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Author Topic:   What is the mechanism that prevents microevolution to become macroevolution?
Quetzal
Member (Idle past 5872 days)
Posts: 3228
Joined: 01-09-2002


Message 91 of 301 (345885)
09-01-2006 10:35 PM
Reply to: Message 90 by NosyNed
09-01-2006 10:14 PM


Re: Degree of remaining overlap
Hi Nosy. Don't get confused here. I was talking about overlap in the sense of shared alleles between populations, not genetic similarity between species. I'm not sure there's much if any correlation between the two concepts.

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 Message 90 by NosyNed, posted 09-01-2006 10:14 PM NosyNed has not replied

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


Message 92 of 301 (345908)
09-01-2006 11:35 PM
Reply to: Message 76 by crashfrog
09-01-2006 12:58 PM


Re: That one bacterium again
I'm talking about experiments that are designed to prove that mutations are a source of genetic diversity in populations. The experiments accomplish this by eliminating all sources of diversity except mutation, and then monitoring the population's subesquent rise in genetic diversity.
OK, that's really all I needed to have confirmed, thanks. I just tend to forget. No need for anything more technical.
Yes. If, later in the population, we find bacteria with alleles that are different than the original one, we know those arose through mutation, because we've designed the experiment to eliminate all other sources of alleles. Further proof is the fact that we can add chemicals that promote mutations - mutagens - and watch the diversity climb even faster.
So these mutations are apparently either neutral or beneficial?

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


Message 93 of 301 (345913)
09-02-2006 12:02 AM
Reply to: Message 64 by crashfrog
08-31-2006 11:00 PM


Re: Faith Logic
Yes that one shows that mutation alone can bring about microevolution, but it also raises the questions just what mutation is {edit: Is it really a mistake?, is it really random?, is this one in bacteria really a mutation at all?
I thought we were pretty clear on what mutations are, but, I mean, in an enclosed bioreactor, there's no outside influence; the bacteria are haploid so sexual recombination isn't happening; and they're all the clonal decendants of a single bacteria so we know that any alternate alleles that we discover in the population are the result of the only source left for them that we know about - mutation.
It could be, you know, mind beams from Alpha Centauri or something, but why don't we stick with the processes that we know occur? In the case of these experiments, that doesn't leave anything but mutation.
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. I'm not sure what information would show me this one way or another but so far I'm still mostly in the dark about it. I'm very sure getting more technical isn't going to do it.
Even if most of the results are neutral it seems this might be a fair way to characterize it. And since the actual number of examples given so far of what are termed beneficial mutations is so small I'm just not buying that mutation figures much in normal genetic transmission.
and whether the same kind of thing can be shown in any other organism.
The rules of genetics are the same for all living things on Earth.
Yes but.
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. I found an article where they were theorizing about why this might be. I think this is a major difference between bacteria and other creatures myself but the full implications of it await a bolt of illumination.
In a population of chipmunks (thinking of a ring-species example from many months ago}, for instance, the main cause of phenotypic change from one population to another is the shuffling of already-present alleles brought about by a splitting or selection process, and often this involves the actual loss of some alleles to the population, even both old and new populations.
Yes. But we can structure the experiment to limit the alleles in our population. In the case of bacteria, which reproduce asexually, we can limit the number of alleles per gene to 1, because that's the maximum number of alleles an individual bacterium can have, and we can develop a whole population from a single individual. When we do that the population is called a "monoculture."
It is hard to explain why I just don't trust this bacteria bit. 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. In this light mutations are just some sort of intrusion.
There are so many alleles already present in such a population there is no need for mutations to fuel microevolution {and how would you recognize a mutation in such a case anyway?
We recognize mutations after the fact when an individual presents with a unique allele that none of his ancestors had.
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?
But if it is a mutation, then every time one is identified it needs to be identified according to what it does to the organism. Is it a mistake, is it a disease process, is it really just basically destructive etc.?
Since mutation is the only natural source of new alleles, it's the only explanation for a new allele in the population.
But ruling out the possibility of rare alleles coming to expression can't be a sure thing.
And again, if they are mutations, are these really viable alleles mutation is bringing about? Do they look like normal alleles? Do they code the same way? And what effects do they cause?
Further, gene sequencing analysis can show us the difference between the gene in the individual and the gene he should have inherited from its parents.
OK, so you know you have a mutation. Then the questions about what the change actually does are the main thing.
If you breed a population from two chipmunks then you can control the number of alleles, but how often does a mutation show up to make your point in that case?
In mammals, we expect roughly one point substitution mutation per every 3.2 billion base pair replications.
And what does that work out to in a human time frame? How many viable new alleles per unit of time?
The problem is, as always, identifying the ACTUAL action of mutations in such a population.
Well, we know what mutations do - change gene sequences. And we know what genes do. (Many of them, anyway.) I don't see the major difficulty in perceiving the role of mutations, unless you mean to suggest that, contrary to the accepted understanding of biology for the last 100 years, DNA is not the molecule of inheritance of phenotype?
No I'm just as usual pondering their sounding like something deleterious although they sometimes get called beneficial and I'm not convinced. 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.

