Are mutations enough to explain natural selection?

Scott and Fred,More light, less heat, please. If you need help please let me know.--------------------EvC Forum Administrator

Dear Eximius,E: Thanks Fred for your clarification and everyone else for the responses. Your answers have been very helpful but to keep the discussion going and to stop the topic straying too far into areas I am not very familiar with (I again apologise for my shortcomings) I would like to reiterate my original question:
How does natural selection favour a mutation that, while advantageous, is not likely to increase the carriers chance of survival or reproduction.PB: Usually the carrier has a diminished ability of reproduction. From antibiotic/drug resistence we know that as long as selective constraint are present such organism have an advantage. As soon as the constraint is removed the wild type takes over. Thus, only under permanent selective constraint traits can be maintained. Still, the genomes of all organisms are characterised by redundancies.
As mentioned, their is an increasing recognition that selection cannot explain biology as we know it now. I already mentioned genetic redundancies. But, more dramatically, even certain cells can be knocked out, without being lethal/affecting the fitness of the organism (for instance mast cell knock outs). Or, illustratively the design redundancy in the 100% perfect gliders of the Zanonia macrocarpa. It is an insoluble problem for evolutionism. As a bio-scientist I know that evolutionism is false and should be replaced by another theory, for instance by the GUToB. In a real search for truth I am not objected by the idea of a Creative Force.E: For evolution to work, every transitional step between, say, the light-sensitive skin-patch and the human or cephalopod eye has to be not only advantageous but advantageous *enough* to increase the individuals chance of reproduction. I sometimes have trouble seeing how that could happen, but I suppose it's like Gzus said and every time an adaptation evolves the situation is unique, so there is no single answer.PB: Who is gzus that he knows this? The only single answer is that it didn't happen that way. But to sound explanatory evolutionists have introduced meaningless terms like "almost neutral purifying selection". Everyone with a working brain knows it is bull. Evolutionism as a theory explaining microbe to man is dead. Killed by contemporary biology. People who deny it, don't know better (and should be educated properly) or prefer to be blind (a lot on this board). Therefor I registered to this board. To demonstrate that evolutionism cannot hold in the light of modern knowledge on biology. And thus evolutionism keeps people from what is really going on on this planet.E: As for the Dawkins quote, I didn't read it, it's from a television debate, and I agree that you don't need a great understanding of genetics to understand evolution. Darwin is proof of that. Besides that, I admire scientists that are comprehensible and interesting to the layman and I think Dawkins fits this category.PB: So you got Dawkins opinion from 'mind control'? Better catch up with real science instead being blinded by Dawkin's blathering on random mutations and selection, his outdated belief that 97% of DNA is junk, and his selfproclaimed search for thruth. Read some contemporary work on evolution and you will find out that molecular scientist now find out that evolution (= MPG in action) is not random. (e.g. LH Caporale is very accessible for layman. And read L. Spetner's Not by Chance: the complete refutation and overthrow of NDT. Also easy to read). Leave Dawkins for what he is: a great story teller. They were very popular in the middle ages, too. Fairytales, I mean, not science.Best wishes,
Peter

I tried to do affine transforms at Cornell to represent biochange but when this was going by the boards I reverted to simply asking the evolutionists how to count the #peas (per pod or per branch). Not only did know one know how many geese were in a gaggle no one answered another PROFS (not me as undergraduate) as to what a "gene" was. Today we know better (at least I do about genes) but I still do not know how to count a "hybrid swarm" of painted turtles. It seems all the arguing made the red on the southern painter of no account and yet that would not do if one insisted to use heritbility. you see the NUMBER ( of fish or birds etc) is not something that we can facutal really yet dissus even though it can not be objected that if ytou asserted NINE it really was ATE. That is not meant as rhetoric but is veild insight. Reject it if ytou must. The concept of mutation seems threaded a bit too plurivocally here for me to target the answer less directly than with the next number and that is not good enough.

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Originally posted by Fred Williams:
5) He can also use oil of Hyssop with its "50% antibacterial" (I dunno, 5 months old?)

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LOL!

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I am not quite sure why YOU would think that is funny. You made the claim and were proved wrong. Nervous laughter, I suppose.

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Speaking of the Rice paper, don’t you remember I already refuted their misleading claims?

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How can one remember something that did not occur? You claiming to have done something is hardly evidence that it occurred.
But it is strange that the only person that seems to think that a demonstration of a principle of sexual recombination/evolution in a laboratory environment is "misleading" is a creationist electrical engineer.
Oh wait - no it isn't.

