Register | Sign In


Understanding through Discussion


EvC Forum active members: 65 (9162 total)
4 online now:
Newest Member: popoi
Post Volume: Total: 915,815 Year: 3,072/9,624 Month: 917/1,588 Week: 100/223 Day: 11/17 Hour: 0/0


Thread  Details

Email This Thread
Newer Topic | Older Topic
  
Author Topic:   Population Genetics
PaulK
Member
Posts: 17822
Joined: 01-10-2003
Member Rating: 2.2


Message 16 of 90 (364041)
11-16-2006 7:28 AM
Reply to: Message 15 by Modulous
11-16-2006 6:57 AM


Yes, ReMine does pretty much claim that the limit is nucleotides
quote:
My immediate response is, "Who are they kidding." I would feel differently about their posturing if the public could recall a serious history of leading evolutionists claiming a limit of 1,667 beneficial nucleotides is "not a problem." But no such history exists. Even the 1,667 limit itself was the trade secret of evolutionary genetics.1 I was the first to bring it to public attention.
And if ReMines argument on that doesn't make sense then why trust what he says elsewhere ?

This message is a reply to:
 Message 15 by Modulous, posted 11-16-2006 6:57 AM Modulous has not replied

  
crashfrog
Member (Idle past 1466 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 17 of 90 (364064)
11-16-2006 10:00 AM
Reply to: Message 11 by Hyroglyphx
11-15-2006 11:08 PM


The argument is not about the genetic difference between divergent organisms. The figures were first supported by many eminent evolutionists before 1957. He is simply reiterating an argument posed by an evolutionist, Haldane, who candidly offered the theorum in the interest of scoence, not the special interest of evolution.
Haldane is wrong. It's that simple. Not only does every population geneticist know that Haldane is wrong, Haldane himself knew he was wrong.
What wasn't clear about my post? To the extent that ReMine bases his arguments on Haldane, he's wrong. Because Haldane was wrong. You don't seem to have spoken to that point at all.
The rest of the ReMine material you post is just a hand-waving accusation of fraud among evolutionists with absolutely no evidence to support it. He claims that evolutionists somehow "didn't tell the public" about Haldane's Dilemma, but that's obviously false - Haldane published in the peer-reviewed journals just like everybody else. He didn't toss his manuscript into a file cabinet that ReMine discovered, or something. Haldane's research has been publically avaliable since he published in 1957.
2. In addition, Haldane used assumptions that favor evolution.
No, he didn't. As I told you, he used assumptions that invalidated his own model. He used assumptions that are contradicted by reality.
As for the specious plea that genetics has developed more since the 1950's, one first has to consider that the backbone of genetics have not changed, such as Mendelian genetics.
In fact, as a student of genetics, I can tell you that this is absolutely false. Mendelian genetics is the sole staple of a high school genetics program simply because that's the only genetics a high school student can be expected to understand.
In truth, very, very few genes operate in a strictly Mendelian way. The greatest advance in genetics, of course, came well after Haldane - the elucidation of the molecular structure of DNA and the confirmation of its role as the mechanism of gene expression and heredity.
The backbone of genetics is DNA, and the research on DNA was in its infancy in 1957. And you're really going to try to tell me that we've learned nothing new since 1957? Really? Funny; I've been to all the garage sales but I can't seem to find a PCR-RFLP kit from back then. Or a gel electrophoresis setup. Or a list of primer sequences and restriction enzymes from 1957.
I wonder why that might be?
How does he misstate Gould?
I just told you how. What wasn't clear about my post?
He is saying that, (actually, Haldane is saying, he is simply agreeing), that there is a finite number of possible mutations, whether by insertions, deleterious, or otherwise.
Strawman argument. Nobody's saying that, given a finite stretch of time, an infinite number of mutations is possible. Clearly, that's not something we should expect to see.
But 1667 is far, far too few. Haldane knew it; everybody seems to know it but ReMine. Most importantly, it's contradicted by direct observation so clearly any model that predicts so few possible mutations is structurally flawed. We conclude that it is flawed in the same way we conclude that any equation where 1 = 0 is flawed. When the outcome is contradicted by the reality we know the model is flawed, simple as that.