This message is a reply to:
 Message 64 by crashfrog, posted 08-31-2006 11:00 PM crashfrog has replied

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


Message 94 of 301 (345915)
09-02-2006 12:08 AM
Reply to: Message 77 by jar
09-01-2006 1:08 PM


Re: On predictions and tests.
Yes, that would be a good test. Any way to conduct it?
Forget anything "before Creation." That wouldn't falsify what I'm predicting but simply bring in some whole other frame of reference.

This message is a reply to:
 Message 77 by jar, posted 09-01-2006 1:08 PM jar has replied

Replies to this message:
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jar
Member (Idle past 394 days)
Posts: 34026
From: Texas!!
Joined: 04-20-2004


Message 95 of 301 (345917)
09-02-2006 12:18 AM
Reply to: Message 94 by Faith
09-02-2006 12:08 AM


Re: On predictions and tests.
Well as Quetzal pointed out in Message 79 it has been done. In his words:
Well, a lot of that's been done. The Ensatina article shows quite clearly increasing divergeance between the two populations. 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. 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).
This isn't the only example, either. See, for instance, Jiggins CD, Mallet J, 2000, "Bimodal Hybrid Zones and Evolution", Trends in Ecology and Evolution, 15:250-255 (available cached here. Also see Via S, 2002, "The Ecological Genetics of Speciation", Am Nat 159:51-57 (I don't know if it's on-line somewhere). Anyway, there's a bunch of research out there. The entire line of argument is bogus.

Aslan is not a Tame Lion

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 Message 94 by Faith, posted 09-02-2006 12:08 AM Faith has replied

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


Message 96 of 301 (345921)
09-02-2006 12:28 AM
Reply to: Message 79 by Quetzal
09-01-2006 1:42 PM


Re: On predictions and tests.
Well, a lot of that's been done. The Ensatina article shows quite clearly increasing divergeance between the two populations.
But divergence we expect, remember. It's the genetic diversity we expect to decrease while the phenotype changes.
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.
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.*.
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. *.
*. {Edit: In other words, ALL the alleles for a particular gene would have to be lost to the organism, and lost for many genes, which would mean the loss of many entire genes, before the genome would appear appreciably smaller. **.
--Here is where I look inquiringly toward the "junk DNA"}
{Edit: **. This wouldn't happen in the normal course of sexual recombination, however, even with any amount of severe isolation or selection, even the most drastic bottlenecks, because there would always be at least one allele for all the loci and the cheetah does just fine with that condition, considering. What brings about extinction is probably mutations that cause diseases and that themselves kill alleles.
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, : No reason given.
Edited by Faith, : No reason given.

This message is a reply to:
 Message 79 by Quetzal, posted 09-01-2006 1:42 PM Quetzal has replied

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


Message 97 of 301 (345926)
09-02-2006 12:55 AM
Reply to: Message 79 by Quetzal
09-01-2006 1:42 PM


Re: On predictions and tests.
They don't. 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).
But novelty can arise in a new split-off population just by the fact that previously suppressed alleles may now be expressed. Gene flow if anything would keep them suppressed. In the new populations gene flow will then smooth out the new phenotype over time as it were, until the whole population will have developed its new characteristics around the novel newly expressed alleles, and then the whole group can be distinguished from the other, but gene flow BETWEEN the populations would only interfere with this diverging process.
Edited by Faith, : No reason given.

