Happy to oblige: Through the powers invested in me by all those of reason, you are hereby awarded The Quote Miner's Award of Excellence.Rhed said:Rhed said:Citation please.
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Happy to oblige: Through the powers invested in me by all those of reason, you are hereby awarded The Quote Miner's Award of Excellence.Rhed said:Rhed said:Citation please.
Well, I have repeated part of your earlier post to emphasise the problem that everyone (except you) noticed: there was nothing in the blog which could give a rational person that idea. Hype about how ENCODE defined "function" is not a sleight on evolution.Rhed said:I read your post Inferno, and all I read is that evolutionists don't like the ENCODE's research because it disagrees with evolution. I could not find any retractions from ENCODE. What I found is the interpretations of what function means (and you agree):
"3) Much of the ENCODE hype rests on the definition of the term “function”."
D
red said:Well, I have repeated part of your earlier post to emphasise the problem that everyone (except you) noticed: there was nothing in the blog which could give a rational person that idea. Hype about how ENCODE defined "function" is not a sleight on evolution.
You are comparing chimps and chumps.Rhed said:The term "function" was a misunderstanding and deals with interpretation of what that term means. That's it. Sooner or later we will still find more and more function in non-coded DNA. Evolutionists know to far to well about hype. 99% similar to chimp; then is was 98.7%, 98.6%, 95%, and now 92%. Notice a trend? The less we are similar and know that non-coded DNA is less junk and more functional, the less believable of human-chimp evolution.
Rhed said:he_who_is_nobody said:Intelligent design creationists are not known for their reading comprehension. I believe their poor reading comprehension comes from spending years in the Quote Mines.
Copy and paste a snippet from an ENCODE research paper that retracts the 80%.
[url=http://sandwalk.blogspot.ca/2014/05/what-did-encode-consortium-say-in-2012.html?m=1 said:Sandwalk[/url]"]Now, none of these editors and experts are ENCODE Consortium authors so it's quite possible that they have all misinterpreted the 'entrée' paper. This is the view now being suggested by the Consortium leaders (Kellis et al., 2014). They now argue that Genetic, Evolutionary, and Biochemical descriptions of "function" are all reasonable approaches to understanding junk DNA and genome composition. They now claim that just having the data available is their most important contribution and not claims about how much of the genome is functional.
The implication is that they really didn't mean to say that 80% of our genome is functional. It was all a misunderstanding. They are now saying that the goal of the Consortium wasn't to discover function at all but merely to provide maps of places that might be functional, depending on your definition.In contrast to evolutionary and genetic evidence, biochemical data offer clues about both the molecular function served by underlying DNA elements and the cell types in which they act, thus providing a launching point to study differentiation and development, cellular circuitry, and human disease. The major contribution of ENCODE to date has been high-resolution, highly-reproducible maps of DNA segments with biochemical signatures associated with diverse molecular functions. We believe that this public resource is far more important than any interim estimate of the fraction of the human genome that is functional.
Rhed said:The term "function" was a misunderstanding and deals with interpretation of what that term means. That's it. Sooner or later we will still find more and more function in non-coded DNA. Evolutionists know to far to well about hype. 99% similar to chimp; then is was 98.7%, 98.6%, 95%, and now 92%. Notice a trend? The less we are similar and know that non-coded DNA is less junk and more functional, the less believable of human-chimp evolution.
They're not results, they are interpretations of data. The ENCODE project did transcription mappings, that doesn't mean they found any new functions (in fact, they haven't, none of the ENCODE papers demonstrate that any new function has been found).Rhed said:SpecialFrog said:I suggest you read this: http://sandwalk.blogspot.ca/2014/05/what-did-encode-consortium-say-in-2012.html.
The 80% figure is wrong (and possibly not even what the ENCODE researchers claimed).
Where ole where do I find a retraction from ENCODE about the 80%??? All I find is different interpretations of the term function. And evolutionary scientists are not happy (mega-rants and tirades actually) with the results so must disagree with the scientific results.