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Me: I will be very curious to see this, since I know that multi-gene traits make the 1667 number worse.

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Dr.Page: You know this, do you? Amazing. How about explaining it all to us?

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Say a new beneficial mutation occurs that impacts a quantitative trait. Say this trait is controlled by 5 genes. In order for one offspring to inherit the precise combination of genes, 2^5 offspring would be needed. That’s 32, for my math-deficient young apprentice.

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Yes, I guess I must be math deficient. However, world-renowned astronomer/mathematician Fred Hoyle is not, and he wrote in his last book that 'Haldane's dilemma' is "an illusion."
I will take his word - the word of an anti-darwinian with legitimate math credentials - over the rants of creationist electrical engineers any day. Even those proclaiming to be experts in information theory Anyway -
I have asked about this before and you fell silent.You say:"In order for one offspring to inherit the precise combination of genes, 2^5 offspring would be needed. That’s 32..."emphases mine.Please explain - dumb it down for us non-math folk - how it will take 31 other offspring to provide one with the 'right' combination.I heard on the news the other day that the odds of winning the powerball lottery here is something like 1 in 165 million (or something like that).
Yet somebody won.As Williams the elctrical engineer creationist 'explains' it, it sounds an awful lot like he thinks that 31 non-beneficient 'offspring' will have to be born for the 32nd to possess the desired mutant.That makes no sense whatsoever to me, and it should make no sense to anyone else.Each conception is an independant event. Therefore, assuming Williams numbers are correct (there is little reason to do so, based on his past performances) each conceptus has a 1 in 32 chance of possessing the mutant.
Now, that could very well be the first born, could it not?

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But surely there are going to be combinations where the phenotypic expression is not going to be recognizable by natural selection. So the actual barrier falls somewhere between 50% and 97% in the example I gave above. Since Haldane is assuming sing-trait genes, he is assuming 50% all of the time. This is clearly a favorable assumption for his model.

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And is offset by his ocnstant population size requirement, which you conveniently have decided not to duscuss anymore.Hmm - didn't Haldane offer several models for different types of alleles, such as recessives and such? Why, yes - yes he did!But surely, you remember the FGF-3 receptor gene?Surely you have heard of the HOX genes and other developmental regulatory genes?Genes whose expression during development influences and/or directs morphological development?How do they fit in?Surely you must know that many if not most evolutionary biologists now consider these genes to be much more important than genes that control or influence single traits?Oh, and while you are at it, perhaps you can produce one of your content-packed posts with an explanation for why the 1667 number (ala ReMine) has any relevance at all.BTW - your intellectual mentor ReMine has written that the fact that Pandas have to eat lots of bamboo to live is supportive of his "Message theory" (myth is a more applicable name) because the creator wouldn't design critters that would deforest the planet...If you can't see the idiocy of that position, I can explain it to you...[This message has been edited by SLPx, 01-04-2003]

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Originally posted by peter borger:
And read L. Spetner's Not by Chance: the complete refutation and overthrow of NDT. Also easy to read).

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Yes, it is easy to read comics, isn't it?

[deleted duplicate][This message has been edited by peter borger, 01-05-2003]

dear Dr Page,quote:
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Originally posted by peter borger:
And read L. Spetner's Not by Chance: the complete refutation and overthrow of NDT. Also easy to read).
--------------------------------------------------------------------------------Page: Yes, it is easy to read comics, isn't it?PB: Why don't you go to the library and get Prof L. Caporale's book "Darwin in the genome"? She demonstrates beyond any doubt the existence of non-random mutations. You better get used to the idea that the NDT era is terminated by these non-random mutations. But even more dramatic, these non-random mutations have far reaching consequences for phylogenetic analysis. I will mail them soon, so we can discuss them.Best wishes,
Peter

Surely if 'bird 10' can catch more fish, it can support
more young than a 'bird 9' individual, and so make
a greater contribution to the gene pool by virtue of larger
numbers of offspring.

It depends what you mean by redundancy ...I think you are referring to redundancy in the
'triple redundancy' sense in which you have a number of
working alternatives so that if one goes wrong there is
a back-up.P.Borger means 'unused' or 'non-functional' when he says redundant.This only requires a modification/mutation that adds a stop or
start without creating a dead critter ... some might contend
that that is impossible and that's another debate.There is a New Scientist article recently that suggests that
these may not even BE redundant (in PB's terms) but functionalstepping stones in the chain of events leading to protein synthesis.