This message is a reply to:
 Message 11 by Hyroglyphx, posted 11-15-2006 11:08 PM Hyroglyphx has replied

Replies to this message:
 Message 22 by Hyroglyphx, posted 11-16-2006 1:37 PM crashfrog has replied

  
Hyroglyphx
Inactive Member


Message 18 of 90 (364077)
11-16-2006 11:37 AM
Reply to: Message 14 by PaulK
11-16-2006 6:19 AM


Can you explain why ReMine's claim of a maximum of 1667 beneifical nucleotide substitutions should be considered valid ?
Again, this isn't ReMine's baby, its Haldane's. The figures were first compiled and tabulated in the 1950's be a host of evolutionists seeking to better understand population genetics. ReMine is just sort of rediscovering the issue and wondering why something this profound was overlooked. For evolution to occur, it requires the substitution of new beneficial mutation into the population to create new biological adaptations that survive the ax of natural selection. The number itself derives from Haldane's calculation that organisms with low reproduction rates, such as humans, (reproducing 0-8) offspring in a parents lifetime) could substitute a new beneficial mutation no more frequently than 1:300 generations. Now, if you really think about, this is completely true and its very straightforward.
The best place to start this with a trial error is the human/simian lineage because its relatively easy to quantify. The ancestry between ans apelike ancestor begins around 10 million years ago, which is often offered as the most reasonably generous to give as much leeway as possible, without completely undermining the integrity of the experiment. Mathematically, this is already presenting a problem for possible beneficial mutations. The problem is further compounded when considering that the human adaptations in question are alleged to have evolved mostly within the last two million years. But at the end of the day, no low reproducing lineage could substitute more than 1667 beneficial mutations. That's extremely low. So low as to make all the alleged changes impossible.
Larger mutations - transpositions, substitutions and deletions - are reasonably common and can include dozens or even hundreds of nucleotides. Why should we ignore these ?
Well, that's a good question. According to evolutionary geneticists, each of those substitutions is typically represented as one nucleotide, not thousands of nucleotide differences. This is because a change in nucleotides, even in a small amount, can prove fatal to an organism. We all know that DNA has to be in precise order to function properly. Even if we take a small fraction of the 1,667 figure, it becomes less likely to have occured. The odds of having as much as 84 nucleotide change is an astronomical figure that greatly exceeds 1050, which is mathematically representative of "absolute zero."
If you evidence that such a high number of mutations can occur, benefically, in any organism and still live to pass that on, I'd love to hear about it. You also have to factor in genetic death or genetic load as a substitution cost for every good mutation. You'll see that you'll start to get into the negatives rather quickly at the rate necessary for evolution to have occured efficiently.
How do you measure the number of nucleotide changes in a substitution ? Given a polymorphic gene (multiple alleles in the pool) what is the baseline ? Does ReMine's claim even make sense ?
ReMine goes over this, because you aren't the only one to offer gene clusters as a possible solution, such as pleiotropy or really anything considered polygenous. He states that this is grossly oversimplified to grant the impossible the possibility. Even under terrific circumstances where each gene acts independently of other genes, the figure is still too low.
"Evolutionists must accept what nature doles out - and we can observe what nature doles out. The issue is fundamentally empirical and observable, not one of telling stories about regulatory genes... when Haldane calculated the total cost of a substitution (=30), he assumed selection coefficients approaching zero, which gives the absolute lowest possible total cost of substitution. The figure rises for higher selection coefficients, and rises especially rapidly when selection coefficients get above one-tenth (s>0.1). Therefore, if evolutionary scenarios invoke high selection coefficients (such as mutations for antibiotic resistance or pesticide resistance), then the total cost of substitution gets quite high - and the number of substitutions (previously at 1,667) goes to a much lower limit.
In summary, whatever the blend of substitutions, (a) they must correspond to what we observe in nature, and (b) they must meet the cost constraints, (higher selection coefficients will lower the plausible number of substitutions)."
-Walter ReMine

Faith is not a pathetic sentiment, but robust, vigorous confidence built on the fact that God is holy love. You cannot see Him just now, you cannot fully understand what He's doing, but you know that you know Him." -Oswald Chambers

This message is a reply to:
 Message 14 by PaulK, posted 11-16-2006 6:19 AM PaulK has replied

Replies to this message:
 Message 19 by Wounded King, posted 11-16-2006 12:18 PM Hyroglyphx has not replied
 Message 20 by crashfrog, posted 11-16-2006 12:48 PM Hyroglyphx has replied
 Message 21 by PaulK, posted 11-16-2006 12:57 PM Hyroglyphx has not replied

  
Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


Message 19 of 90 (364087)
11-16-2006 12:18 PM
Reply to: Message 18 by Hyroglyphx
11-16-2006 11:37 AM