Did you know that evolutionary scientists actually started out believing the entire genome was functional? The rationalization was that natural selection would get rid of stuff that isn't used because it costs energy to replicate it. Turns out on closer inspection that was wrong, and a lot more complicated than initially thought.Can any evolutionists guess what the next rescuing device will be if our genome is actually 80% functional? :lol:
ENCODE did not find any functionality. They interpreted their transcrition mappings to be indication of function, that's it. No function was actually discovered.Rhed said:Inferno said:I'd rather you read my blog post on the subject. I'm happy to say it was cited by Ryan T. Gregory, a researcher on the topic of the c-value paradox, as a "good resource" on the topic.
Of course Larry Moran's post is better, but I think mine has a broader approach.
I read your post Inferno, and all I read is that evolutionists don't like the ENCODE's research because it disagrees with evolution. I could not find any retractions from ENCODE. What I found is the interpretations of what function means (and you agree):
"3) Much of the ENCODE hype rests on the definition of the term “function”."
And you obviously don't like ENCODE's scientific papers either:
"A further update comes from a 2013 paper in “Genome Biology and Evolution”. The paper is discussed over at Pharyngula and it basically rips into ENCODE’s papers. There’s a lot of technical stuff I needn’t cover, so I’ll limit myself to mentioning one thing: Other researchers have found only 10% true functionality, that’s 70% less than the folk over at ENCODE."
False as already explained. It would help your case a lot if you could get beyond handwavey dismissals and actually try to bring arguments about to show:Rhed said:The term you used "rips" into ENCODE" means to me "tearing apart".; in other words, don't like their papers. You and evolutionists don't like the factual results because it makes evolution nothing more than a fairytale.
It would be more correct to say natural selection fixes alleles in the population.Rhed said:Rhed said:What's the mechanism? Random mutations without natural selection?Rumraket said:No, the mechanisms are the same. Mutations, selection, drift, migration and so on. The mechanisms aren't different, their relative importance is. It has been recognized that drift players a much larger role at the genomic level than previously thought.
That doesn't mean natural selection no longer exists, they are not mutually exclusive.
Natural Selection (NS) conserves traits; not create.
After the fact of mutation, yes. Newly arisen mutants will be subject to selection.Rhed said:The NS mechanism is after the fact; not before the fact.
Correct. Newly arisen mutants will either go to 100% or 0% frequency in the population.Rhed said:Genetic Drift loses genetic diversity, and smaller the population, faster the genetic lose.
Yes they do, your statement is unambigously, provably and factually incorrect.Rhed said:Mutations don't work in evolution's favor:
That's what they did in Lenski's Long-term experiment. Quoting Lenski:Rhed said:To test this theory, add mutations to a genome and see how it responds, a phenomenon called Epistasis:
Richard Lenski said:Fitness Unlimited
This latest paper is an interesting one because it uses our most old-fashioned assays – the kind that was the heart of the LTEE when it started, and which also formed the core of that first paper back in 1991. That is, the results are based on measurements of relative fitness, coupled with new models – both descriptive and dynamical. (Although this blog post emphasizes the descriptive model, the Science paper also presents new theory showing that the descriptive model can be derived from a dynamical model of evolution that incorporates two phenomena – clonal interference and diminishing-returns epistasis – that are known to occur in the LTEE and other studies of evolving asexual populations.)
Fitness is the central phenotype in evolutionary theory; it integrates and encapsulates the effects of all mutations and their resulting phenotypic changes on reproductive success. Fitness depends, of course, on the environment, and here we measure fitness in the same medium and other conditions as used in the LTEE. We estimate the mean fitness of a sample from a particular population at a particular generation by competing the sample against the ancestral strain, and we distinguish them based on a neutral genetic marker. Prior to the competition, both competitors have been stored in a deep freezer, then revived, and acclimated separately for several generations before they are mixed to start the assay proper. Fitness is calculated as the ratio of their realized growth rates as the ancestor and its descendants compete head-to-head under the conditions that prevailed for 500 … or 5000 … or 50,000 generations.
The exciting new result is that the fitness of these evolving bacteria shows no evidence of an upper bound or asymptote. A two-parameter power law fits the data much better than does a two-parameter hyperbolic model. According to both models, the rate of fitness increase decelerates over time, as it clearly does. However, the power-law model has no asymptote, whereas the hyperbolic model has an upper bound.
No, you actually don't need positive epistasis. That is simply unambigously false.Rhed said:bla bla bla stuff we already know...
