Summations Only

Hey David Coppedge, do you go by the name of Kleinman nowadays?I mean, David Coppedge used to work as a computer specialist in that industry where he pretended to know more about biology than biologists and more about geology than geologists and more about maths than mathematicians and more about physics than physicists. Didn't bode too well for him in the end.He's just another crackpot.Kleinman, are you a YEC?Edited by Pressie, : No reason given.Edited by Pressie, : No reason given.Edited by Pressie, : No reason given.

Let it be noted that I found the flaws in Kleinman's argument before he got around to properly presenting it (He still hasn't, but he has gone far enough to show that I was correct)

Excuse me for coming in late in the discussion. I have received your pdfs but not had time to look them over yet. Can you answer a simple question for me, even if it has already been asked?What is the probability that a mutation will be beneficial?I think we can all agree that mutations are random -- leaving aside for the moment that the probability of mutations varies with the section of DNA involved -- and that some are immediately deleterious or immediately beneficial, while others are immediately neutral and their relative deleterious\beneficial value can be important later.We also have cases where a mutation is somewhat deleterious but leads later to beneficial results because of changing environmental conditions.So how can we predict the probability of a mutation being beneficial?Enjoy

I wanted Kleinman to cover two topics, how the mathematics of RM/NS makes evolution impossible, and how the evolution from dinosaurs to birds is impossible. As near as I can tell his answers didn't change when he moved from the first topic to the second. There was no additional math or details, and the arguments remained the same.Would there be any objections if I dropped this thread into summation mode? I won't do that if anyone thinks there is still some productive discussion remaining.

As a novice on anything about biology or genetics or anything like that, I don't have any objections. Maybe Kleinman can try to start a discussion on one of the subjects he flew around, without being able change subjects at will all the time?Edited by Pressie, : No reason given.

Really? So, if a group of grizzly-like bears moves north and starts living off a diet of seals, they couldn't make multiple adaptations to multiple pressures? They couldn't evolve meat ripping teeth, ice-gripping claws, larger feet for ice walking and swimming, longer necks for swimming, and a suitable camouflage because these are multiple adaptations to multiple pressures and, according to the Kleinman theory of evolution, changes involving many mutations can't happen?You seem to have a problem with the idea that eight or more genes might be involved in the difference between scales and feathers. Why? Siblings can have different alleles on more than eight genes, so why shouldn't diverging populations of dinosaurs and proto-birds?You also seem to think that population groups have to be threatened with extinction before significant change takes place. Things like dinosaurs to birds, tree squirrels to "flying" squirrels, and non-polar to polar bears have much more to do with highly successful models diversifying into new niches. There's no hurry. There's also no target.Mrs. Bird winning a lottery with one million participants is a one in a million chance, but someone winning is 1/1. Evolution doesn't care what wins.

Why do that? I want to hear the Kleinman theory. I want to know what the limit is to the number of new alleles that can go to fixation by positive selection in a population group of 100,000 in 1,000,000 generations, and why it wouldn't be enough to transform a land animal into a flier.I'm fascinated! Please let it roll! (Or you could suggest that Kleinman opens a thread outlining his "falsification" of evolutionary theory, and we could discuss it there).Edited by bluegenes, : spellin

It is a bit glacial, isn't it? Still, we may as well see if anything else is going to happen.

Little-Man is David Coppedge? Really? That creationist idiot who claimed that scientists believe that humans 6000 years ago were all ape-men? That one?

The main problem with your HIV example is that the beneficial mutations are not additive. In most situations, beneficial mutations are additive.What I mean by additive is if A and B are both beneficial mutations on their own, then an individual with both A and B will be more fit than individuals with just A or B. In the case of multi-drug treatment and HIV, there is no way for an amplification of just A or just B because the individual viruses with just one potentially beneficially mutation do not reproduce at a higher rate.We could use an example in humans to show why your HIV example doesn't work. In humans, there has been selection for both malaria resistance and melanin production. Individuals with either darker skin or resistance to malaria will do better than individuals without either trait in lower latitudes that experience endemic rates of malaria. Both traits will be selected for independently. Individuals who receive both traits will be even fitter than individuals with just one of those traits.As we can see, your HIV model fails to model real life, both because it lacks additive fitness and it lacks sexual recombination. In human populations, you don't have to wait for dark skin to become fixed before malaria resistance can be selected for. Both can be selected for in individual lineages, and through sexual recombination you can have individuals inherit both beneficial mutations.Edited by Taq, : No reason given.

