly one experiments, it's a class of experiments. Like rat-pellet experiments. The same basic organism and equipment, thousands of different parameters. I've been generalizing to avoid getting bogged down in specifics. All that's relevant right now, all you need to remember, is that you have a sealed chamber full of nutrient broth, designed so that you can add more broth and take some away, and then one single bacterium is introduced and allowed to reproduce. If mutation doesn't occur, isn't the source of new alleles, then all subsequent members of the population should be exact clones.
They aren't. So we know that mutations are giving rise to new alleles.
And I assume you examine the genome of the bacteria before and after the mutation event, so what exactly are you seeing there in the basic genetic stuff? Is it possible to pinpoint the mutation, identify what it did to the DNA, and the protein it codes for and all that?
Yeah, you could. I don't know if they need to do that in every single case - like I said, we're actually talking about a thousand different experiments here - but there's no reason you couldn't do exactly that, except maybe expense.
Please show me that mutations occur often enough even to make a difference in the development of a new phenotype in a ring species.
Every single individual should have somewhere between 5 and 50 mutations, or even more.
Is that often enough? I don't know how to prove it is, I guess.
I don't know what the relevance of getting them in bacteria is to chipmunks.
We know they happen the same way in chipmunks, because we know that the rules of genetics apply to all organisms.
What new alleles? I think you are mostly assuming new alleles rather than proving they exist. I mean truly novel chemical coding stuff that codes for something the cell can actually use. You have claimed this happens but all I've seen is processes that would bring up previously suppressed alleles, recessive alleles and so on.
I'm sorry, I guess I wasn't being clear enough? Bacteria don't have recessive alleles, suppressed alleles, or any of that. Bacteria have one chromosome, one copy of all their genes. One allele per gene.
There are no recessive alleles, there are no suppressed, hidden genetic "possibilities". There isn't even any "junk DNA", remember? If you grow a population from one individual, that population can only have one allele per gene. Period.
Except for mutation. There are no hidden alleles in the population. No recessive or suppressed ones. There are only the one original allele per gene, plus whatever new alleles arise. And if new alleles arise we know they did so by mutation.
Please again reference these experiments.
I'm going to hold off on doing that because I don't want to confuse the issue. First we have to get down exactly what's going on with what I've already told you, first.
You say all the pre-existing stuff mutated there. You are merely ASSUMING that it mutated there. I assume it was created there in the very beginning.
And I'm telling you that, in the experiment, we're taking out everything that was "created in the very beginning", or, from my perspective, had already evolved in the population. Except for what a single individual can carry. In the case of bacteria, that's only one allele per gene. That's all that they can really hold.
Well, drat, Crash, this is what I assumed was the case way back, that the adaptive potential was already present in the population and merely selected out in the presence of the antibiotic.
Yes. But what I'm telling you is, because of the way we've designed the population - as a monoculture where everybody's decended from a single individual - we know that the adaptation developed by mutation. Then, if we add the antibiotic, it gets promoted by selection.
Mutation and selection working together to cause adaptation. It's the classic formula for evolution. Mutations create traits at random; then, subsequently, environmental pressures select certain traits over others.
But we are talking about population level changes.
Not if we're talking about traits. Phenotype only expresses, and is selected, in individuals. The population changes as a result of individuals being selected.
Don't discount the individual. The individual is all that is real. The "population" is a construct. The "species" is a construct. Only the individual is real. Everything else is a fiction we use in our heads to understand the reality.
And if what you said above is the case, that the different bacteria were already in the population, then scrap the whole show because that fits MY model.
You're still not apparently understanding the timeline at work here.
In the beginning of the experiment, there are not resistant bacteria. Later, there are resistant bacteria, even though they haven't encountered the antibiotic. After we introduce the antibiotic, all bacteria are resistant, because the wild type (not resistant) were killed.
The resistant bacteria are in the population only because of mutation. This isn't something we assume, it's something that we proved because we designed an experiment where, if diversity in bacteria increased, it could only have done so by mutation.
But anyway, how can you expect mutation to be anywhere near the kind of influence you are all claiming given its rarity, its high proportion of uselessness which may in fact be destructive in the end, and so on?
Because it happens a little bit in each individual, and there are a countless number of individual living things. If you buy one lottery ticket a year, you won't ever win, probably. If you buy a million tickets every second you might win very soon. Repetition makes improbabilities certainties. That's basic math.
It isn't enough to do what you all claim it must do. It just isn't. Astronomically far from it.
If you say so, I guess I'd like to see your math on that.
But then I do have to wonder why the cheetah hasn't experienced this.
Cheetahs reproduce slowly. Their generational time is very long, compared to bacteria which have a new generation every 30 minutes. Evolution takes longer when it takes longer to reproduce.