The contribution of epistasis to the architecture of fitness in an RNA virus
Rafael Sanjuán, Andrés Moya, and Santiago F. Elena
http://www.pnas.org/content/101/43/15376.abstractThe tendency for genetic architectures to exhibit epistasis among mutations plays a central role in the modern synthesis of evolutionary biology and in theoretical descriptions of many evolutionary processes. Nevertheless, few studies unquestionably show whether, and how, mutations typically interact. Beneficial mutations are especially difficult to identify because of their scarcity. Consequently, epistasis among pairs of this important class of mutations has, to our knowledge, never before been explored. Interactions among genome components should be of special relevance in compacted genomes such as those of RNA viruses. To tackle these issues, we first generated 47 genotypes of vesicular stomatitis virus carrying pairs of nucleotide substitution mutations whose separated and combined deleterious effects on fitness were determined. Several pairs exhibited significant interactions for fitness, including antagonistic and synergistic epistasis. Synthetic lethals represented 50% of the latter. In a second set of experiments, 15 genotypes carrying pairs of beneficial mutations were also created. In this case, all significant interactions were antagonistic. Our results show that the architecture of the fitness depends on complex interactions among genome components
So in order for neo-Darwinian evolution to work, you need positive epistasis
You should actually try to read the paper you link before you link it, instead of just quotemining the abstract:Rhed said:and beneficial mutations. That did not happen.
Here, we took a direct approach for characterizing the distribution of epistatic effects (8, 9). The starting point for our experiments was a collection of 91 single-nucleotide substitution mutants of vesicular stomatitis virus (VSV) created by site-directed mutagenesis (14). In a first set of experiments, we chose 28 of these genotypes that fulfilled the following two conditions (14): (i) the genomic position to be mutated and the nucleotide incorporated were both randomly chosen, and (ii) mutations had deleterious (although nonlethal) fitness effects. We randomly picked 47 pairs of these mutants and constructed the corresponding double-mutant genotypes.
In a first set of experiments, we chose 28 of these genotypes that fulfilled the following two conditions (14): (i) the genomic position to be mutated and the nucleotide incorporated were both randomly chosen, and (ii) mutations had deleterious (although nonlethal) fitness effects. We randomly picked 47 pairs of these mutants and constructed the corresponding double-mutant genotypes.
In a second set of experiments, we chose six genotypes for which the mutation incorporated had a beneficial fitness effect (14) and created all of the 15 possible double mutants resulting from combining these single mutations.
Very well in fact.Rhed said:So how does evolution work again?
Give scientific paper that claims this.Rhed said:red said:Well, I have repeated part of your earlier post to emphasise the problem that everyone (except you) noticed: there was nothing in the blog which could give a rational person that idea. Hype about how ENCODE defined "function" is not a sleight on evolution.
The term "function" was a misunderstanding and deals with interpretation of what that term means. That's it. Sooner or later we will still find more and more function in non-coded DNA. Evolutionists know to far to well about hype. 99% similar to chimp
Give scientific paper that claims this.Rhed said:then is was 98.7%
Give scientific paper that claims this.Rhed said:98.6%
Give scientific paper that claims this.Rhed said:
Give scientific paper that claims this.Rhed said:and now 92%.
Even if the trend was true, and even if there was no junk-DNA, neither of these would entail your conclusion.Rhed said:Notice a trend? The less we are similar and know that non-coded DNA is less junk and more functional, the less believable of human-chimp evolution.
Rumraket said:If all our (and Chimpanzee) DNA was functional, why the hell would that affect the comparative relationships between our two species? I can give you two subspecies of E coli that have fully functional genomes (likely not even a single redundant base-pair), and they clearly and unambigously evolved from a common ancestor (we know this because we observed it happen in an experiment). So tell me again why the percentage of functionality of the genome should affect the inference of common descent? Is there any logic to that statement?
Rumraket said:You should actually try to read the paper you link before you link it, instead of just quotemining the abstract:
Here, we took a direct approach for characterizing the distribution of epistatic effects (8, 9). The starting point for our experiments was a collection of 91 single-nucleotide substitution mutants of vesicular stomatitis virus (VSV) created by site-directed mutagenesis (14). In a first set of experiments, we chose 28 of these genotypes that fulfilled the following two conditions (14): (i) the genomic position to be mutated and the nucleotide incorporated were both randomly chosen, and (ii) mutations had deleterious (although nonlethal) fitness effects. We randomly picked 47 pairs of these mutants and constructed the corresponding double-mutant genotypes.
