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Hybridization as a Challenge to Common Descent?

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Here’s an article from New Scientist that will be open for the next seven days to registered viewers. It’s about the “metamorphosis” of species from larval to adult stages, and brings in the views of Donald Williamson.

Here’s a link to his 2006 paper, and the entire abstract (it’s worth it!):

Examples of animal development that pose problems for Darwinian evolution by ‘descent with modification’ but are consistent with ‘larval transfer’ are discussed. Larval transfer claims that genes that prescribe larval forms originated in adults in other taxa, and have been transferred by hybridization. I now suggest that not only larvae but also components of animals have been transferred by hybridization. The ontogeny of some Cambrian metazoans without true larvae is discussed. The probable sequence of acquisition of larvae by hemichordates and echinoderms is presented. I contend (1) that there were no true larvae until after the establishment of classes in the respective phyla, (2) that early animals hybridized to produce chimeras of parts of dissimilar species, (3) that the Cambrian explosion resulted from many such hybridizations, and (4) that modern animal phyla and classes were produced by such early hybridizations, rather than by the gradual accumulation of specific differences.

Another day; another bad day for Darwinism!

Comments
wd400, What is umm "expected" is NOT what always happens. Also "selection" does not "act" on anything- natural slection is an oxymoron and a result of three processes- an after-the-fact assessment. What is your evidence that newly arising mutatnts can become fixed? I don't care about "quite common" that is BS backpeddling. And i did NOT say new mutations will never become fixed. I said they are unlikely to become fixed. And the data supports my claim. OTOH you don't have any data to support your claims. As for delitrious mutations, well they tend to wipe out and "benefit" of the beneficial one. How did fixed differences come about? By design, as they were designed in.Joseph
October 7, 2011
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OK Joseph, one last go. The math just shows the distribution of gametes. It does NOT show the distribution of offspring. Nope. The maths is explicitly about diploid populations with sex. Amusingly enough, you can actually get the expected offspring distribution form the gamete distribution. But in the really simple case above. I'm sure you'll agree the probability that any offspring receives any given allele is 0.5 right? Doesn't matter it's "+" "-" or "blue eyes" or whatever - parents have two each offspring gets one. That means half of a mutants offspring will have the the newly arising allele. You wanted to know how many offspring you'd need to be sure to get the "+" into the next generation, and that's pretty easy maths too. The probability of offspring1 and offspring2 having the "+" is independent (different eggs or sperm) so you can mulitly them. So, the chance of getting 4 "-"s in a row is 0.5^4 ~ 0.06 and the probability of getting at least one "+" is 1-0.06 = 0.94. I don't know why you think background deleterious alleles are a problem here. Individuals with a new beneficial mutation have no more or less chance of having a bad one somewhere else. Moreover, sex means genes get broken up by recombination, so selection acts on individual genes. Finally, I'm happy to admit I read a graph in that paper incorectly. But that paper as a whole doesn't support your claim since (a) newly arising mutants can become quite common (b) quite common alleles can go to fixation. From that it follows mutations can go to fixation. And as I said, non-adaptive alleles go to fixation (read the Kimura paper). If they didn't, how would fixed differences between populations or species come about?wd400
October 6, 2011
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Elizabeth- The math just shows the distribution of gametes. It does NOT show the distribution of offspring. Also as far as getting a new allele fixed wd400 choked on that. She/ he also choked on the fact that even someone carrying a beneficial mutation will most likely pass on deletrious mutations as well.Joseph
October 6, 2011
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Joseph, s/he just did. It's just math (though the math is quite complicated!) Check out Kimura's classic paper here.Elizabeth Liddle
October 5, 2011
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You are going to back away because you cannot support the nonsense you post.Joseph
October 5, 2011
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So, what you are saying is you are so convinced you are right you are willing to deny the Binomial Theorem (the source of those numbers)? I'm going to back away slowly now.wd400
October 5, 2011
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If (a) selection can get new mutations into populations and up to a decent level and (b) selection can drive existing alleles to fixation then it follows newly arising alleles can go to fixation!
"Ifs" don't help your case. Imagination doesn't help your case. And unfortunately those are all you have.
Moreover, non-adaptive alleles can (and do) go to fixation.
Evidence please.
Quite a lot of population genetics is about comparing the rate of substitution rate to mutation rate to see if alleles are fixed faster than mutation would allow.
Quite a lot of population genetics takes place on paper and does not translate to the real world. As for "selection", well nature doesn't select- natural selection is an oxymoron.Joseph
October 5, 2011
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How many of their offspring would have the “+” allele? How can you tell?
High school math?
Nope- reality.
The expectation is half of the offspring, with variance n/2*(0.5) where n is the number of offspring
Doubtful. Do you have any real-world data to support your claim? How many offspring would they have to have to ensure ONE “+” allele gets passed on?
4 would give you a 94% chance
And the evidence to support your claim is? What happens when the -/- the one +/- mated with has deletrious alleles?
Well, that’s the thing about sex isn’t it. The alleles get broken up every generation.
Non-sequitur.
But that’s all gish anyway, it wasn’t part of your orignal claim,
You don't have any idea what my original claim was as you have trwisted it with most of your posts.
only added on when you started to realise your confidence was misplaced.