Dear dr Page,Page: Surely you have heard of the HOX genes and other developmental regulatory genes?PB: They are 99.3% identical in human and chimp. They probably vary on some neutral postions. So, that will not be the difference. They difference between man and chimp is more likely to be found in the fractal code of the DNA. Huh, another level of complexity in the genome? Yes, Dr Page, another level. Surprised?Best wishes,
Peter

[QUOTE]Originally posted by peter borger:
[B]Dear dr Page,Page: Surely you have heard of the HOX genes and other developmental regulatory genes?PB: They are 99.3% identical in human and chimp. They probably vary on some neutral postions. So, that will not be the difference.[/quote]Did I say they were? I di dnot realize that I had limited my comments only to the chimp/human question.

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Originally posted by peter borger:
Re: Lynn Caporale.

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Funny - this paper by her does not seem to indicate what you think her book 'proves':

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http://www.ceptualinstitute.com/...caporale/Caporale_IJ2.htm

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Looking at the description of the book and the reviews of it, I think what we have is just another example of Borger's shall we say, "unique" interpretations...

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Page: But it is strange that the only person that seems to think that a demonstration of a principle of sexual recombination/evolution in a laboratory environment is "misleading" is a creationist electrical engineer.

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Of course you know I did not say the above was misleading. What I said is misleading is their claim that recombination is an advantage to evolution:

The author’s conclusion essentially is that beneficial mutations have a better chance of fixation in a sexual species over an asexual species, because the high level of harmful mutations in an asexual species wreak greater havoc than they do in a sexual species. If there were not such a powerful current of harmful to slightly harmful mutations at work, then beneficial mutations would clearly proliferate more easily in an asexual species. But the authors fail to emphasize this fact, so the reader can easily be left with the impression that recombination is an advantage to evolution (as happened to Dr Page). It is NOT per se an advantage to evolution. It is only an advantage when contrasted to asexual reproduction in a harmful mutation environment. Recombination remains an "enigma" to evolution.

Link: 404 Not Found

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Fred Hoyle wrote in his last book that 'Haldane's dilemma' is "an illusion."

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What is it about Hoyle’s argument that convinces you it’s an illusion?

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You say:
"In order for one offspring to inherit the precise combination of genes, 2^5 offspring would be needed. That’s 32..."
emphases mine.
Please explain - dumb it down for us non-math folk - how it will take 31 other offspring to provide one with the 'right' combination.

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Say daddy has 5 genes that contribute to a trait: A, B, C, D, E. Mommy has a different gene version at each respective locus: A`, B`, C`, D`, and E`. Say some phenotype is advantageous with the combination A, B`, C`, D, E. The odds of getting A with the first offspring is .5. The odds of getting A & B` is .5 x .5 = .25 (1 in 4), The odds of getting A, B`, C` is .5 x .5 x .5 = .125 (1 in 8), etc. To get 5 is 2^5 or 1 in 32. So on average one out of every 32 offspring will inherit the precise combination (thus 32 offspring are needed to have an even chance).

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I heard on the news the other day that the odds of winning the powerball lottery here is something like 1 in 165 million (or something like that). Yet somebody won.

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This is a meaningless statement. It appears you are headed directly toward a very common fallacy in statistics. See the Fallacies & Traps chapter in Forgotten Statistics (or any other stats book that covers the traps).

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As Williams the elctrical engineer creationist 'explains' it, it sounds an awful lot like he thinks that 31 non-beneficient 'offspring' will have to be born for the 32nd to possess the desired mutant.
That makes no sense whatsoever to me, and it should make no sense to anyone else.
Each conception is an independant event. Therefore, assuming Williams numbers are correct (there is little reason to do so, based on his past performances) each conceptus has a 1 in 32 chance of possessing the mutant.
Now, that could very well be the first born, could it not?

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It could, but the average hurdle is nevertheless 1 in 32 (as opposed to 1 in 2 to inherit a trait controlled by a single mutated gene). Thus, for species that do not commonly produce 32+offspring, the already low frequency of beneficial mutations is reduced further since most new beneficial mutations will never even make it to the 2nd generation.Multigene families are common and probably average more than 5 genes. This would have a major impact on Haldane’s cost, and in turn makes the 1 in 300 substitution rate unrealistically too high.