So for one of their experiments, they generate random mutations and then deliberately picked only deleterious mutations to research their epistatic interactions:
In a first set of experiments, we chose 28 of these genotypes that fulfilled the following two conditions (14): (i) the genomic position to be mutated and the nucleotide incorporated were both randomly chosen, and (ii) mutations had deleterious (although nonlethal) fitness effects. We randomly picked 47 pairs of these mutants and constructed the corresponding double-mutant genotypes.
Then they turned their attention towards another experiment, where they only picked beneficial mutatants to explore their epistatic interactions:
In a second set of experiments, we chose six genotypes for which the mutation incorporated had a beneficial fitness effect (14) and created all of the 15 possible double mutants resulting from combining these single mutations.
So actually, random mutations did in fact generate beneficial mutations, otherwise the experiment would simply not have been possible.
After having picked their beneficial mutants they turned to generate double-mutants with beneficial-only mutations to see how their interacted. What they found was that, while the double-mutant still had higher fitness than the ancestral unmutated wild-type, the double-mutant had lower fitness than the single-mutants. So while the epistatic interaction reduced the fitness effect from the individual beneficial mutations when they were both were present, it was still in fact a net fitness gain.
So while it was negative epistasis, it was a net gain in fitness over the wild-type. The double mutant would still be more fit than the wild-type with no mutations. But the single-mutant would be more fit and outcompete the double-mutant in this case.
Either case would still constitute evolution by natural selection. Thank you for bringing more evidence for evolution.
he_who_is_nobody said:If I could venture a guess, it has to do with Rhed reading about the percentage of our relationship with chimpanzees going from 98% to 95% at around the same time he read about functional DNA going from ~8% to 80%. Basically a causation/correlation fallacy based off of Rhed's ignorance of genetics.
Rhed said:he_who_is_nobody said:If I could venture a guess, it has to do with Rhed reading about the percentage of our relationship with chimpanzees going from 98% to 95% at around the same time he read about functional DNA going from ~8% to 80%. Basically a causation/correlation fallacy based off of Rhed's ignorance of genetics.
Well help a brother out. Are Humans and chimps 98% similar including the non-coding and junk DNA?
[url=http://www.theleagueofreason.co.uk/viewtopic.php?p=167187#p167187 said:Rumraket[/url]"]This question is also answered by Larry in the blog post you link first, at the bottom.
It includes Junk-DNA. In fact most (and I emphasize MOST, not ALL, as Larry also explains) of the differences between human and chimp are IN the junk-DNA, because the functional parts are under varying levels of purifying selection.
Why do you link material you don't read?
I also covered it earlier, albiet definitionally, repeating from the post: there is a variety of ways to calculate DNA percentages, giving different outcomes of the similarity between chimpanzees and humans. The 1.2% chimp-human distinction, for example, measures only substitutions in the base building blocks of those genes which chimpanzees and humans share. A comparison of the entire genome, however, indicates that segments of DNA have also been deleted, duplicated over and over, or inserted from one part of the genome into another. Counting these differences leads to an additional 4 to 5% distinction between the human and chimpanzee genomes.he_who_is_nobody said:[url=http://www.theleagueofreason.co.uk/viewtopic.php?p=167187#p167187 said:Rumraket[/url]"]This question is also answered by Larry in the blog post you link first, at the bottom.
It includes Junk-DNA. In fact most (and I emphasize MOST, not ALL, as Larry also explains) of the differences between human and chimp are IN the junk-DNA, because the functional parts are under varying levels of purifying selection.
Why do you link material you don't read?
Why not help us all out by reading our posts
I'm not, you are, because it is clear you are unfamiliar with the terminology.Rhed said:Sorry but I have to be blunt. You are wrong wrong wrong. And more wrong. You are so wrong I cannot even describe it to you. (sigh...)
Yeah, site-directed mutagenesis is still random with respect to fitness. That's what the random in random mutation means.Rhed said:Where to begin? For one they used Site-Directed Mutagenesis for mutations.