Do you have a reference for this?

I don't have a reference at hand, but I may find time to find one.I think my example of melanin production and malaria resistance should suffice, unless someone can explain how darker skin will not be selected for unless someone also has mutations that confer malarial resistance (and visa versa).

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Kleinman writes:

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And I'm pretty sure I've had a lot more training in mathematics and physics than you.

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And I'm sure you haven't. After all, you haven't answered any of my questions about mathematics:

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You have a standard deck of 52 cards. You randomly choose a card.

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What is the probability of having drawn the Ace of Spades?
What is the probability of having drawn an Ace?
What is the probability of having drawn a Spade?
What is the probability of having drawn a black card?
What is the probability of having drawn a card?

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What is the probability of having drawn the Ace of Spades given no information?
What is the probability of having drawn the Ace of Spades given that it is an Ace?
What is the probability of having drawn the Ace of Spades given that it is a Spade?
What is the probability of having drawn the Ace of Spades given that it is a black card?

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How boring! Let's do something fun. Let's do a card drawing problem that has a relationship to population genetics.You have a standard deck of 52 cards. You randomly choose 3 cards, 1 at a time with replacement. Write the probability function that you choose either a queen or an ace or king in the 3 draws.

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Suppose you have a single-gene trait with two alleles with perfect dominant/recessive expression. If you are homozygous for dominant allele or heterozygous, you display the dominant trait. Only if you are homozygous for recessive allele do you display the recessive trait and you always do if you are homozygous recessive. Suppose the current rate of recessive display is 1-in-1,000. Suppose that those who display recessive trait are sterile and cannot reproduce while those who display dominant trait (either homozygous dominant or heterozygous) have no difference in reproductive capability.

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How many generations would need to pass in order to reduce the appearance of recessive trait from 1-in-1,000 to 1-in-1,000,000?

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To help you start: What is the value for p? What is the value for q?

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That calculation is already done: http://pba.ucdavis.edu/files/149789.pdfLet's do a different problem. Let's think about how a population can evolve resistance against two selection pressures simultaneously.Start with a population size N. In a single generation of replication of that population with a given mutation rate, what is the probability that some members will get a beneficial mutation to one of the selection pressures, other members will get a beneficial mutation to the other selection pressure and what is the probability that some members will get beneficial mutations to both selection pressures?Since you like hints, I'll give you a hint. The members that get beneficial mutations to the first selection pressure are one subset of the population, the members which beneficial mutations to the second selection pressure are a second subset of the population and the members which get both beneficial mutations are the intersection of the two subsets.

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Kleinman writes:

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Early in my career, I worked in the aerospace industry

Hey David Coppedge, do you go by the name of Kleinman nowadays?
I mean, David Coppedge used to work as a computer specialist in that industry where he pretended to know more about biology than biologists and more about geology than geologists and more about maths than mathematicians and more about physics than physicists. Didn't bode too well for him in the end.

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Who is David Coppedge. The multiplication rule of probabilities does not bode well for the theory of evolution.

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Kleinman, are you a YEC?

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I already answered that question in a previous post. Pay attention.

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... What I do remember is that they listed at least 8 genes necessary to be transformed. ...

Excuse me for coming in late in the discussion. I have received your pdfs but not had time to look them over yet. Can you answer a simple question for me, even if it has already been asked?

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What is the probability that a mutation will be beneficial?

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Your question hasn't been asked and my answer is I don't know. But this is not a number which you have to know to understand how rmns works.

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I think we can all agree that mutations are random -- leaving aside for the moment that the probability of mutations varies with the section of DNA involved -- and that some are immediately deleterious or immediately beneficial, while others are immediately neutral and their relative deleterious\beneficial value can be important later.

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We also have cases where a mutation is somewhat deleterious but leads later to beneficial results because of changing environmental conditions.

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So how can we predict the probability of a mutation being beneficial?

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Most people say that most mutations are neutral. Mutations are fairly rare to begin with. Most DNA replication is done with high fidelity. As you read my papers on rmns, you will see that I address the possibility that even though a mutation occurs at the correct site in a genome, it has to be the correct mutation to improve fitness. Just getting an accurate mutation rate is a challenging problem and then determining the fraction of the mutations which are beneficial, neutral and detrimental is even more challenging. But the mutation rate is not the dominant factor in the rmns problem, it is the multiplication rule of probabilities that drives this phenomenon. It is the joint probability that two or more beneficial mutation occur on a lineage which drives this problem.