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And is offset by his ocnstant population size requirement, which you conveniently have decided not to duscuss anymore.

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I’d love to duscuss (sic) it, I have stated that it is at worst a favorable assumption and at best a NULL assumption. If you think a shifting population size somehow lessens the substitution rate, I’d love to hear how.

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Hmm - didn't Haldane offer several models for different types of alleles, such as recessives and such? Why, yes - yes he did!

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What’s your point? The cost to fix recessives is exponentially higher!

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But surely, you remember the FGF-3 receptor gene?
Surely you have heard of the HOX genes and other developmental regulatory genes?
Genes whose expression during development influences and/or directs morphological development?
How do they fit in?

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Very badly. My understanding is that copying errors to HOX genes are far more likely to cause harm than copy errors to non-HOX genes. Thus, the cost required to pay for lethals increases (more offspring to account for these genetic deaths), increasing the overall substitution rate. Methinks you are attempting a red herring?

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Surely you must know that many if not most evolutionary biologists now consider these genes to be much more important than genes that control or influence single traits?

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Exactly my point. And don’t call me Surely.

[QUOTE]Originally posted by Fred Williams:
[B]

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Page: But it is strange that the only person that seems to think that a demonstration of a principle of sexual recombination/evolution in a laboratory environment is "misleading" is a creationist electrical engineer.

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Of course you know I did not say the above was misleading. What I said is misleading is their claim that recombination is an advantage to evolution:[/quote]Snip sophism.
Please explain how removing deleterious mutations while accelerating the fixation of beneficial ones is not an advantage to evolution.

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Fred Hoyle wrote in his last book that 'Haldane's dilemma' is "an illusion."

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What is it about Hoyle’s argument that convinces you it’s an illusion?

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Haven't read it. Have you?
But like I said - I would take his word over yours any day.

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You say:
"In order for one offspring to inherit the precise combination of genes, 2^5 offspring would be needed. That’s 32..."
emphases mine.
Please explain - dumb it down for us non-math folk - how it will take 31 other offspring to provide one with the 'right' combination.

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To get 5 is 2^5 or 1 in 32. So on average one out of every 32 offspring will inherit the precise combination (thus 32 offspring are needed to have an even chance).

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You said that before. However, I must now question whether or not you took even undergraduate statistics, as you clearly have no clue whatsoever what statisical inferences indicate.You do not seem to realize that conceptions are independant events. That is, each conception would therefore have a 1 in 32 chance of getting the combination you used in your worst case scenario.
As such, that means that, in fact, it could very well be the first born.
I am flabbergasted at this sophomoric gaffe on your part - you had me convinced at one point that you actually knew what you were talking about. This demonstrates the shortcomings of pontificating on subjects that one has o business doing so on.Unless you are just making one of your 'patented' "shortcomings of the medium" deals...

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I heard on the news the other day that the odds of winning the powerball lottery here is something like 1 in 165 million (or something like that). Yet somebody won.

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This is a meaningless statement. It appears you are headed directly toward a very common fallacy in statistics. See the Fallacies & Traps chapter in Forgotten Statistics (or any other stats book that covers the traps).

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I suggest that you re-read the book. Or better yet learn some elementary statistics. When you do this, you should also read some elementary developmental biology books. Perhaps then you might - MIGHT - realize that each conception is an independant event.
If your "explanation" above had any basis in reality, then there would necessarily have to be 165 million lottery tickets sold in order for a winner to emerge, and, what is more, premised directly on your above claim, the winner would be the very last ticket purchaser.

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As Williams the elctrical engineer creationist 'explains' it, it sounds an awful lot like he thinks that 31 non-beneficient 'offspring' will have to be born for the 32nd to possess the desired mutant.
That makes no sense whatsoever to me, and it should make no sense to anyone else.
Each conception is an independant event. Therefore, assuming Williams numbers are correct (there is little reason to do so, based on his past performances) each conceptus has a 1 in 32 chance of possessing the mutant.
Now, that could very well be the first born, could it not?

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It could, but the average hurdle is nevertheless 1 in 32 (as opposed to 1 in 2 to inherit a trait controlled by a single mutated gene).

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And you thus directly contreadict your claim above.Which is is Fred?The 32nd is the one, or each event a 1 in 32 chance?You cannot have it both ways.

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Thus, for species that do not commonly produce 32+offspring, the already low frequency of beneficial mutations is reduced further since most new beneficial mutations will never even make it to the 2nd generation.

