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Survival of the Fittest?

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Here’s a news article about 400,000 antelopes dying off in a short period of time. Looks like it’s due to some sort of bacterial attack, though they’re not fully sure what caused this massive die-off.

There’s lots of questions that come to mind. Here’s one or two:
(1) How do we define the “fittest”?

Are they the “strongest”, the “fastest”, the most “aggressive”? What are they? Maybe they’re the “weakest.” Maybe they were so weak that they couldn’t forage with the rest of the herds, and so stayed behind and didn’t get infected. So, how do we define “fitness” here?

(2) In the annals of NS, no one has likely ever seen anything like this. The selection factor is 0.5 (half the population has died off). What other small, gradual change could be this destructive? And it seems it all has to do with bacteria. So, are the “fittest” the ones with the best “immune systems”? If that’s the case, with this kind of selection factor at work, you’d expect that the survivors, the ‘fittest’, would have incredibly good immune systems. Yet, something like this huge die-off happened not too long ago (1988). So, if something this lethal leads to hardly any change, then what great change is NS going to bring about when the selection pressure is far, far less.

Again, the “survival of the fittest” doesn’t befall the “strongest,” “fastest”, “most aggressive”, most “anything,” but, apparently to almost any member of the population. If 400,000 out of 800,000 antelopes die, and they’re none for the better, then what does NS do anyway? Have we wildly exaggerated what it is able to do? (Read The Edge of Evolution to find out more)

Comments
DNA_Jock: Have been very busy, and have had to replace my modem. As to the improbability: the calculation is straightforward. It's 1 in 2^30. No problem. Nevertheless, it demonstrates the constraints that Darwinism labors under. It is possible, but not probable, that this worst case scenario could happen. IOW, the Darwinian mechanism is not robust. Behe demonstrates this in "The Edge of Evolution." But let's look at it from the neutral drift angle. Kimura calculates that it will take 4N_e generations to "fix" an allele in the population. With a population size of 800,000, that means 3.2 MILLION years for it to become fixed in that population. Now, what if 5 specific amino acid substitutions had to take place for some very minor "adaptation"? To be sure that this has taken place, we would need 20N_e generations, or, 16 million years. Now, you might say that due to these reductions in population--these collapses--N_e is half of the 800,000. This, then, would mean that for some simple, likely insignificant change to sweep through the population, 8 million years would be needed. What's the word which means the opposite of "robust"? That's the word I would attach to such a scenario. No fair-minded scientist can be persuaded by these numbers.PaV
September 21, 2015
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Roy: IIRC, I got that number from Wikipedia. Maybe you can revoke their license to criticize population genetics.PaV
September 21, 2015
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The genome size for mammals is 3.2 x 10^9 nucleotides.
That is not even wrong. Your license to criticise population genetics is hereby revoked. Understand then criticise.Roy
September 15, 2015
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Arthur: It's intriguing what you say about cytochrome c. I just can't see how what you say is right. Can you expand?PaV
September 12, 2015
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Earth to Arthur Hunt- Your position cannot account for any proteins. If you could then you would win a Nobel Prize.Virgil Cain
September 10, 2015
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Arthur Hunt, your poster child protein turf13 was not produced by unguided material processes but was produced, in direct contradiction to 'random' neo-Darwinian thought, by the cell modifying its own genome.
De Novo Genes: - Cornelius Hunter - Nov. 2009 Excerpt: Cells have remarkable adaptation capabilities. They can precisely adjust which segments of the genome are copied for use in the cell. They can edit and regulate those DNA copies according to their needs. And they can even modify the DNA itself, such as with adaptive mutations,,,,One apparent de novo gene is T-urf13 which was found in certain varieties of corn. http://darwins-god.blogspot.com/2009/11/de-novo-genes-evolutionary-explanation.html Revisiting The Central Dogma (Of Evolution) In The 21st Century - James Shapiro - 2008 Excerpt: Genetic change is almost always the result of cellular action on the genome (not replication errors). (of interest - 12 methods of 'epigenetic' information transfer in the cell are noted in the paper) https://uncommondescent.com/intelligent-design/central-dogma-revisited/
Moreover, TURF-13 is a constitutively transcribed mitochondrial gene that is derived from two already existing genes.
