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Author Topic:   What is the mechanism that prevents microevolution to become macroevolution?
crashfrog
Member (Idle past 1494 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 61 of 301 (345556)
08-31-2006 9:21 PM
Reply to: Message 59 by Faith
08-31-2006 1:39 PM


Re: Faith Logic
What is a fantasy -- utterly without evidence, simply assumed -- is this idea that mutation drives evolution.
It's no fantasy. It's trivial to construct an experiment where a population develops where the only source of alternate alleles is mutation. That evolution happens in these populations is proof that mutation is one of the driving forces of evolution and a true source of genetic novelty.

This message is a reply to:
 Message 59 by Faith, posted 08-31-2006 1:39 PM Faith has replied

Replies to this message:
 Message 62 by Faith, posted 08-31-2006 9:44 PM crashfrog has replied

crashfrog
Member (Idle past 1494 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 64 of 301 (345582)
08-31-2006 11:00 PM
Reply to: Message 62 by Faith
08-31-2006 9:44 PM


Re: Faith Logic
You are talking about ONE kind of experiment with bacteria and ONLY bacteria, correct?
Bacteria experiments are the easiest, but it's not difficult to do with any kind of organism.
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.
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.
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."
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. Since mutation is the only natural source of new alleles, it's the only explanation for a new allele in the population. 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.
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.
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?

This message is a reply to:
 Message 62 by Faith, posted 08-31-2006 9:44 PM Faith has replied

Replies to this message:
 Message 72 by Faith, posted 09-01-2006 10:14 AM crashfrog has replied
 Message 93 by Faith, posted 09-02-2006 12:02 AM crashfrog has replied

crashfrog
Member (Idle past 1494 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 76 of 301 (345728)
09-01-2006 12:58 PM
Reply to: Message 72 by Faith
09-01-2006 10:14 AM


Re: That one bacterium again
I'm still hoping to get to your post here, but right now I seem to have forgotten again what this bacteria example is supposed to demonstrate and must ask that you explain it again.
I don't have the time right now to walk you though the experiment, but let me just jump to the end: 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.
You get a whole population from a single bacterium with its one allele -- a whole population of that one kind of bactera with that one allele. And does this allele then mutate somewhere in that population, is that what this is all about?
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.
If this isn't enough I'd be happy to try to explain again, or answer any other questions. We can even go to a specific experiment if you like, but I warn you that it will be quite detailed and technical.

This message is a reply to:
 Message 72 by Faith, posted 09-01-2006 10:14 AM Faith has replied

Replies to this message:
 Message 92 by Faith, posted 09-01-2006 11:35 PM crashfrog has replied

crashfrog
Member (Idle past 1494 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 1494 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

crashfrog
Member (Idle past 1494 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 106 of 301 (346030)
09-02-2006 1:08 PM
Reply to: Message 95 by jar
09-02-2006 12:18 AM


Re: On predictions and tests.
I just want to say - I'm not following where Faith is substantively wrong, either.
Here's the contention, as I see it - imagine a population and a gene with 20 different alleles in that population, which we'll use to measure diversity. We'll say that population has a diversity of 20.
Imagine then that the population is divided by some speciating process. What was one contiguous gene pool has become two, and from simple statistics we might imagine that all the individuals with one of the alleles went in the first population, and all the individuals with another of the alleles went to the second population.
So, where we had one population with 20 alleles, now we have two populations, and each of them has 19 alleles for that gene.
No alleles have actually disappeared, but some of them have become inaccessable to members of each population, so to those individuals, they might as well not exist at all.
I see that as a reduction, however slight, in diversity for each of those subpopulations. That's the claim I see Faith making. Where am I going wrong? Obviously, you could count both populations together and see the same amount of diversity you had before, but that seems incoherent. I wouldn't count the alleles found in the African elephant when trying to assess the diversity of the human species, so why would I count both of these populations together if they're already permanently seperated?

This message is a reply to:
 Message 95 by jar, posted 09-02-2006 12:18 AM jar has replied

Replies to this message:
 Message 107 by jar, posted 09-02-2006 1:43 PM crashfrog has replied
 Message 109 by NosyNed, posted 09-02-2006 2:00 PM crashfrog has not replied
 Message 114 by Quetzal, posted 09-02-2006 2:39 PM crashfrog has not replied

crashfrog
Member (Idle past 1494 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 116 of 301 (346118)
09-02-2006 7:59 PM
Reply to: Message 107 by jar
09-02-2006 1:43 PM


Re: On predictions and tests.
IMHO that is wrong because it is just a snapshot at one moment of a dynamic process.
It seems like it's more like before and after, to me.
I get that it's not as simple as I portray, and that indeed, it's a fallacy to imply that you can say "at this one point, they were one species, and now at this next moment, they are two."
It looks like one population got a whole bunch of copies of MGC8902 and very likely did not get a copy of some other gene so there was very likely a temporary reduction in diversity. However, over time, there was an increase in diversity as some of those copies of MGC8902 were available to be modified to perform new functions.
Obviously, I don't mean to contend that genetic diversity can never rise. Clearly mutation has that effect.
But assuming there's an indentifiable instant of speciation, it doesn't seem unreasonable to assert that genetic diversity is equal or lower in each subpopulation than in the whole population. I don't see how it can go up, except subsequently, due to mutation.