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Please retrune to the board AFTER you educate yourself on elementary statistics and developmental biology.

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Multigene families are common and probably average more than 5 genes. This would have a major impact on Haldane’s cost, and in turn makes the 1 in 300 substitution rate unrealistically too high.

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Do you have any clue what a multi-gene family is?Really, Fred, you are showing your miserable knowledge of these topics here.
You do not, unfortunately for you, get to make your own terminology, nor do you get to apply real terms as you personally see fit.Find out what a gene family is.

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And is offset by his ocnstant population size requirement, which you conveniently have decided not to duscuss anymore.

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I’d love to duscuss (sic) it, I have stated that it is at worst a favorable assumption and at best a NULL assumption. If you think a shifting population size somehow lessens the substitution rate, I’d love to hear how.

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100,000 starting pop.
5% have a beneficial mutant after origination and drift.
Environemtal shift occurs.
5,000 are left, all those with the beneficial allele.New population size of 5000.Cost already paid.
Savvy?

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But surely, you remember the FGF-3 receptor gene?
Surely you have heard of the HOX genes and other developmental regulatory genes?
Genes whose expression during development influences and/or directs morphological development?
How do they fit in?

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Very badly. My understanding is that copying errors to HOX genes are far more likely to cause harm than copy errors to non-HOX genes.

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Your memory is pathetic. One of the citations I had offered demonstrating the futility of the "no new information" please dealt with duplication of a HOX gene that altered phenotype and corrected deleterious mutations in one copy.
Keep up your studies.

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Thus, the cost required to pay for lethals increases (more offspring to account for these genetic deaths), increasing the overall substitution rate. Methinks you are attempting a red herring?

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You can think whatever you want. I am pointing out that thngs are not the way you like to portray them.

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Surely you must know that many if not most evolutionary biologists now consider these genes to be much more important than genes that control or influence single traits?

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Exactly my point. And don’t call me Surely.

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If that was your point, I have to wonder why you prattled on about single trait genes and all that.Apparently, you have not learned a thing in all these years.I am planning (again) to wind down my 'net activity.So, hit me with your next round of gaffes and illinformed nonsense and that will be it...

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Haven't read it. Have you?

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Yep. But it is not an easy read. If you check it out you will see what I mean. It will take some digging to really begin to understand where he is going. I just haven't had the time because it would be a significant effort (ie dusting off Calc 3 and Diff Equation books). Maynard Smith is an evolutionist who has gone through it and admits it is not convincing. The one thing I recall is that Hoyle estimated the rate would be more like 10 generations instead of 300.

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You do not seem to realize that conceptions are independant events.

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Yes. I also realize you are equivocating/hairsplitting again. Your comment about the lottery already clued me in you were heading to a big, black, fallacy hole. To your defense it is an *extremely* common fallacy. My point remains that the reproductive hurdle goes from 50% to somewhere between 50 and 97% (using my example). Haldane assumes 50%. A very favorable assumption for his model, one that we have learned in the years since his model is grossly unrealistic.

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...you had me convinced at one point that you actually knew what you were talking about.

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I did? When?

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Do you have any clue what a multi-gene family is?

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Yes. I meant multi-gene (quantitative) traits, as I wrote several times earlier. I "miswrote" when I said "family" in my latest post. Perhaps you will save this "gaffe" in your "Williams" file? I suspect I have "multi-family" on the brain from reading all those posts between you and Peter, you know, the ones where you are taking one devastatingly severe whoopin'!

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100,000 starting pop.
5% have a beneficial mutant after origination and drift.
Environemtal shift occurs.
5,000 are left, all those with the beneficial allele.
New population size of 5000.
Cost already paid.
Savvy?

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I can't count the times this has been shown to be bogus. Small populations will invariably reduce the fitness of the species because genetic drift works against selection. That is, the spread of mutations is driven by randomness and not selection, and thus the far more prevalent deleterious mutations will spread more than they would in a much larger population where selection can work. Do you seriously think reducing fitness is good for evolution. Don't feel bad, you are not alone. Many on this board and elsewhere have implied the same thing! Doesn't it get tiring defending the indefensible? "Alice really did see a rabbit, doggonit!"

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I am planning (again) to wind down my 'net activity.

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Yea, right, when have I heard this before! Actually, I do say this in good humor. I don't know how many times I've told myself to "wind down my net activity", only to find myself back on the boards a couple weeks later. Good luck on your attempt, maybe you will be more successful than I.