According to evolutionary geneticists, each of those substitutions is typically represented as one nucleotide, not thousands of nucleotide differences. This is because a change in nucleotides, even in a small amount, can prove fatal to an organism. We all know that DNA has to be in precise order to function properly. Even if we take a small fraction of the 1,667 figure, it becomes less likely to have occured. The odds of having as much as 84 nucleotide change is an astronomical figure that greatly exceeds 1050, which is mathematically representative of "absolute zero."
Care to substantiate any of that?
According to evolutionary geneticists, each of those substitutions is typically represented as one nucleotide, not thousands of nucleotide differences.
'Typically' covers a multitude of sins. As was discussed in the recent threads about human/chimp divergence the mutation rate for length mutations is roughly 1/10 that of single nucleotide substitutions but length mutations account for almost four times as much of the divergence between chimps and humans.
This is because a change in nucleotides, even in a small amount, can prove fatal to an organism.
Well it can also prove beneficial or prove completely neutral and the same holds true for single nucleotide substitutions as well as length mutations.
We all know that DNA has to be in precise order to function properly.
I certainly don't know that. Some sequence of DNA need to be in a specific order to function correctly but there are also large independent sections of chromosome that could quite easily be transferred wholesale somewhere else with no ill effects. Similarly while the particular order of exons in a gene might be important that gene could almost certainly still withstand a considerable change in its nucleotide composition and even in the amino acid sequence of its product.
The odds of having as much as 84 nucleotide change is an astronomical figure that greatly exceeds 1050, which is mathematically representative of "absolute zero.
Care to show us your working? This looks like a calculation for 84 specific mutations to have occurred. Are you claiming this is the probability of any 84 beneficial nucleotide substitutions to have occurred? If so Haldane and ReMine seem to both think that it would only take 504,000 years for the impossible to happen at least once assuming it takes 300 generations for each beneficial allele to become fixed and a generation is ~20 years. Is the impossible really that easy or is your entire probability argument specious from the get-go.
TTFN,
WK
Edited by Wounded King, : No reason given.

This message is a reply to:
 Message 18 by Hyroglyphx, posted 11-16-2006 11:37 AM Hyroglyphx has not replied

  
crashfrog
Member (Idle past 1466 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 20 of 90 (364090)
11-16-2006 12:48 PM
Reply to: Message 18 by Hyroglyphx
11-16-2006 11:37 AM


ReMine is just sort of rediscovering the issue and wondering why something this profound was overlooked.
Because everybody knew Haldane was wrong. Just like everybody but ReMine seems to understand that ReMine is wrong. His work is consistently rejected in peer review.
The number itself derives from Haldane's calculation that organisms with low reproduction rates, such as humans, (reproducing 0-8) offspring in a parents lifetime) could substitute a new beneficial mutation no more frequently than 1:300 generations. Now, if you really think about, this is completely true and its very straightforward.
There's nothing at all straightforward about it to me. Could you elaborate? Usually people say "this is obvious" when they don't understand a step in the reasoning but they're hoping no one will ask them to explain it.
Look, it's pretty obvious to me that in a sexual reproducing species, you can fix a large number of beneficial mutations simultaneously. In fact sexual reproduction makes this a lot more likely to occur, which is part of the evolutionary advantage of sexual reproduction. So this idea that you can only fix one gene at a time, and only over 300 generations, simply doesn't hold up for me. It's prima facie ridiculous.
If you evidence that such a high number of mutations can occur, benefically, in any organism and still live to pass that on, I'd love to hear about it.
Open a phylogenetics text. It's well-understood that, in mammals (for instance), we can expect roughly one uncorrected nucleotide substitution during DNA replication per every ~3 billion base pairs. That means that every new individual mammal should have somewhere between 5 and 100 mutations. (6 gbp genome, two copies of each genome per offspring, plus mutations that may occur during the very earliest stages of cell cleavage, which would have a similar effect as germline mutations inherited from parental gametes.)
So I don't see 86 mutations as a really large amount. You almost certainly have way more than 86 mutational differences between the genes you had as a zygote and the genes you should have inherited on your parent's chromosomes.
ReMine operates from the ridiculous assumption that multiple genes can't be fixed at a time; that beneficial mutations have to be fixed in linear chronological order, one at a time. Neither he nor you seem to have offered any support I can detect for this position. Please correct me if I'm mistaken.

This message is a reply to:
 Message 18 by Hyroglyphx, posted 11-16-2006 11:37 AM Hyroglyphx has replied

Replies to this message:
 Message 25 by Hyroglyphx, posted 11-16-2006 7:31 PM crashfrog has replied

  
PaulK
Member
Posts: 17822
Joined: 01-10-2003
Member Rating: 2.2


Message 21 of 90 (364091)
11-16-2006 12:57 PM
Reply to: Message 18 by Hyroglyphx
11-16-2006 11:37 AM


quote:
Again, this isn't ReMine's baby, its Haldane's.
False. The idea that the substitution rate typically refers to single nucleotides is ReMines - not Haldanes.
And Haldanes numbers were based on assumptions that are certainly not guaranteed to hold (e.g. the assumption that all selection is "hard" selection)
quote:
Well, that's a good question. According to evolutionary geneticists, each of those substitutions is typically represented as one nucleotide, not thousands of nucleotide differences.
That isn't even what ReMine says ! If you can really show me an evolutionary geneticist saying that we should count a large insert or transposition as a single nucleotide change - when in fact it is many - please go ahead. Personally I just think you are spouting words you don't understand.
quote:
The odds of having as much as 84 nucleotide change is an astronomical figure that greatly exceeds 1050, which is mathematically representative of "absolute zero."
A simple case of garbage in, garbage out. The fact that you don't explain what you are calculating or how just makes it nonsense.
quote:
ReMine goes over this, because you aren't the only one to offer gene clusters as a possible solution, such as pleiotropy or really anything considered polygenous
But I wasn't offering a solution or referring to gene clusters or pleiotropy. I was simply asking how you could measure how you could measure the number of nucleotide substitutions when a gene is polymorphous to start with (i.e. has more than one allele). And you don't offer a real answer, instead you ustt quote ReMine.