Genetic and molecular basis of cytoplasmic male sterility in maize - 2007 Excerpt page 51: The specific virulence of B. maydis towards CMS-T maize was found to be due to mitochondrial gene Turf 13, which is also responsible for the CMS phenotype in CMS-T. It is a constitutively transcribed gene which produces a 13 kd polypetide (Williams et al., 1992). Such a polypeptide is not found in CMS -S, CMS -C or normal maize cytoplasm. Turf 13 is a chimeric region gene which is a recombination product of 5’ region of the atp 6 gene and 3’ region of the 265 ribosomal gene (rrn 26). Its transcription is presumably under the control of the atp 6 promoter (Stamper et al., 1987). It is located in 3547-nucleotide mt DNA sequence that contains two open reading frames, one coding for urf 13 and the other for orf 221, which codes for a 25 kd polypeptide consisting of 221 amino acids and is 77 nucleotides downstream of urf 13 (Levings, 1990). The orf 221 encodes a membrane bound protein that has been identified as ATP4 (Heazlewood et al., 2003). http://agrobiol.sggw.waw.pl/~cbcs/articles/CBCS_2_1_7.pdf
As well, as if that was not bad enough, the adaptation was degenerative not constructive
On the non-evolution of Irreducible Complexity – How Arthur Hunt Fails To Refute Behe Excerpt: furthermore, T-urf 13 involves a kind of degradation of maize. In the case of the Texas maize–hence the T—the T-urf 13 was located by researchers because it was there that the toxin that decimated the corn grown in Texas in the late 60?s attached itself. So the “manufacturing” of this “de novo” gene proved to make the maize less fit. This is in keeping with Behe’s latest findings. https://uncommondescent.com/intelligent-design/on-the-non-evolution-of-irreducible-complexity-how-arthur-hunt-fails-to-refute-behe/comment-page-3/#comment-373178
bornagain77
September 9, 2015
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Arthur Hunt its funny that you guys always say that Axe is wrong, but you guys never actually demonstrate the origin of proteins by unguided material processes. Been there, done that.Arthur Hunt
September 9, 2015
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Arthur Hunt its funny that you guys always say that Axe is wrong, but you guys never actually demonstrate the origin of proteins by unguided material processes. Don't you think you guys would have far more credibility, scientifically speaking, with the general public, as opposed to your atheistic cheerleaders, if you were to actually back up your grandiose claims for Darwinian evolution in the lab? Or is actual experimental evidence, that would physically substantiate your grandiose claims for how all life arose on earth, beneath the dignity of the Darwinian elites?
Show Me: A Challenge for Martin Poenie - Douglas Axe August 16, 2013 Excerpt: Poenie want to be free to appeal to evolutionary processes for explaining past events without shouldering any responsibility for demonstrating that these processes actually work in the present. That clearly isn't valid. Unless we want to rewrite the rules of science, we have to assume that what doesn't work (now) didn't work (then). It isn't valid to think that evolution did create new enzymes if it hasn't been demonstrated that it can create new enzymes. And if Poenie really thinks this has been done, then I'd like to present him with an opportunity to prove it. He says, "Recombination can do all the things that Axe thinks are impossible." Can it really? Please show me, Martin! I'll send you a strain of E. coli that lacks the bioF gene, and you show me how recombination, or any other natural process operating in that strain, can create a new gene that does the job of bioF within a few billion years. http://www.evolutionnews.org/2013/08/a_challenge_for075611.html Doug Axe PhD. on the Rarity and 'non-Evolvability' of Functional Proteins - video (notes in video description) https://www.youtube.com/watch?v=8ZiLsXO-dYo When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied. http://www.biologicinstitute.org/post/18022460402/when-theory-and-experiment-collide Can Even One Polymer Become a Protein in 13 billion Years? – Dr. Douglas Axe, Biologic Institute - June 20, 2013 - audio http://radiomaria.us/discoveringintelligentdesign/2013/06/20/june-20-2013-can-even-one-polymer-become-a-protein-in-13-billion-years-dr-douglas-axe-biologic-institute/ Correcting Four Misconceptions about my 2004 Article in JMB — May 4th, 2011 by Douglas Axe http://www.biologicinstitute.org/post/19310918874/correcting-four-misconceptions-about-my-2004-article-in The Hierarchy of Evolutionary Apologetics: Protein Evolution Case Study - Cornelius Hunter - January 2011 http://darwins-god.blogspot.com/2011/01/hierarchy-of-evolutionary-apologetics.html “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain – Michael Behe – December 2010 Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain. http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/
etc.. etc.. etc..bornagain77
September 9, 2015
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Estimating the prevalence of protein sequences adopting functional enzyme folds: Doug Axe: Axe was (and is) wrong. Note that Axe has never responded to the core criticism in this piece, that his deliberate use of an enfeebled temperature-sensitive variant invalidates the use of sensitivity to mutation as any sort of measure of functional sequence space.Arthur Hunt