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


Message 98 of 301 (345927)
09-02-2006 12:58 AM
Reply to: Message 95 by jar
09-02-2006 12:18 AM


Re: On predictions and tests.
Quetzal doesn't yet completely grasp what we are arguing. Those supposed answers don't answer it, and in fact I've addressed that post in my two posts above.
Edited by Faith, : No reason given.

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


Message 99 of 301 (345946)
09-02-2006 1:53 AM
Reply to: Message 80 by EZscience
09-01-2006 2:20 PM


Using diversity in a different sense
Faith writes:
And what demonstrates this? I haven't seen anything in the above that shows evidence of an increase in diversity, but most likely the opposite. That would imply an increase in alleles and that hasn't been shown. It is probably assumed, but it hasn't been shown.
The increase in diversity is observable at the level of the population in that it consists of a much greater range of genotypes than would be observed if it was all one gene pool.
Then here is where he is not understanding what I'm talking about because diversity at the level of the population is expected, while genetic diversity decreases. {Edit: Realizing the hazard of the term "diversity" in this context. What I mean is change. Change at the level of the population. observable change, change in the phenotype} Greater range of genotypes means a greater range of phenotypes doesn't it? I may have the technical picture off here somehow but I think this is just another way of saying what I'm saying. Because there are different frequencies of alleles, including very possibly a complete absence of some alleles, we now have entirely new combinations that didn't exist in the former combined population. Is this what you are saying?
THIS kind of diversity {change} is expected, but it is brought about by a DECREASE in the number of alleles or in what I've been calling genetic diversity, i.e., the number of allelic possibilities in the population. The use of the term "genotype" may bring in a factor that makes this harder to express, but in any case it is describing a change in individuals that is different from what existed in the previous population, and this is at least because of a change in allele frequencies or even a reduction in the number of alleles caused by the elimination of some altogether.
Diversity at the level of the population can arise in many ways other than simply an increase in the number of alleles occurring at specific loci.
Well, what I am saying is the exact opposite. I'm saying that a DECREASE in the number of alleles occurring at specific loci is what brings about more diversity {change} at the level of the population, by which I mean new phenotypes, which I believe implies new genotypes but I haven't been thinking at the level of genotypes exactly except that they have fewer alleles to work with.
{IMPORTANT EDIT: OK, I'm realizing there's some terminological confusion here. You are talking about increasing PHENOTYPIC/GENOTYPIC DIVERSITY, but I'm only talking about forming new phenotypes, period, not thinking about how diverse the options may be, more perhaps how striking the observable differences may be {between the phenotypes of the two populations.} The "diversity" is at the allele level and I haven't used the term in any other sense. At the population level, I'm talking about producing new traits -- diversity or numbers of such new traits isn't of any importance in what I'm saying. There may or may not be a lot of them and it doesn't matter. I'm talking about simply creating a new phenotype, period. I assume that a variety of new traits will show up in the new populations from the new frequencies of alleles due to the separation, and that over time, from interbreeding within each population these traits will get more or less blended in the population so that a typical phenotype will come to represent that population, one which differs in a number of traits from the original population, yet of course individuals will still possess some variety of different alleles.
AGAIN, in all this discussion diversity of these traits is not the subject. I'm glad I caught this. The subject is confusing enough. Let's stick to diversity of alleles or genetic diversity and simple production of new traits without worrying about how many of them there are.}
For example, the linkage disequilibrium Quetzal refered to refers to a multi-locus effect.
I've pretty much assumed this without saying it in so many words: That is, in both populations there is an absence of some alleles at a number of loci, caused by this population split.
Lets assume 2 loci, A and B, with two alternative alleles at each, A/a and B/b. Assuming diploid sexual reproduction, meiosis yields four types of possible gametes:
AB
ab
Ab
ab
The first two are referred to as 'coupling' gametes and the second two as 'repulsion' gametes.
Now, if there is no linklage between these alleles (or meiotic drive of any kind), we expect these gametes to be formed at equal rates and be present in equal proportions (.25) in the population.
When there are statistical deviations from the .25 frequency (when coupling gametes outnumber repulsion gametes or vice versa), this can be considered evidence for selection favoring one type of gene combination over another. Thus AB and ab may be the most advantageous gametes to produce in one particular population, and aB and Ab the most advantageous in another population. These populations are then different, i.e. they are genetically 'diverse' relative to one another even though there is no increase in the number of alleles, or even any difference in the actual alleles possessed by them.
Hope this is helpful.
Sorry, you lost me there, got way too technical. I'm trying to stick to the level of simple presence or absence of different alleles plus the proportions in which they occur in the two populations -- for example,
no alleles at all for genes 1 2 3 4 and 5,
3 alleles for gene 6
and 10 for gene 7, etc.,
as compared to the other population's
5 for gene 1,
3 for gene 2,
2 for gene 3,
1 each for genes 4 and 5,
none for gene 6 and 1 for gene 7.
{Edit: This situation could come about from the division of a population that originally contained all of the alleles in both new populations: 5 alleles for gene 1, 3 for gene 2, 2 for gene 3, 1 each for 4 and 5, ALL of these being lost to one of the new populations but retained in the other, and 3 for gene 6, in this case all going to the first population and lost to the second, and 11 for gene 7. I should have had more genes that retained some alleles, to be realistic, say a gene 8 with 12 alleles that split 5 to the first population and 7 to the second and so on}
{EDIT: Somehow the above list seems to imply that alleles will only be split and fails to account for the fact that most of them will be shared but in different proportions. Oh well now my brain is too tired to figure out how to express this.}
These differences are going to make for very different phenotypes and genotypes in the two populations.
You are bringing in other qualities at this point that I think only confuses the issue unnecessarily.
EDIT: I'm afraid this post is rather confused because I didn't grasp that you were using "diversity" in such a different sense than I was until the end. I tried to correct it by putting in "change" where you had used "diversity" in that sense, to delineate our two different views, but I'm not sure I succeeded at clarifying anything. I hope I didn't make it less clear.
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, : No reason given.
Edited by Faith, : No reason given.