This message is a reply to:
 Message 18 by Hyroglyphx, posted 11-16-2006 11:37 AM Hyroglyphx has not replied

  
Hyroglyphx
Inactive Member


Message 22 of 90 (364095)
11-16-2006 1:37 PM
Reply to: Message 17 by crashfrog
11-16-2006 10:00 AM


Haldane is wrong. It's that simple. Not only does every population geneticist know that Haldane is wrong, Haldane himself knew he was wrong.
What wasn't clear about my post? To the extent that ReMine bases his arguments on Haldane, he's wrong. Because Haldane was wrong. You don't seem to have spoken to that point at all.
You haven't addressed in what way either of then are wrong. You made a couple of points on what you thought he meant. I even posted ReMine's answer to his critics. Some of which were your objections. But you haven't addressed it, and simply saying, "he's wrong, he's all wrong," does nothing to offer your argument. Likewise, RAZD simply saying, "the math is wrong, its all wrong," doesn't explain how or why. If its wrong, I want to be shown why. If anyone can take ReMine's challenge or demonstrate why its wrong, I and ReMine would certainly concede.
The rest of the ReMine material you post is just a hand-waving accusation of fraud among evolutionists with absolutely no evidence to support it. He claims that evolutionists somehow "didn't tell the public" about Haldane's Dilemma, but that's obviously false - Haldane published in the peer-reviewed journals just like everybody else. He didn't toss his manuscript into a file cabinet that ReMine discovered, or something. Haldane's research has been publically avaliable since he published in 1957.
Right, Haldane peer reviewed it, and no one could answer the question. It simply faded into obscurity until years later. The point ReMine is making is that it wasn't solved then, and it hasn't been solved now. If there was really a simple solution to overcome the dilemma, why hasn't anything of rigor been offered? Heck, even Maynard-Smith, a very prominent evolutionist, admitted that it really did present a large challenge to the prevailing wisdom.
In fact, as a student of genetics, I can tell you that this is absolutely false. Mendelian genetics is the sole staple of a high school genetics program simply because that's the only genetics a high school student can be expected to understand.
Calling Mendelian genetics the staple of high school genetics is like saying that Newtonian law is the staple of high school law of gravitation. That's reducing its importance to the field to mere child's play.
In truth, very, very few genes operate in a strictly Mendelian way. The greatest advance in genetics, of course, came well after Haldane - the elucidation of the molecular structure of DNA and the confirmation of its role as the mechanism of gene expression and heredity.
First of all, DNA was already known long before Crick and Watson. This is a bit of a misnomer here. DNA was first discovered in the late 1800's by Friedrich Miescher. Aside from which, Darwin and Wallace and the rest of the gang all knew there were heritable traits before DNA. It didn't take a genius to figure out that animals produce like animals, or that little Timmy bore a striking resemblance to his father.
Now, by the time the double-helix was co-discovered in 1953, Haldane published his peer review a whole four years after. Yes, that's in its infancy, but then again, this is all pointless. The backbone, the rules of inheritance, were known long before with Mendelian genetics. DNA is simply a pathway or a mechanism that explains why inheritance does what it does.
The backbone of genetics is DNA, and the research on DNA was in its infancy in 1957. And you're really going to try to tell me that we've learned nothing new since 1957? Really? Funny; I've been to all the garage sales but I can't seem to find a PCR-RFLP kit from back then. Or a gel electrophoresis setup. Or a list of primer sequences and restriction enzymes from 1957.
I never said we haven't learned anything beyond 1957. I said we haven't learned so extraordinary since the 1957 that would pose a legitimate challenge to Haldane's Dilemma. But if you are so certain, you can start by taking the challenge.
quote:
How does he misstate Gould?
I just told you how. What wasn't clear about my post?
I offered a solution. You haven't offer a rebuttal.
Nobody's saying that, given a finite stretch of time, an infinite number of mutations is possible. Clearly, that's not something we should expect to see.
Where did I, Haldane, or ReMine say anything about an 'infinite' number of mutations? I said that there is a 'finite' number of possible mutations-- meaning there is a specific limit.
But 1667 is far, far too few.
Of course it is. That's the thrust of the argument.
Haldane knew it; everybody seems to know it but ReMine.
Of course Haldane knew it. That's why he wrote a paper on it. It sought for someone to reconcile the implications this had.
Most importantly, it's contradicted by direct observation so clearly any model that predicts so few possible mutations is structurally flawed. We conclude that it is flawed in the same way we conclude that any equation where 1 = 0 is flawed. When the outcome is contradicted by the reality we know the model is flawed, simple as that.
What??? Name me one organism that has a high number of beneficial mutations as the result of point mutations. You know what they offer as examples of beneficial mutations? Yeast, bacteria, and viruses-- all prokaryotes where a single mutation is bound to something good. Big deal. We are talking about a much more complex organism, namely, humans. So, what about eukaryotes? Would the deletion of a single nucleotide lead to a frameshift mutation? Would the 1,667 figure change dramatically if 3 nucleotides changing simultaneously, yet beneifically, offer any real solution? No, it would still be too slow to allow for human evolution. Aside from which, it wouldn't act beneficially because the entire sequence following the mutation would translate into a chain of garbled amino acid sequences. Afterall, this is what we normally expect of mutations. Evolutionists just cling to the hope that so many mutations would have been beneficial, even though finding any such evidence is scant.
Edited by nemesis_juggernaut, : No reason given.