September 9, 2015
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Art and wd400, seeing as you guys are into pop gen, perhaps you will enjoy this recent podcast interview of Richard Sternberg, who has a PhD in evolutionary biology. He seems to find a fairly large problem with the math of pop gen. Listen: Evolutionary Biologist Richard Sternberg on the Problem of Whale Origins - September 9, 2015 http://www.evolutionnews.org/2015/09/listen_richard099201.html Casey Luskin interviews Dr. Richard Sternberg, evolutionary biologist and CSC Senior Fellow, whose discussion of whale origins is featured in Illustra Media's new documentary, Living Waters: Intelligent Design in the Oceans of the Earth.bornagain77
September 9, 2015
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Arthur Hunt, seeing as you have the math all figured out so that 'the probability, per Hoyle, comes out to be pretty close to 1', perhaps if you can do the same math trick for a naturally occurring code then you can toss your hat in the ring for this following prize (small caveat, they want to actually see you produce a code naturally)
The Origin of Information: How to Solve It Technology Prize for Origin of Information $100,000 For Initial Discovery $3 million USD if Patentable Non-Disclosure Agreements Required Natural Code LLC is a Private Equity Investment group formed to identify a naturally occurring code. Our mission is to discover, develop and commercialize core principles of nature which give rise to information, consciousness and intelligence. Natural Code LLC will pay the researcher $100,000 for the initial discovery of such a code. If the newly discovered process is defensibly patentable, we will secure the patent(s). Once patents are granted, we will pay the full prize amount to the discoverer in exchange for the rights. Our investment group will locate or develop commercial applications for the technology. The discoverer will retain a small percentage of ongoing ownership of the technology. http://cosmicfingerprints.com/solve/
bornagain77
September 9, 2015
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"the probability, per Hoyle, comes out to be pretty close to 1." Just be sure never to ask a neo-Darwinist for an actual demonstration of that 100% probability of cytochrome c arising all by itself. Such as say how this post demonstrates the 100% probability of Intelligence generating functional information.
Estimating the prevalence of protein sequences adopting functional enzyme folds: Doug Axe: Excerpt: The prevalence of low-level function in four such experiments indicates that roughly one in 10^64 signature-consistent sequences forms a working domain. Combined with the estimated prevalence of plausible hydropathic patterns (for any fold) and of relevant folds for particular functions, this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences. http://www.toriah.org/articles/axe-2004.pdf
bornagain77
September 9, 2015
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No, the worst case scenario is the one I mentioned, where it takes all of 30 years for the tNM to appear, and then it is culled away; and, then this is repeated. That is the worst scenario, one for which I made the calculation.
It's kind of obvious now that you are making this up as you go along... but what possible relevance does this calculation have to anything?wd400
September 9, 2015
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Fred Hoyle has done the calculation for you. It’s in his “The Mathematics of Evolution.” I mean, if were going to talk about improbabilities…. Actually, if you correct Hoyle's calculations, allowing for all of the amino acid substitutions that are seen in the universe of cyt C sequences, then the probability, per Hoyle, comes out to be pretty close to 1.Arthur Hunt
September 9, 2015
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What are the odds of cytochrome c arising all by itself? Would you like to calculate those odds? Fred Hoyle has done the calculation for you. It's in his "The Mathematics of Evolution." I mean, if were going to talk about improbabilities....PaV
September 9, 2015
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Oh dear. Even if we go along with your deranged insistence that the tNM only ever arises in the generation immediately preceding a cull, you are now arguing that it is culled every single time. So out of 60 cullings, it is present (at only one copy, wtf?) at 30 cullings, right? The probability that tNM survives at least one culling is 1 - 0.5^30, that is 99.9999999% Yikes.DNA_Jock
September 9, 2015
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No, the worst case scenario is the one I mentioned, where it takes all of 30 years for the tNM to appear, and then it is culled away; and, then this is repeated. That is the worst scenario, one for which I made the calculation.PaV
September 9, 2015