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


Message 100 of 301 (345980)
09-02-2006 8:23 AM
Reply to: Message 81 by Quetzal
09-01-2006 2:50 PM


Re: Increased phenotypic diversity by changing allele frequencies?
You explained the situation to Ben just as I am thinking of it, except for the part where you bring in selection pressures, and I think mutation, though you don't name it.
The different allelic frequencies between the two populations may cause them to not really resemble each other very much if the daughter has a vastly different distribution of alleles.
Yes, nothing needed for the change in phenotype except "vastly different distribution of alleles" working their way through the new populations in subsequent generations.
It's only when there's some isolating mechanism that limits or prevents gene flow between the two that we start to see the two populations really genetically diverging (evolving) on separate trajectories, as each starts accumulating unique alleles in response to their own particular selection pressures.
This part doesn't seem at all necessary to add. For one thing geographic isolation is more or less implied in the first paragraph, already meeting this requirement. Certainly the less gene flow the more divergence, and in this case, the mere "vastly different distribution of alleles" should explain even dramatic divergence, or even the accumulation of unique alleles. Neither further selection pressures nor mutation (which you didn't name, but perhaps implied in "unique alleles") is needed. Unique alleles are most likely simply alleles that occurred in low frequency in the previous combined population that now have an opportunity to be expressed in the normal pattern of sexual recombination. Selection pressure MIGHT enhance this but it is not needed for this to occur. Mutation is not necessary at all, and whether it might occur or not in any beneficial way is very much open to question.
Even if the pressures are mostly the same, as long as there is sufficient isolation, we'll start seeing novel alleles (and hence divergeant phenotypes) appearing.
OK, fine, here you're saying what I'm saying. I should have read on. But I'll leave my statement that emphasizes this. Yes, all it takes is isolation.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.

This message is a reply to:
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Faith 
Suspended Member (Idle past 1444 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 101 of 301 (345985)
09-02-2006 9:11 AM
Reply to: Message 84 by NosyNed
09-01-2006 3:21 PM