Faith is not a pathetic sentiment, but robust, vigorous confidence built on the fact that God is holy love. You cannot see Him just now, you cannot fully understand what He's doing, but you know that you know Him." -Oswald Chambers

This message is a reply to:
 Message 17 by crashfrog, posted 11-16-2006 10:00 AM crashfrog has replied

Replies to this message:
 Message 23 by Chiroptera, posted 11-16-2006 2:07 PM Hyroglyphx has not replied
 Message 24 by crashfrog, posted 11-16-2006 3:39 PM Hyroglyphx has not replied
 Message 27 by RAZD, posted 11-16-2006 8:41 PM Hyroglyphx has not replied

  
Chiroptera
Inactive Member


Message 23 of 90 (364105)
11-16-2006 2:07 PM
Reply to: Message 22 by Hyroglyphx
11-16-2006 1:37 PM


The abuse of models.
quote:
Likewise, RAZD simply saying, "the math is wrong, its all wrong," doesn't explain how or why.
RAZD doesn't have to explain how or why. The overwhelming abundance of data provides conclusive evidence that common descent is the correct explanation for features in the world that we see around us. Evolution happened, and humans evolved from earlier primates. Any math that shows otherwise is flawed, either in the mathematic manipulations or in the assumptions that went into the model.
It is like in mathematics (my field). If I claim to have proven a new theorem and someone else shows an example that contradicts the theorem, then she does not have to show me where my error lies; she has done her part in demonstrating that my "theorem" is false. It becomes my job to find my error and see if I can correct it.
This is how it works in science (and I have also done some scientific modelling). Models rarely prove or disprove theories. Models are used to see whether or not we understand the unseen processes that drive the phenomena under question. Whatever Haldane's Dilemma is supposed to do, it has absolutely nothing to do with whether or not the descent of humans from earlier primates is true. The truth of the descent of humans from earlier primates can only by determined by looking at the actual physical evidence. At best, Haldane's calculations can only be used to check whether scientists understand the mechanisms that led to the evolution of humans.
If Haldane's Dilemma has any validity (and I am not saying that it does), then it is up to the people making this claim to figure out why the predictions of the calculations are at odds with reality. It is up to them to try to figure out where in the calculations they have gone wrong, which assumptions are incorrect, or, at the most extreme case, what are the correct processes that drove human evolution.

Kings were put to death long before 21 January 1793. But regicides of earlier times and their followers were interested in attacking the person, not the principle, of the king. They wanted another king, and that was all. It never occurred to them that the throne could remain empty forever. -- Albert Camus

This message is a reply to:
 Message 22 by Hyroglyphx, posted 11-16-2006 1:37 PM Hyroglyphx has not replied

  
crashfrog
Member (Idle past 1466 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 24 of 90 (364126)
11-16-2006 3:39 PM
Reply to: Message 22 by Hyroglyphx
11-16-2006 1:37 PM