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PaV, the calculation that is hopelessly wrong is the one you offered in comment 38. Here you calculated that, thanks to the 50% culls that you reckon occur every 33 years, any (particular) favorable allele would have a 1 in 2^60 ( i.e. 1 in 10^18) chance of surviving 2,000 years, i.e. through 60 successive culls. This calculation assumes that allele X arose only once, 2,000 years ago, and is present at precisely one copy immediately preceding every one of the 60 culls. That's hilarious. In comment 57, you introduce a different calculation, wherein you calculate that the "needed" mutation only has a 50% chance of arising in 33 years. Ignoring (for now) the error inherent in "the needed mutation" (tNM), your math is still hopelessly wrong. In the worst case scenario, tNM occured immediately preceding the cull, and has a 50% chance of surviving the cull, giving a 25% chance (50% * 50% = 25%) of being present post-cull. But most of the time tNM will have occurred somewhere 5 to 25 generations prior to the cull, and be present in, say, ten or more different animals, and thus have 49.95% chance (50% * (1 - 2^10)) of being present post-cull. IOW the intermittent culls don't have the earth-shattering effect you think. Annual culls would merely reduce the effective population size by 50%, and thus make drift more important, relatively speaking. But we should master basic math before moving on to pop-gen, amirite?DNA_Jock
September 9, 2015
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No wd400, the 2.4/(3.2 x 1.5) calculation is a separate calculation, that just happens to yield exactly the same value as PaV was using for the effect of the cull. What are the chances? Perhaps we can borrow a design detector from one of the denizens at UD...DNA_Jock
September 9, 2015
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Yo are (incorrectly as far as I can tell, what is 2.4/(3.2 x 1.5) ?) trying to calculate the probability of a specific mutation arising once, staying a frequency 1/2N then surviving a halving of the population? And you think this biologically relevant?wd400
September 9, 2015
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DNA-Jock: Point out where it is "hopelessly" wrong. I've already done one calculation. Through the limitations that the die-offs represent, there is only a 50% chance that the needed mutation would occur in the thirty year period. If it never 'arises,' then how does it 'spread' through the population. You can argue that statistically, given enough chances, it will reach that point. Then, and only then, would the math falter. But let's look at the big picture: we're talking about ONE amino acid change. That's the whole argument of Behe's "Edge of Evolution." It appears, based on the malarial parasite example, that the most one can expect of "evolution" is two two-amino-acid changes. This is "hopelessly" inadequate, wouldn't you agree?PaV
September 9, 2015
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Poperian: Again, it seems as if your strategy to deny evolution is true is to only accept misconceptions of it. Read Michael Denton's, "Evolution: A Theory in Crisis," or Behe's "The Edge of Evolution." There are problems with Darwinian theory. And, in "Darwin's Doubt," Meyer argues forcefully that Darwinian theory does not have the "explanatory" power necessary to explain the Cambrian Explosion.PaV
September 9, 2015
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No PaV, post 38 (which is about drift), contains math that is hopelessly wrong, whatever prism you try to squint through. But if you want to talk about the OP, sure: What is the evidence that supports your claim that the 1988 die-off led to "hardly any change"? Careful though, it's a trap...DNA_Jock
September 9, 2015
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PaV:
The OP was meant to underscore problems with common analyses used in population genetics. If you have a problem with NS, take it up with them. I’m afraid that I am not interested in having the discussion.
The OP is titled: "Survival of the Fittest?" This underlies the entire premise of the OP. For example, you wrote....
(1) How do we define the “fittest”? Are they the “strongest”, the “fastest”, the most “aggressive”? What are they? Maybe they’re the “weakest.” Maybe they were so weak that they couldn’t forage with the rest of the herds, and so stayed behind and didn’t get infected. So, how do we define “fitness” here?
Are you suggesting that question, based on a misconception, really isn't relevant to the OP? You went on to write:
Again, the “survival of the fittest” doesn’t befall the “strongest,” “fastest”, “most aggressive”, most “anything,” but, apparently to almost any member of the population. If 400,000 out of 800,000 antelopes die, and they’re none for the better, then what does NS do anyway? Have we wildly exaggerated what it is able to do? (Read The Edge of Evolution to find out more)
Again, I wrote:.....
So what has been achieved during this period? [Evolution] has not optimized the functional adaptation of a variant gene to its environment, but the relative ability to propagate itself though the population. From the point of view of the species and it’s individual members, the effect of evolution was a disaster. However, evolution does not care in this sense. It merely favors the genes that spread best though the population.
Pav:
But again: the title of the OP is “survival of the fittest.” This is not about neutral drift, but about the problems inherent with defining “fitness,” and with the role of “selection.”