You have to look up the measured fitness effects of the double-mutant compared to the wild-type and the single mutants, It's in supplementary info, which you can find here:Rhed said:For the set of beneficial mutations, all changes introduced were nonsynonymous: two mutants contained one change in the N gene, three in the M gene, and one in the G gene
For two, not sure where you get this "net-gain".
See the measured fitness of double mutants. In several cases, the net effect is still positive (but less than the fitness gain of the single-mutant. So I'm not wrong, you are wrong.The first 47 rows correspond to the randomly selected deleterious mutations, whereas the last 15 rows correspond with mutations of beneficial fitness effect.
Quantifying the Strength and Direction of Epistasis. Fitness was determined for each double mutant (W ij) as well as for their corresponding single mutants (W i and W j). Under the null hypothesis of nonepistatic effects, the expected fitness for the double mutant equals the product of the fitness estimated for each single mutation (i.e., W ij = W i W j). If deleterious mutations were to interact in a synergistic way, then the observed fitness for the double mutant would be lower than expected by multiplying the fitness of both single mutations, and hence the difference between observed and expected fitnesses would became negative. By contrast, if deleterious mutations were to interact in an antagonistic way, then the observed fitness would be larger than expected under the null hypothesis of multiplicative fitness effects, and thus the difference between observed and expected fitnesses would became positive. From this argument, a convenient way of detecting the existence (and sign) of epistasis is by computing the index εij = W ij - W i W j (1). For deleterious alleles (W i < 1 and W j < 1), synergistic epistasis is defined by εij < 0, whereas antagonistic epistasis is defined by εij > 0. For beneficial alleles (W i > 1 and W j > 1), the signs of εij must be inverted.
The first 47 rows correspond to the randomly selected deleterious mutations, whereas the last 15 rows correspond with mutations of beneficial fitness effect.
Rhed said:The tests were so bad, they even called it decompensatory epistasis!
After studying each genotype separately, eight cases showed significant antagonistic epistasis (t tests, P ≤ 0.027) but none showed synergistic epistasis.</I>
Rhed said:Six antagonistic cases remained significant even after correcting the significance level with Bonferroni's sequential method (17). Actually, in five of these instances, the fitness of the double mutant was even less than that of either single mutant.</B>
Rhed said:<I><B>This particular case of antagonism between mutational fitness effects is known as decompensatory epistasis
Yes, and I have not claimed otherwise. Suppose a double mutant arises against a background of wildtype, it will still have superior fitness compared to the unmutated wild-type in several cases.Rhed said:(1). Therefore, on average, a viral genotype carrying two beneficial mutations does not get the entire benefit individually associated with each mutation. Indeed, when epistasis is decompensatory, both beneficial alleles involved in the interaction cannot spread to fixation in the population, because the double mutant is less fit than each single mutant
No, I have to ask, did you read the paper? The whole paper, including the supplementary information, and did you understand what you read? Apparently not.Rhed said:I have to ask...did you even read the paper??? :?
The red line corresponds to neutrality (fitness = 1.0).Relationship between observed and expected (multiplicative) fitnesses for 65 VSV genotypes carrying pairs of nucleotide substitutions. The solid line represents the null hypothesis of pure multiplicative effects. Deviations from this line are a consequence of the existence of epistatic fitness effects (εij = W ij - W i W j ≠ 0). Filled circles correspond with genotypes carrying two deleterious mutations; open circles correspond with genotypes carrying two beneficial ones.
Rhed said:Sorry but I have to be blunt. You are wrong wrong wrong. And more wrong. You are so wrong I cannot even describe it to you. (sigh...)
Rumraket said:They go to great lengths to explain and define how they measure fitness.