You haven't addressed in what way either of then are wrong.
I thought I was as clear as I could possibly be. ReMine and Haldane are wrong because 300 generations to fix a gene doesn't mean only one gene fixed every 300 generations. Multiple genes can fix simultaneously - in fact, sexual reproduction makes this a given.
Right, Haldane peer reviewed it, and no one could answer the question.
No, that's not true. Bruce Wallace answered it in 1991 in his book Fifty Years of Genetic Load - An Odyssey. When you correct Haldane's misapprehension that two genes take twice as long to fix as one, the genetic cost of fixation disappears entirely.
If there was really a simple solution to overcome the dilemma, why hasn't anything of rigor been offered?
It has been. ReMine has simply ignored it, and so have you. That's why you keep avoiding the rebuttals, and why ReMine can't publish except in the vanity press.
That's reducing its importance to the field to mere child's play.
It is child's play. That's what I'm telling you - we teach it to children because it's a lot easier than molecular genetics, because it applies to so many fewer cases.
Most genes are not strictly Mendelian. (Mitochondrial genes are not at all Mendelian.) Phenomena like penetrance and epistasis are regularly observed, but Mendel had no explanation for them.
Molecular genetics is the true understanding of inheritance, and more importantly, the mechanism of inheritance, not simply it's pattern. Mendel simply observed a pattern of inheritance that he could not truly explain. Molecular genetics explains both Mendel's patterns and the non-Mendelian patterns, like epistasis.
First of all, DNA was already known long before Crick and Watson.
I never said it wasn't. Crick and Watson figured out what it did and how it did it, which proved that DNA was the molecule of heredity. This was suspected but not confirmed until their work.
Aside from which, Darwin and Wallace and the rest of the gang all knew there were heritable traits before DNA.
Sure. But nobody knew how that worked, or why some traits were inherited but some were not. Even Mendel didn't know; he just observed the patterns of inheritance of four specific characters in one specific species. Even his attempts at developing an explanation were clumsy. It took Thomas Morgan to develop the chromosomal theory of inheritance; the first steps into molecular genetics.
I said we haven't learned so extraordinary since the 1957 that would pose a legitimate challenge to Haldane's Dilemma.
Why would we need to? I told you that even Haldane himself eventually rejected his own "dilemma".
I offered a solution. You haven't offer a rebuttal.
A rebuttal to what? Look, you're hopelessly confused. Let me spell out this portion of our exchange. You quoted ReMine saying that Gould's punctuated equilibrium proposed long periods of genetic stasis.
This is false. Punctuated equilibrium does not propose genetic stasis, it proposes morphological stasis. Genetic changes continue during the morphological stasis, that's how sudden morphological change occurs when stasis ends - because of genetic changes that had been occuring the whole time.
That's how ReMine misrepresents Gould. Maybe you're simply not clear on the difference between morphology and genetics? You need to get back to Mendel, I guess.
Of course it is. That's the thrust of the argument.
Yes. It's why the argument is wrong.
What exactly is unclear, here? ReMine's model predicts fewer fixations in a population than we observe. Hence, his model is wrong. You can't use a model to disprove what's right in front of your face. That's such a basic idea of epistomology that it shouldn't even have to be made explicit.
Name me one organism that has a high number of beneficial mutations as the result of point mutations.
Name you one? I'll go much better than that - all organisms have beneficial mutations that are the result of point substitutions.
Yeast, bacteria, and viruses-- all prokaryotes where a single mutation is bound to something good.
Huh? No, there's plenty of mutations that are fatal to prokaryotes. Seriously. "Bound to do something good"? Where do you get this stuff?
We are talking about a much more complex organism, namely, humans.
Er, well, now you're leaving behind ReMine's argument, which was an argument from population genetics, to delve into the actual molecular chemistry of proteins, genes, and mutations. That wasn't the scope of ReMine's argument. Are you sure you're ready to leave that behind? You should probably open a new thread if you want to talk about how a mutation could be beneficial, even in a human.
Aside from which, it wouldn't act beneficially because the entire sequence following the mutation would translate into a chain of garbled amino acid sequences.
No. A point substitution won't change the read frame. You have to have an addition or a deletion to affect the read frame. And even if you do, a subsequent addition or deletion down the line restores the read frame anyway, leaving the disruption limited to the space between the two mutations. Anyway you can usually alter up to 60% of the primary structure of a protein with little to no effect on its function.
Look, until you're up to speed with molecular genetics, you're not going to be able to deal with the evidence from genetics. And the fact that you think any change at all in a gene "garbles" the gene shows me that you have no idea what's going on, here.

This message is a reply to:
 Message 22 by Hyroglyphx, posted 11-16-2006 1:37 PM Hyroglyphx has not replied

  
Hyroglyphx
Inactive Member


Message 25 of 90 (364177)
11-16-2006 7:31 PM
Reply to: Message 20 by crashfrog
11-16-2006 12:48 PM