Re: What is macroevolution / answering fallacycop
Ben is the only one who answered fallacycop with a fair representation of what I'm arguing, in his Message 85. Quetzal, in Message 83 is claiming all kinds of things are wrong with my argument and MJFloresta's but he is very far from having demonstrated any such thing. His examples have all tended to support our argument, and he has not made any kind of case whatever for mutation in any of the processes we have discussed.
I just wanted to comment on a few things in NosyNed's post. I understand that one problem with pursuing any particular creationist argument is that there are many different creationist arguments and terminological uses, and elements from those may be assumed wrongly to be involved in a particular argument when they are not.
microevolution: any changes to the population genetics that does not produce a speciation event.
This is a case in point. The term "speciation" has been very problematic for creationists because it often is used to imply macroevolution in itself. But speciation is really only variation within the Kind and it would help if creationists would all get on the same page about this. It is a common occurrence, most dramatically demonstrable in domestic breeding programs, but very frequent in nature under all kinds of situations that isolate populations just as domestic breeding does.
In fact microevolution IS speciation.
It isn't, for the most part, the genetic changes that allow speciation to happen. This is way it really is of value to discuss micro and macro evolution. It actually does, most of the time, require some other mechanisms to allow speciation to occur.
Geographic isolation should in fact bring about the genetic changes that lead to speciation, by simply altering the frequency of alleles in the isolated populations. The smaller the new population the more dramatic the change because the fewer alleles there will be available for developing the new phenotypes.
The most obvious is geographic separation.
This will do it all by itself.
With a population split into two between which there is no (or very little) gene flow the ongoing genetic changes which have to happen are not "smoothed" out but rather can accumulate in each of the populations.
I guess by "ongoing changes" you are implying mutation? There is no need to assume mutation in any of this. Geographic isolation would all by itself tend to change the allelic frequencies sufficiently to bring new traits into the population and form new phenotypes.
I have no idea what you mean by "ongoing genetic changes which have to happen." You mean this change in allele frequency or mutation or both or what? I also don't know what you mean by "smoothed out" or "can accumulate."
I assume no useful mutations in everything I say. I see no need for them to explain any of these processes.
Maybe your terms imply the following: With changed allelic frequency you get some new traits appearing in the first generations of a new population. These traits may very well accumulate in the population over time with inbreeding, and over time these traits will get more or less "smoothed out" by being intermingled over and over again, until a phenotype that characterizes that new population emerges in an identifiable way. Perhaps this is what you had in mind. I agree with this picture if so.
Over time the accumlated differences gradually reduce the likelyhood of the success of any pairings from the two populations.
Yes.
The time frames can be very short for some organisms (generations) and, more often, very long (millions of years) for others. Eg tigers and lions have not yet completed the total separation.
I agree with the general point except of course the millions of years part.
The accumulated differences are, just like the changes of microevolution, the same set of kinds of mutations that always occur.
All of the accumulated differences ARE microevolution, and while mutation keeps being mentioned it's kind of like a third thumb, it has no role in any of this. Ordinary sexual recombination of different frequencies of alleles in isolated populations is all it takes to bring about new phenotypes and even speciation.
There is no difference in the nature of the changes on either side of the line. The only difference is that gene flow is not (for some reason) available to keep the populations more or less homogeneous.
As I've been trying to show, there is a point at which further change in the ordinary processes of speciation becomes impossible, and this is the barrier to macroevolution and provides the means to define the Kind. If normal sexual recombination of a reduced allelic set (which is the case in domestic breeding and in natural selection and geographic isolation etc) is all it takes to produce new phenotypes, and it is, this demonstrates that the reduced allelic set is the operative principle. Reduced number of alleles means less genetic diversity and this is what brings about phenotypic change all the way to speciation. Taken through many repetitions of the same processes the allelic set will be SO reduced that further change of any kind becomes impossible. This is fortunately a rare occurrence in most species so far, because it is a precursor, not to macroevolution but to extinction. This is what has happened to the cheetah. Again, THIS is the line that defines the Kind, that defines the limit of evolution at the outer edges of microevolution and means that macroevolution simply does not happen.
This is what the "kind" folk don't seem to grasp or deal with. They look at the over all phenotypes but don't see that the genetic changes between even rather widely separated branches of the tree of life just more and more of the same thing.
Oh we see that just fine, but it's an illusion if you are really grappling with what goes on in the genetic processes that arrive at speciation. These genetic processes are an inexorable reduction in genetic diversity. This is what brings about new phenotypes and eventually speciation and eventually the extremity at which no further change is possible.
You guys get yourselves all confused with this background assumption of mutation that nobody ever demonstrates is really going on but gets tossed into any discussion about population genetics. The actual observed facts of speciation 1) do not require mutation at any point, 2) would even be interfered with by mutation because speciation requires allelic reduction not addition,* and 3) do not in fact show any actual evidence whatever of mutation in anything yet discussed.
I'm not totally sure but I think there has been a few decade old history of the creationist idea of "kind". Once upon a time it was a species just as it is clear the bible means. As speciation events became demonstratable they backed "up" the taxonomic chart and have also gotten very fuzzy. They've been forced high enough up that humans and the other primates become one kind so they start to waffle. It is most amusing to watch.
This is a bogus problem, purely a matter of terminological confusion. "Species" is simply the Latin (or Greek?) word for "Kind." But the way it is used in practice it actually refers to varieties of a Kind, and this is why creationists have had to keep adjusting the terminology.
Kind must be defined in terms of genetics but there isn't anything there to point at.
This is true, and this is exactly what I've been doing and have in fact done. What I'm pointing at is the end result of a process that has to be grasped conceptually. It can only be demonstrated in the unfortunate cases of extreme genetic depletion as in the case of the cheetah, and you have to throw out that utterly useless notion that mutations have anything to do with it if you are going to understand what I'm talking about.
{Edit: * The only exception to the allelic reduction formula is recombination or gene flow between two separated populations or hybridization, and in this case mutation is also not needed. This will reintroduce formerly lost alleles to the combined population and this will produce new phenotypes. Gene drift is a similar process. Without any mechanisms of selection or isolation or reduction new phenotypes can be produced this way, and ultimately the change may be striking enough to be called a new species. But this is more of a homogenizing and stasis-producing process. I don't see how you would ever get macroevolution out of it. To get macroevolution you need to select, and if you select you reduce numbers of alleles, and that means reduced genetic diversity, and then we are back at what I'm describing above, in other words the utter defeat of any possibility of macroevolution since all the processes that would be needed to bring it about actually make it impossible.
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, : No reason given.