My confiemce is still high and you have yet to provide any evidence to support your nonsense. The point being, as I have already eluded to, is your equations do not deal with reality.
They do.
No, they don't.
Do you really think every evolutionary biologist in the world is unaware that newly arising mutations can be lost in the first generation.
Has any biologist applied the equations to a population in the wild? We have to a population of fruit flies and no new alleles became fixed- YOU LOSE.Joseph
October 5, 2011
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Well, I'm happy to admit I read that paper wrong. Seems the only alleles that were fixed were ones that already existed in the population. But that doesn't really help with your case. If (a) selection can get new mutations into populations and up to a decent level and (b) selection can drive existing alleles to fixation then it follows newly arising alleles can go to fixation! Moreover, non-adaptive alleles can (and do) go to fixation. In fact, for a neurtral allele the the rate of fixation is equal to the mutation rate. Selection just makes that go faster. Quite a lot of population genetics is about comparing the rate of substitution rate to mutation rate to see if alleles are fixed faster than mutation would allow.wd400
October 4, 2011
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How many of their offspring would have the “+” allele? How can you tell? High school math? The expectation is half of the offspring, with variance n/2*(0.5) where n is the number of offspring. How many offspring would they have to have to ensure ONE “+” allele gets passed on? 4 would give you a 94% chance What happens when the -/- the one +/- mated with has deletrious alleles? Well, that's the thing about sex isn't it. The alleles get broken up every generation. But that's all gish anyway, it wasn't part of your orignal claim, only added on when you started to realise your confidence was misplaced. The point being, as I have already eluded to, is your equations do not deal with reality. They do. It's ok to be wrong. Just stop, and think about it. Do you really think every evolutionary biologist in the world is unaware that newly arising mutations can be lost in the first generation. Or maybe that they're aware of it, thought about it, tested it and, in the case of the nearly neutral theory, built new theories about it.wd400
October 4, 2011
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Our work provides a new perspective on the genetic basis of adapta- tion. Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles. This is notable because in wild populations we expect the strength of natural selection to be less intense and the environment unlikely to remain constant for,600 generations. Consequently, the probability of fixation in wild populations should be even lower than its likelihood in these experiments. This suggests that selection does not readily expunge genetic variation in sexual populations, a finding which in turn should motivate efforts to discover why this is seemingly the case.
OOOPS....Joseph
October 4, 2011
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Next I never said anything about new mutations not being selected for. wd400
You said they’d be lost.
I never said anything about new mutations not being selected for. Also, from the paper:
Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.
YOU LOSE. And becoming common does not mean becoming fixed. And that was under controlled lab conditions which means in the wild you lose too.Joseph
October 4, 2011
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Next I never said anything about new mutations not being selected for. You said they'd be lost. But in fact they arise and a lot of them become very commmon (like 0.8) Please reference the new alleles that became fixed. See the dots with allele frequency = 1 in their graphs? For both methods of calling genotypes? Those are fixed allles.wd400
October 4, 2011
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wd400:
Imagine a population of 10 000 fixed for an allele we’ll call “-”. A new mutation pops up making the allele “+”, and the finesses are “-/-” : 0.98 “+/-” : 0.99 “+/+” : 1.0
So, to start we would have 9999 individuals with "-/-" and 1 with "+/-". That would mean the +/- would be mating with a -/-. How many of their offspring would have the "+" allele? How can you tell? How many offspring would they have to have to ensure ONE "+" allele gets passed on? What happens when the -/- the one +/- mated with has deletrious alleles? The point being, as I have already eluded to, is your equations do not deal with reality.Joseph
October 4, 2011
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You are just confused. First I said sexual reproduction- I never said anything about the recombination that can take place during meiosis. Next I never said anything about new mutations not being selected for. Please reference the new alleles that became fixed. try again, indeed...Joseph
October 4, 2011
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But some did become fixed and others moved from 1/population.size to like 0.8 So... sexual recombination doesn't prevent new mutations from being selected for. Try again.wd400
October 4, 2011
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Yes I read the paper- no new alleles became fixed. I never said mutations cannot increase fitness- which is a total BS term wrt biology anyway- but the fact that even mutations that increased fitness did not become fixed, supports my claim.Joseph
October 4, 2011
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Did you read this paper. New mutations increased the fitness of their holders. In a sexually reproducing species.wd400
October 4, 2011
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wd400:
You started by saying sexual recombination meant “very beneficial” mutations can’t be fixed.
No, I did not say that.
But, in fact, even in the scenario I talked about with not very beneficial mutations and the chance of being lost in the first generation the probability that the newly arising allele is fixed in about 50%.
Too bad you don't have any real world evidence that supports your claim. You don't even have experimental evidence. IOW all you have is your bald assertion. OTOH I have provided a peer-reviewed paper that supports my claim.
Take one cell, grow a few clones and split them into two dishes.
LOSER- what part of sexual reproduction don't you understand? But anyways thanks for proving that you don't have any clue nor do you have any positive evidence for your claims.Joseph
October 4, 2011