Look, it's pretty obvious to me that in a sexual reproducing species, you can fix a large number of beneficial mutations simultaneously. In fact sexual reproduction makes this a lot more likely to occur, which is part of the evolutionary advantage of sexual reproduction.
Why is this 'obvious?' Lets look at the only known cases of speciation as presented by TalkOrigins. Most of their instances are all in the plant kingdom. Of the few in the animal kingdom, they're all flies-- simple on the molecular level. Now, I'm not even going to go into how many different ways I object to the Drosophila, rather, lets assume they are all legitimate cases of speciation due to beneficial mutations? Of their beneficial mutations, they to cite Sickle Cell Anemia, as if the trade-off between SCA and malaria is really worth mentioning. Beneficial mutations aren't obvious. They are so rare as to be absurd to hang the theory upon them, or to account for all of life's diversity is hinged on their success. And the cases of speciation are so sparse, so as to render evolution as an unwitnessed event that bases its beliefs on inferences rather than empiricism-- which, consequently, is the exact same charge they have against ID.
Here's the point of Haldane's Dilemma. Even if a beneficial mutation survived, for it to become fixed in a population, the organisms not carrying it must be eliminated because it will just become swamped in the gene pool. This is the 'cost of substitution.'
I don't see 86 mutations as a really large amount. You almost certainly have way more than 86 mutational differences between the genes you had as a zygote and the genes you should have inherited on your parent's chromosomes.
Most mutations that occur in the average human do not have any affect on our progeny. I think we'd all agree that the most frequent type of mutation is a single nucleotide substitution, that pretty much will go away when we die-- meaning it poses no kind of affect in any evolutionary sense. For a mutation to make a significant impact on an organism and their morphology, is for a mutation to occur during the production of haploid production. An accident in replication anywhere else in the body will only affect the specific cell where the injury occurred. We have these kinds of mutations all the time in our body, but it doesn't go anywhere. They die with us. So, really, mentioning that we have so many mutations already is inconsequential.
Edited by nemesis_juggernaut, : Having problems formatting properly

Faith is not a pathetic sentiment, but robust, vigorous confidence built on the fact that God is holy love. You cannot see Him just now, you cannot fully understand what He's doing, but you know that you know Him." -Oswald Chambers

This message is a reply to:
 Message 20 by crashfrog, posted 11-16-2006 12:48 PM crashfrog has replied

Replies to this message:
 Message 26 by crashfrog, posted 11-16-2006 8:23 PM Hyroglyphx has not replied
 Message 28 by Wounded King, posted 11-17-2006 6:46 AM Hyroglyphx has not replied
 Message 30 by Allopatrik, posted 02-17-2007 3:49 AM Hyroglyphx has not replied

  
crashfrog
Member (Idle past 1466 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 26 of 90 (364186)
11-16-2006 8:23 PM
Reply to: Message 25 by Hyroglyphx
11-16-2006 7:31 PM


Why is this 'obvious?'
Because every individual is the result of two genetic heritages.
Thus, fixation happens at least twice as fast as Haldane's model.
Now, I'm not even going to go into how many different ways I object to the Drosophila, rather, lets assume they are all legitimate cases of speciation due to beneficial mutations?
...ok, you've lost me. I thought we were talking about Haldane's dilemma, not speciation. Speciation isn't the topic of this thread and it doesn't have anything to do with Haldane's dilemma. Are you just not interested in pursuing this topic? Or did you just not understand the topic before you posted on it, and so now you don't know how to respond to rebuttals except to bring up irrelevant, off-topic subjects?
Even if a beneficial mutation survived, for it to become fixed in a population, the organisms not carrying it must be eliminated because it will just become swamped in the gene pool. This is the 'cost of substitution.'
Right. Where's the dilemma? Eventually, every member of a sexual population can trace it's ancestry back to two single shared individuals; one male and one female. (No, this isn't proof of Noah's Ark or some such nonsense.)
Most mutations that occur in the average human do not have any affect on our progeny.
You seem to have misunderstood. I was referring specifically to germline mutations, not somatic mutations. In fact, you'll pass on half of the mutations you were born with (statistically; it depends obviously on which of your chromosomes are passed on to your offspring) to each of your children.
I think we'd all agree that the most frequent type of mutation is a single nucleotide substitution, that pretty much will go away when we die
If it occurs in a germline cell, it has an equal chance of being passed on, so I don't know where you're getting this idea that they'll "go away when you die." If your offspring get that chromosome it'll live on long after you.
So, really, mentioning that we have so many mutations already is inconsequential.
Again, you apparently didn't read closely. I was not referring to the somatic mutations you've accrued from decades of living in an environment with mutagens, etc. I was referring specifically to the germline mutations you aquired from your parents (or just after) at conception. You have between 5 and 100, maybe more, and since your own germline cells are decendants of your original single cell, your offspring will get some of them too. (Have gotten, I think you mentioned before you have children.)
I mean, counting all mutations, you surely have billions by now. I was just talking about the germline mutations since they're the evolutionarily relevant ones.

This message is a reply to:
 Message 25 by Hyroglyphx, posted 11-16-2006 7:31 PM Hyroglyphx has not replied

  
RAZD
Member (Idle past 1405 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 27 of 90 (364190)
11-16-2006 8:41 PM
Reply to: Message 22 by Hyroglyphx
11-16-2006 1:37 PM


math is not reality.
Likewise, RAZD simply saying, "the math is wrong, its all wrong," doesn't explain how or why. If its wrong, I want to be shown why.
It's wrong because it doesn't explain the facts. That is WHY it is wrong.
No matter what the math is or how it is developed or what assumptions it is based on, evaluation of the math is unnecessary when it doesn' t model reality: it is wrong.
This is also why all those calculations of probability are inherently wrong: life exists, either it happened naturally or was created makes no difference, the calculation cannot show that it could not happen naturally.
Enjoy.