Quantifying the Strength and Direction of Epistasis. Fitness was determined for each double mutant (W ij) as well as for their corresponding single mutants (W i and W j). Under the null hypothesis of nonepistatic effects, the expected fitness for the double mutant equals the product of the fitness estimated for each single mutation (i.e., W ij = W i W j). If deleterious mutations were to interact in a synergistic way, then the observed fitness for the double mutant would be lower than expected by multiplying the fitness of both single mutations, and hence the difference between observed and expected fitnesses would became negative. By contrast, if deleterious mutations were to interact in an antagonistic way, then the observed fitness would be larger than expected under the null hypothesis of multiplicative fitness effects, and thus the difference between observed and expected fitnesses would became positive. From this argument, a convenient way of detecting the existence (and sign) of epistasis is by computing the index εij = W ij - W i W j (1). For deleterious alleles (W i < 1 and W j < 1), synergistic epistasis is defined by εij < 0, whereas antagonistic epistasis is defined by εij > 0. For beneficial alleles (W i > 1 and W j > 1), the signs of εij must be inverted.
So a deleterious fitness effect is a value less than 1, and a beneficialt fitness effect is a value greater than 1. Exactly equal to 1 is effectively neutral. Let's look at the table in supplementary info, under "Double mutant fitness":
Orange = Deleterious double mutant
Green = Beneficial double mutant.
0.869± 0.022
1.060 ± 0.073 Oh look at me, I'm not supposed to exist.
0.899 ± 0.025
0.694 ± 0.013
0.637 ± 0.012
0.582 ± 0.007
0.837 ± 0.016
0.935 ± 0.016
0.972 ± 0.017
0.841 ± 0.016
1.000 ± 0.013 * Seems to be strictly neutral.
1.014 ± 0.015
1.014 ± 0.015 Wait a minute, what's all these beneficial double mutants doing here when they were produced by combining deleterious single-mutants?
0.671 ± 0.016
1.041 ± 0.041 Another one.. weird!
0.959 ± 0.018
1.023 ± 0.024 Oops, I did it again!
0.757 ± 0.037
0.687 ± 0.010
0.769 ± 0.008
0.889 ± 0.017
lethal
0.992 ± 0.019
0.664 ± 0.010
lethal
0.650 ± 0.014
0.934 ± 0.013
0.836 ± 0.010
lethal
1.022 ± 0.052 Call the creationism police, something's wrong here. How can double deleterious mutants result in synergistic positive epistasis?
0.867 ± 0.014
1.002 ± 0.031
0.866 ± 0.011
0.986 ± 0.014
0.658 ± 0.007
0.625 ± 0.010
0.657 ± 0.005
0.739 ± 0.015
0.665 ± 0.008
0.613 ± 0.009
0.778 ± 0.021
1.012 ± 0.015
0.996 ± 0.021
1.013 ± 0.029
0.950 ± 0.038
0.592 ± 0.035
0.936 ± 0.016
0.885 ± 0.016
0.920 ± 0.012
1.026 ± 0.015
0.978 ± 0.009
0.930 ± 0.013
0.998 ± 0.013
0.942 ± 0.014
1.063 ± 0.020
1.064 ± 0.017
1.091 ± 0.031
1.082 ± 0.024
0.928 ± 0.012
1.112 ± 0.031
1.116 ± 0.026
The first 47 rows correspond to the randomly selected deleterious mutations, whereas the last 15 rows correspond with mutations of beneficial fitness effect.
Rhed said:The tests were so bad, they even called it decompensatory epistasis!
After studying each genotype separately, eight cases showed significant antagonistic epistasis (t tests, P ≤ 0.027) but none showed synergistic epistasis.</I>
Rumraket said:Which merely means the combined effect of two mutations was less beneficial than the effect of a single mutation. In several cases, as you can see on the supplementary information table, the net effect of both mutations was still beneficial.Rhed said:Six antagonistic cases remained significant even after correcting the significance level with Bonferroni's sequential method (17). Actually, in five of these instances, the fitness of the double mutant was even less than that of either single mutant.</B>
Rumraket said:But still higher than the wild-type (look at the numbers). I'm still right, you're still wrong.Rhed said:<I><B>This particular case of antagonism between mutational fitness effects is known as decompensatory epistasisRhed said:(1). Therefore, on average, a viral genotype carrying two beneficial mutations does not get the entire benefit individually associated with each mutation. Indeed, when epistasis is decompensatory, both beneficial alleles involved in the interaction cannot spread to fixation in the population, because the double mutant is less fit than each single mutant
Rumraket said:Yes, and I have not claimed otherwise. Suppose a double mutant arises against a background of wildtype, it will still have superior fitness compared to the unmutated wild-type in several cases.Rhed said:I have to ask...did you even read the paper??? :?