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Joseph, You really are a laugh. You started by saying sexual recombination meant "very beneficial" mutations can't be fixed. But, in fact, even in the scenario I talked about with not very beneficial mutations and the chance of being lost in the first generation the probability that the newly arising allele is fixed in about 50%. Obviously it's much higher for those "very beneficial" mutations you were talking about. If you want to see this for yourself download popG from Joe Felsenstein's page and set up some populations. As for real world examples - there are thousands. But one I like is "Growth Advantage is Stationary Phase" (GASP). Take one cell, grow a few clones and split them into two dishes. Add the first colony to a flask of medium and it will grow unconstrained until it reaches the end of the resources and reaches "stationary phase" where the number of cells in the flask reaches equilibrium. That's a dynamic equilibrium, cells are dieing and others are reproducing and eating the remains of other cells. Now. Take some of those cells that have already been in stationary phase and an equal number of cells from the other cloned colony you had to start with and grow them up into another stationary phase. If mutations are unlikely to prosper, then there is no reason to think either colony will do better than the other. But every time the cells that have already been through a stationary phase out compete their counterparts and when you sequence the cells you find fixed mutations that arise in their earlier stationary phase that made them fit their environement (remember, they were clones, so it can't be existing differences). Not that I suppose anything can change your mind about how right you are though.wd400
October 4, 2011
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Thanks very much for this, WD400, you've given me enough to go on here.Chris Doyle
October 4, 2011
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OK Mark- what % of offspriing will have the beneficial mutation and what % of those will have it on the dominant (as opposed to recessive) side? Heck Sir Ronald Fisher- one of the architects of the modern synthesis- he has shown that most mutatnts- even those with very beneficial effects, will be wiped out via random effects. Not only that there will be competeing mutants.Joseph
October 4, 2011
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Loser, loser, loser wd400:
I’m asking your for a estimate of the rate of fixation for an allele such as I described.
And I am asking for REAL LIFE examples- something which YOU will NEVER provide. Do you have anything dealing with the real world? I would say in your example the allele will never reach fixation and the fact is you cannot demonstrate otherwise. And that is the problem with your position-> it is untestable in the real world and relies solely on imagination.Joseph
October 4, 2011
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wd400:
(1) Williamson is crazy, there is no reason for a ‘Darwinist’ or anyone else to take him seriously.
This is a very closed-minded view. Exactly the problem of Darwinists. Why don't you just simply say: "I refuse to entertain such ideas." (Of course, there's no rational basis to this. You haven't refuted Williamson's contention.) I might not agree with Williamson's views, but I would want to look at his evidence and his thought process. You've shown no such tendency. Is this how science is to be conducted?
Of course, Shapiro is erecting a strawman there.
Aren't you guilty of the very thing you're accusing Shapiro of? Haven't you just made a strawman argument of Shapiro's position. Haven't you just thrown out all the substance and subtlety of his argument? As to "transition bias", does such a thing actually exist? I cited a 2003 paper that suggests otherwise. And constraints such as "transition bias", should it actually occur, happens at a chemical/quantum-mechanical level. Shapiro talks about "system engineering". This represents a very different kind of "constraint".PaV
October 4, 2011
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Excuse me, but how is it possible for none of one parent’s genes to get passed on?
You are right. I am getting confused about when recombination takes place. But the main point is what is the probability of new beneficial mutation being fixed in a population? It is possible for a beneficial mutation to be lost in one generation but the probability is low. The big thing you have left out is that parents on average have many offspring - in some species very, very many.markf
October 3, 2011
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Gish Gish Gish. I'm asking your for a estimate of the rate of fixation for an allele such as I described. If the fact that "even the most beneficial mutation can get lost in one generation" counts for much, natural selection is a non-entity in the population size in the scenario then we must be talking about a small number? Right? So what's the number, roughly, do you think?wd400
October 3, 2011
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1- Environments change, sometimes quite a bit. What do you think ice ages did? 2- Except beneficial is still a relative word 3- No it doesn't for reasons given above- one being even the most beneficial mutation can get lost in one generation. 4- Experiments with stable environments do not support your equation: A random search where the peaks and valleys change- good luck with that and your irrelevant population genetics equations… And with a population of 10,000- your example- natural selection is a non-entity, so all you have left is sheer dumb luckJoseph
October 3, 2011
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1. Yes environments change (a little) and we can talk about that later if you want. But it's not the issue you originally brought up 2. That would just mean one of several possible beneficial mutations would get fixed. 3. Yes it does. What do you think the chances of the beneficial allele fixing are? Just a range 0.1 - 1%?, 5%?wd400
October 3, 2011
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Genome-wide analysis of a long-term evolution experiment with Drosophila A random search where the peaks and valleys change- good luck with that and your irrelevant population genetics equations...Joseph
October 3, 2011
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I was trying to find out what this alleged strawman was and you jumped in with some unrelated nonsense. So that is my point- evos like to throw around bald assertions and false accusations but are always very short on supporting evidence.Joseph
October 3, 2011
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