Again, it seems as if your strategy to deny evolution is true is to only accept misconceptions of it.Popperian
September 9, 2015
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DNA-Jock: Sorry, it's not goofy. It's looking at things in a very specific way, through the prism of huge die-offs every thirty years. If the population cannot produce a "particular" allele in a limited amount of time, die-offs exacerbate the process of any significant genetic change. But again: the title of the OP is "survival of the fittest." This is not about neutral drift, but about the problems inherent with defining "fitness," and with the role of "selection."PaV
September 9, 2015
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PaV:
This “adapting” to pathogens makes the antelope population incapable of almost nothing else.
I agree. Although I suspect that isn’t what you meant. Things work better if you take the time to write carefully. I did take the time to read carefully what you wrote @38.
Just imagine that some member of the population is working towards some adaptive trait. It has, let us say, one of two needed a.a. bases in the right location. There it is in the population, waiting for the next a.a. to come along by chance, and, lo and behold, it’s GONE. Poof! Undone by some virus. The “chance” of this potential favorable mutation to remain in the population is 1 in 2, or 0.5. This same ‘halving’ occurred 30 years before. Let’s say this happens, on average, every 33 years, or 3 times a century. Well, in a thousand years, this means it would have occurred 30 times. Thus, the ability of ANY favorable allele (whatever that means) to survive is 1 in 2^30, or, 1 in 10^9, and, for a 2,000 year period, it would be 1 in 10^18.
Your math is correct (for a specific allele – not “ANY favorable allele” – perhaps you meant to write “any PARTICULAR favorable allele”) if and only if this specific allele magically remains at one copy in the population prior to every one of the 60 culls. As in: “Errr, only if it hasn’t replicated.” Waaay beyond goofy. [sound of weeping bears]DNA_Jock
September 9, 2015
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DNA-Jock: Like I said, Only if it hasn’t replicated.
Just imagine that some member of the population is working towards some adaptive trait. It has, let us say, one of two needed a.a. bases in the right location. There it is in the population, waiting for the next a.a. to come along by chance, and, lo and behold, it’s GONE. Poof! Undone by some virus.
I was stating the fact that the animal was the "only" one in the population with the needed a.a., awaiting the second. Then it dies suddenly. The a.a. is gone, needing to show up once again in the population. Things work easier if you take the time to read carefully. Again, if you read carefully, I said this die-off occurred before in 1988. That's 27 years. I used 33 years to make the math more straightforward. So, we have an effective population of at most 400,000, or, 4 x 10^5. This 'die-off' occurs with a frequency of 30 years, let's say. And let's say there's 200 new mutations per new offspring. Crunching the numbers: 4 x 10^5 x 30 generations x 200 mutations per generation= 24 x 10^8, or, 2.4 x 10^9 mutations. The genome size for mammals is 3.2 x 10^9 nucleotides. To get an a.a. to change requires more than 1 nucleotide base to change. Let's say it needs, on average, 1.5 nucleotide changes. Then, this means the odds of getting the "first" a.a. to change is 2.4/(3.2 x 1.5)= 0.5. So, when I said that there was an animal now with the 'first' a.a. in place, that's a concession. And, important for the antelope population. But, it also means that statistically, on average, 30 years is not enough for the "first" mutation to arise, let alone the second one. So much for neutral drift. How can anything happen at all? And what about elephant populations that are much, much smaller, and which mate only infrequently? What then? You see my point now, right? This "adapting" to pathogens makes the antelope population incapable of almost nothing else. So much for neo-Darwinian evolution.PaV
September 8, 2015
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PaV math:
Half the population died off. The chance that the animal died off without passing on the allele, or of the animal to whom the allele is passed off to, are both 1 in 2.
Like I said, Only if it hasn't replicated. If the potentially favorable mutation occurred a couple of generations before the cull, then there might be two to four animals with the allele, thanks to drift. Chance that the allele survives the cull is now 75% - 93%. (There might also be zero alleles, making the cull irrelevant for that mutation.) Your math assumes that a potentially beneficial mutation arises once every 33 years, and in that generation there is a 50% cull. It's beyond goofy. Now Josie Bruin is sad too.DNA_Jock
September 8, 2015
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Popperian: The OP was meant to underscore problems with common analyses used in population genetics. If you have a problem with NS, take it up with them. I'm afraid that I am not interested in having the discussion.PaV
September 8, 2015
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DNA-Jock: "Only if it hasn't replicated." Is this supposed to be a thoughtful reply? If it is, you'll have to try harder. Half the population died off. The chance that the animal died off without passing on the allele, or of the animal to whom the allele is passed off to, are both 1 in 2. Please don't obfuscate any further.PaV
September 8, 2015
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