Join the effort to unravel {AIDS/HIV} {Protenes} and {Cancer} with Team EvC! (click)

we are limited in our ability to understand
by our ability to understand
RebelAAmericanOZen[Deist
... to learn ... to think ... to live ... to laugh ...
to share.

This message is a reply to:
 Message 22 by Hyroglyphx, posted 11-16-2006 1:37 PM Hyroglyphx has not replied

Replies to this message:
 Message 29 by RAZD, posted 02-10-2007 9:03 AM RAZD has not replied

  
Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


Message 28 of 90 (364287)
11-17-2006 6:46 AM
Reply to: Message 25 by Hyroglyphx
11-16-2006 7:31 PM


Of the few in the animal kingdom, they're all flies-- simple on the molecular level.
In what way are flies any 'simpler' on the molecular level than humans? They may have less genes but they still use the same basic molecular mechanisms, with the arguable exception of DNA methylation.
If you object to bacteria and invertebrates as model organisms what would you accept?
Mice? Monkeys? Only actual human experimentation?
Beneficial mutations aren't obvious. They are so rare as to be absurd to hang the theory upon them
Don't you see the contradiction here? Given that beneficial mutations aren't obvious what rationale do you have for claiming that they are 'so rare as to be absurd to hang the theory upon them', how do you know how rare they are? Do you have a reliable way of measuring the rate of beneficial mutations in humans? Or are you just ignoring the fact that such mutations aren't obvious and basing your rate estimates on the fact that you don't see many egg headed super intellectual psychic mutants roaming the countryside?
TTFN,
WK

This message is a reply to:
 Message 25 by Hyroglyphx, posted 11-16-2006 7:31 PM Hyroglyphx has not replied

  
RAZD
Member (Idle past 1405 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 29 of 90 (384142)
02-10-2007 9:03 AM
Reply to: Message 27 by RAZD
11-16-2006 8:41 PM


Once more for Randman: the difference between model and reality.
It's wrong because it doesn't explain the facts. That is WHY it is wrong.
randman writes:
Message 189
In other words, if data does not support ToE, then the data must be wrong because ToE is a fact. This really is the basic approach of evolutionism.
RAZD echoes the same error.
You build a "model" of the Eiffel Tower using playing cards, making a tower with boxed sides and layers.
I tell you the model is false because it does not model the Eiffel Tower.
You complain that I have not addressed your use of playing cards in making the model and that nobody shows that the use of playing cards is wrong.
It is not the use of playing cards that makes the model wrong. It is wrong because stacks of rectangular boxes do not model the Eiffel Tower.
A house of cards is not reality.
Enjoy.
Edited by RAZD, : changed link readout

Join the effort to unravel AIDS/HIV, unfold Proteomes, fight Cancer,
compare Fiocruz Genome and fight Muscular Dystrophy with Team EvC! (click)


we are limited in our ability to understand
by our ability to understand
RebelAAmericanOZen[Deist
... to learn ... to think ... to live ... to laugh ...
to share.

This message is a reply to:
 Message 27 by RAZD, posted 11-16-2006 8:41 PM RAZD has not replied

  
Allopatrik
Member (Idle past 6187 days)
Posts: 59
Joined: 02-07-2007


Message 30 of 90 (385783)
02-17-2007 3:49 AM
Reply to: Message 25 by Hyroglyphx
11-16-2006 7:31 PM


quote:
Here's the point of Haldane's Dilemma. Even if a beneficial mutation survived, for it to become fixed in a population, the organisms not carrying it must be eliminated because it will just become swamped in the gene pool. This is the 'cost of substitution.'
That is only part of the "dilemma". Leigh Van Valen actually coined the term "Haldane's Dilemma": it was a problem for a population needing to fix beneficial mutations in a rapidly deteriorating environment. The dilemma is, populations of organisms with long generation times cannot fix the mutations needed to adapt to drastic ecological changes fast enough because they do not possess the reproductive excess necessary to prevent disastrous drops in population size.
Haldane's two papers on the subject did not--repeat--did NOT-- make the infamous 1667 beneficial mutations calculation. Remine did, using Haldanes estimate of 1 beneficial substitution every 300 generations. But so what? Since we have no idea how many beneficial substitutions it took (or would take) to differentiate human and chimpanzee from their common ancestor, the number has no known significance. It's an interesting calculation, I suppose, and I have no reason to think it's wrong in any appreciable way. But it doesn't impact evolutionary theory much.
A

This message is a reply to:
 Message 25 by Hyroglyphx, posted 11-16-2006 7:31 PM Hyroglyphx has not replied

Replies to this message:
 Message 31 by RAZD, posted 02-17-2007 9:27 AM Allopatrik has replied

  
Newer Topic | Older Topic
Jump to:


Copyright 2001-2023 by EvC Forum, All Rights Reserved

™ Version 4.2
Innovative software from Qwixotic © 2024