This message is a reply to:
 Message 130 by Faith, posted 09-03-2006 8:30 PM Faith has not replied

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


Message 134 of 301 (346340)
09-04-2006 2:11 AM
Reply to: Message 132 by crashfrog
09-03-2006 10:34 PM


Re: Rise in which kind of diversity?
NO, I am not thinking about this in an individual, but in the population.
Drat, this is now awfully frustrating. My own fault for allowing that misuse of "diversity" to get into this and now the whole thing is a terminological nightmare. I knew better at first and then allowed it against my better judgment. Communication about these things is difficult at best; now it just seems impossible. Anyway.
I can't take the time to get into this again for a while, but I'll just answer one small part of this one post:
Sure. Cheetahs, though, have so little phenotypic diversity that you can skin graft from one unrelated individual to another without rejection. So I don't see how this is an example of increased diversity through a reduction in alleles.
Again, SO sorry I allowed "diversity" into the description of the phenotype. Stupid of me. Please let's try to eliminate the idea of phenotypic/genotypic or organismal diversity or "diversity at the population level" from the discussion. I guess I need to go back through all my posts and edit them all to reject this word. Sigh.
Anyway, about the cheetah: Again, forget "phenotypic diversity." The cheetah is a NEW phenotype, that's all I ever wanted to say, I'm only talking about new phenotypes coming about through these processes of evolution, particularly through the reduction of genetic diversity, a change in phenotype from an earlier type, in the cheetah's case brought about from the old through a bottleneck which severely reduced its alleles for certain loci. The lost alleles could no longer affect the phenotype. 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, differentiated from its parent population back who-knows-when by the dominance of these particular traits and by the loss of those traits it no longer shares with it.
There are some cases where new phenotypes emerge in a population without any increase or decrease in alleles / genetic diversity, such as gene drift, such as population splits where all alleles are retained in both populations but only the frequencies change, etc. Some have said that speciation can occur this way. Point here is that INCREASE in genetic diversity is not needed to bring about new phenotypes/genotypes/organismal or population-level changes.
There is only one situation in which an increase in genetic diversity occurs, and that is hybridization, a reintroduction of alleles where they had once been lost. Nothing new is added but old alleles are recombined. Does hybridization lead to new species?
Or mutation, but that's a big questionmark still.
But loss of alleles is still the general trend over time, and new phenotypes are certainly produced by this loss, and speciation as well. Instead of a mere reduction in frequency that allows other formerly suppressed alleles to be expressed in new traits in the new population, a complete absence of the competing alleles may be the case. Many population splits, say in a ring species, is very likely to bring about this situation, and speciation can certainly result from it.
My claim is that this trend to loss of alleles is general for all species over time, and it comes about in the production of new phenotypes and new species, which requires that some alleles not be expressed while others are, and if the competing alleles are completely gone so much more certainly will the new phenotype come to dominate.
Edited by Faith, : No reason given.

This message is a reply to:
 Message 132 by crashfrog, posted 09-03-2006 10:34 PM crashfrog has replied

Replies to this message:
 Message 135 by qed, posted 09-04-2006 8:54 AM Faith has not replied
 Message 165 by crashfrog, posted 09-05-2006 4:52 PM Faith has replied

qed
Inactive Member


Message 135 of 301 (346380)
09-04-2006 8:54 AM
Reply to: Message 134 by Faith
09-04-2006 2:11 AM


Sciencey stuff not a reply
Ok i did 2/3rds of a BSc in Mol Bio before i ran off to business school these are off the top of my head and pretty basic but i hope it helps clear up some of the communication difficulties here.
Genotype: what the dna in your sex cells says / heritable DNA.
Phenotype: What you look like, in Genetics this term is usually used to describe the physical expression of you genes disregarding environmental factors.
The (most) inportant difference: Genotype contains recessive* or unexpressed information which may not appear for many generations.
Introns: DNA of debated/unknown/no purpose cut out during rna production. Eukaryotes have them everywhere, Prokayotes only in transport and ribosomal rna coding DNA.
Allele: A chunk of dna responsible for ....
Divergence: The gradual seperation of a species into two non-interbreeding species.
Mutation (Evo): Change in genotype caused by an error in transcription or random interaction with oxidisers or radiation. Humans contain 120 on average.
Beneficial Mutation (Creationist): Mutation which provides a species with an observable new characteristic which helps it to reproduce.
Neutral Mutation (Creationist): most (much greater than 99.9%) of mutations fall into this catergory, mutation of no significant observable effect.
Detrimental Mutation (Creationist): Mutation which provides a species with an observable new characteristic which hinders it's reproduction.
The above are also Darwinist concepts however NeoDarwinism considers
all mutations to contribute to diversity provided they allow future reproduction. Diversity = greater chance of survival.
Devolution (Creationist): Reduction in the potential / ability / genetic information of a creature due to evolutionary mechanisms.
Devolution (Evo): A subset of evolution defined by semantics.
Junk DNA: Ok popular science has hijacked this term leading to a heap of confusion, when Eukaryote non-sex cellular dna is replicated the last chunk of the chromosome is not copied, theres a bunch of useless
DNA tagged onto the end and this gets slowly lopped off with each new
generation of cellular division. Prokaryiotes do not have this problem
(easy to work out why if u think about it). Pop science and even wiki use this term for all dna of unknown function, i think it's confusing and caused by the catchiness of the phrase.
Just thought i'd put that that here
*reccessive/dominant PHENOTYPES are not strictly accurate but work for most purposes.
Edited by qed, : more stuff

This message is a reply to:
 Message 134 by Faith, posted 09-04-2006 2:11 AM Faith has not replied

Replies to this message:
 Message 138 by Wounded King, posted 09-04-2006 12:07 PM qed has replied

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