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Faith 
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Posts: 35298
From: Nevada, USA
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Message 102 of 301 (346004)
09-02-2006 10:54 AM
Reply to: Message 89 by Quetzal
09-01-2006 9:31 PM


allozymes and other stuff
Just so you know, I'm working on your Message 89 and expect eventually also to get to RAZD's Message 88.
Cheers.

This message is a reply to:
 Message 89 by Quetzal, posted 09-01-2006 9:31 PM Quetzal has replied

Replies to this message:
 Message 113 by Quetzal, posted 09-02-2006 2:30 PM Faith has replied

Brad McFall
Member (Idle past 5033 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 103 of 301 (346018)
09-02-2006 11:45 AM
Reply to: Message 83 by Quetzal
09-01-2006 3:20 PM


Re: What about the topic?
I do not think that we have been able to promote "our" EvC 'gaze' though(see Gould at bottom of page 443 ("But suppose that we "promote" our gaze and consider evolutionary trends through..."). I am still working on my own contribution.
quote:
by Stephen Jay Gould Harvard University Press

This message is a reply to:
 Message 83 by Quetzal, posted 09-01-2006 3:20 PM Quetzal has not replied

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


Message 104 of 301 (346024)
09-02-2006 12:17 PM
Reply to: Message 92 by Faith
09-01-2006 11:35 PM


Re: That one bacterium again
So these mutations are apparently either neutral or beneficial?
The way we detect the mutations is, we take a sample out of the culture - which is really just a bunch of bacteria floating in a heated nutrient broth - which represents a statistical sample of the whole population.
Remember that we're talking about a population that has pretty quicky grown to K, that is, the largest possible population that the environment will support. So there's no room for bacteria that can't compete. Any detrimental mutations get knocked out pretty much right away because they can't compete with their peers who lack that mutation.
So, yes. Because of the environment of the experiment, the only mutations we're detecting are the ones that are currently either beneficial or neutral. Detrimental mutations won't survive long enough, or produce enough decendants, for us to detect.

This message is a reply to:
 Message 92 by Faith, posted 09-01-2006 11:35 PM Faith has not replied

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


Message 105 of 301 (346028)
09-02-2006 1:01 PM
Reply to: Message 93 by Faith
09-02-2006 12:02 AM


Re: Faith Logic
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."
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, 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.
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? And what about if an environment required a trait that nobody had an allele for?
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. Only mutation allows for potentially limitless variation, and the introduction of new alleles into the population.
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.
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.
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.
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.
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.
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 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.
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."
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.
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.
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.
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.

This message is a reply to:
 Message 93 by Faith, posted 09-02-2006 12:02 AM Faith has replied

Replies to this message:
 Message 126 by Faith, posted 09-03-2006 11:28 AM crashfrog has replied

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