Rumraket said:No, I have to ask, did you read the paper? The whole paper, including the supplementary information, and did you understand what you read? Apparently not.
I read the whole thing. I understood it. But to make sure I went back to see if I missed something or you missed something. I believe I found the error. There is a section in the paper named Epistasis Among Pairs of Beneficial Mutations under The Results:
"Epistasis Among Pairs of Beneficial Mutations. Let us now move our attention to the 15 genotypes carrying two mutations for which the expected fitness effect was beneficial. The average epistatic effect, Formula, was also significantly antagonistic (Fig. 2; t 14 = 4.522, P < 0.001) and the distribution of epistatic interactions was effectively symmetrical (Fig. 2; g 1 = -0.304 ± 0.580; t 14 = 0.524, P = 0.608) and unimodal as well (Fig. 2; g 2 = -0.576 ± 1.121; t 14 = 0.514, P = 0.616). However, the conclusion of a predominance of antagonistic epistasis between pairs of beneficial mutations can be jeopardized by a lack of statistical independence among the 15 genotypes used in this experiment. We created all possible double mutants from six beneficial mutations, but this set of double mutants does not represent a random sample of all possible double mutants on the genome, because several genotypes contain the same mutation. To circumvent this statistical problem, we used a bootstrap approach. One thousand size six random samples were taken from the original dataset, and a Formula value was computed from each sample. Samples of size six were taken simply because six is the number of independent mutations from which the experiment was initiated. The 95% bootstrap confidence interval for Formula ranged between -0.129 and -0.087, slightly more negative than computed above. (The conclusion was completely robust to changes in the sample sizes used during the bootstrap resampling, because 14 of 15 cases had ε < 0.) This result gives even more strength to our conclusion of a predominance of antagonistic epistasis among beneficial mutations. "
They used the bootstrap approach. I knew something was odd with your analyses with the numbers and with the conclusions of the research paper. The observed expected fitness was less than 0. Beneficial mutations had a antagonic epistasis effect. Not one did a beneficial mutation had a synergistic epistasis effect (a requirement for evolution to work). And I quote, "Therefore, on average, a viral genotype carrying two beneficial mutations does not get the entire benefit individually associated with each mutation. Indeed,when ipistasis is decompensatory, both beneficial alleles involved in the interaction cannot spread to fixation in the population".
Rumraket said:Also, THE LONG TERM EVOLUTION EXPERIMENT WITH E COLI. Got a response to that?
You seem to have totally ignored it, and now want to extrapolate the case of evolution in a single viral experiment to generalize the effect of epistasis for all of life. You need to not just look at single cases, in single experiments, to pick out single sentences you apparently don't even understand.
Rhed said:I will in due time.
Rhed said:I will in due time.
Dustnite said:
There's nothing wrong with my analysis, because it isn't an analysis. It is a direct reading of the paper as-is. The numbers are right there, they unambiguously state their methodology.Rhed said:They used the bootstrap approach. I knew something was odd with your analyses with the numbers and with the conclusions of the research paper.
There is no such thing as "observed expected fitness".Rhed said:The observed expected fitness was less than 0.
Yes, because in all cases the observed fitness was less than the product of the two single mutants. But in several cases it was still beneficial, because it still had a fitness above 1.0Rhed said:Beneficial mutations had a antagonic epistasis effect.
Correct, none of the double mutants using beneficial mutations had synergistic epistatic effects. But several of them were still beneficial (Wij > 1).Rhed said:Not one did a beneficial mutation had a synergistic epistasis effect
False. A beneficial double mutant can arise against a background of wildtype, with no higher-fitness single mutants being present. The likelihood of this is of course less than the likelihood that a beneficial single-mutant will also arise in the population.Rhed said:(a requirement for evolution to work).
And there we have it, you missed the key word. On average.Rhed said:And I quote, "Therefore, on average a viral genotype carrying two beneficial mutations does not get the entire benefit individually associated with each mutation.
Because their combination is less fit than their product, but this simply implies both single mutants are present, instead of a scenario where a double mutant arises against a background of no beneficial single mutants.Rhed said:Indeed, when epistasis is decompensatory, both beneficial alleles involved in the interaction cannot spread to fixation in the population".