This message is a reply to:
 Message 107 by jar, posted 09-02-2006 1:43 PM jar has replied

Replies to this message:
 Message 119 by Faith, posted 09-02-2006 8:47 PM crashfrog has replied
 Message 120 by jar, posted 09-02-2006 8:57 PM crashfrog has not replied

crashfrog
Member (Idle past 1494 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

crashfrog
Member (Idle past 1494 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 1494 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

crashfrog
Member (Idle past 1494 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 1494 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

crashfrog
Member (Idle past 1494 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 165 of 301 (346743)
09-05-2006 4:52 PM
Reply to: Message 134 by Faith
09-04-2006 2:11 AM


Re: Rise in which kind of diversity?
The cheetah is a NEW phenotype
I don't see how it is, or at least, I don't see how it's a "new phenotype" that arose through a reduction in allelic diversity. The "cheetah body plan", or the traits that we recognize as the definitive morphological character of cheetahs, didn't arise because of the bottleneck event; they were already there in the population. The pre-bottlenect population of ur-cheetahs would have included individuals that looked like modern cheetahs, and individuals that looked differently.
The bottleneck didn't give rise to anything new, it simply removed other phenotypes, so that the current cheetah "specification" was the only one left.
How is that a new phenotype? That's simply the loss of the old ones - a loss of phenotypic diversity, which is exactly what I've been telling you is the consequence of a loss of allelic diversity.
The phenotype is now completely defined for those particular traits by those single alleles. It is a NEW phenotype compared to the population it was bottlenecked from
No, it's not, because it was in the old population, too.
Let's say that we have a population of tall people and short people, and that that's determined, as it is in pea plants, by a single gene that is dominant for tall.
Now, imagine that aliens come down from space and because they hate tall people, they vaporize everybody who is tall. That leaves only the people who lack any tall alleles, who only possess the short allele. That's a loss of diversity, a loss of an allele (the tall one.)
So, all humans are now a lot shorter. But how is that "new"? All those short people where there in the old population, before the alien bottleneck. So there's no "new" phenotypes - only a loss of old ones. A loss of physical diversity that stemmed from something that reduced genetic diversity.
That's the only thing a loss of genetic diversity can result in - a loss of physical diversity.
But loss of alleles is still the general trend over time
No, it's not. I've already referred to the direct experimental evidence that this is not the case. Alleles increase in diversity over time; that's the trend. Specific events might remove alleles, selection might do that (although for statistical reasons it's actually fairly hard to completely select out an allele, especially if it's recessive. The fewer number of individuals that possess an allele, the harder it is to select against.) But the overarching trend is always one of allelic increase, not decrease. That's been consistently borne out in observation and experiment, and mutations are known - known, Faith! Known like we know lightning is made of electricity! - to be the cause.
and new phenotypes are certainly produced by this loss
If what you're saying is that they're "new" not because they're actually something different than has come before, but merely "new" because now they represent a greater fraction of individuals, that's pretty dumb. Imagine if you had a child that kept bugging you for a new toy.
Now imagine if you took all of their toys but one, and threw them in the trash. Imagine if you tried to convince your incredulous child that their last remaining toy, that ragged stuffed bunny with the missing eye she'd had since she was 2, was now "new" because it represented a greater fraction of her toys - 100% of her toys, in fact - than it had before.
Is that logic you can imagine convincing even a child? No? Then why is that the logic you seem to be bringing in here? What you're glossing over in every one of your posts is why we should consider a phenotype "new" simply because we lost a bunch of the old ones. How does that make any sense at all?

This message is a reply to:
 Message 134 by Faith, posted 09-04-2006 2:11 AM Faith has replied

Replies to this message:
 Message 167 by Faith, posted 09-05-2006 7:15 PM crashfrog has replied
 Message 168 by NosyNed, posted 09-05-2006 7:39 PM crashfrog has replied

crashfrog
Member (Idle past 1494 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


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


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

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

crashfrog
Member (Idle past 1494 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


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


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

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

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

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