Uncommon Descent Serving The Intelligent Design Community

Nachman’s Paradox Defeats Darwinism and Dawkins’ Weasel

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The following is a crude 1-minute silent animation that I and members of the IDCS Network put together. God willing, there will be major improvements to the animation (including audio), but this is a start. Be sure to watch it in full screen mode to see the details.

http://www.youtube.com/watch?v=SrIDjvpx7w4

The animation asserts that if harmful mutation rates are high enough, then there exists no form or mechanism of selection which can arrest genetic deterioration. Even if the harmful mutations do not reach population fixation, they can still damage the collective genome.

The animation starts off with healthy gingerbread men as parents. Each spawns ginger kids, and the red dots on the kids represent them having a mutation. The missing ginger limbs are suggestive of severe mutations, the more mild mutations are represented by ginger kids merely having a red dot and not severe phenotypic effects of their mutation. The exploding ginger kids represent Selection doing its thing and removing the less functionally fit from the population. The persistence of red dots on the ginger kids represents persistence of bad mutations despite any possible mechanism of selection.

Nobel Prize winner HJ Muller (of Muller’s ratchet fame) suggested that the human race can’t even cope with a harmful rate of 0.1 per new born. The actual rate has been speculated to be on the order of 100-300.

The animation uses a conservative harmful rate of 1 and argues (with some attempts at humor) that deterioration would thus be inevitable even with a harmful rate of 1 per new born.

I save discussion in the comment section the relevant but technical topics of truncation selection, sexual reproduction, recombination, synergistic epistasis, compensatory mutations, relief from Muller’s ratchet etc. These highly technical topics should be addressed and were not included in the animation. We can discuss them in the comment section.

However, the essential problem of mutation rates and deterioration is depicted by the animation. How this cartoon is illustrative of reality (when we consider the technicalities such as recombination, sexual reproduction, synergistic epistasis), can be discussed in the comment section.

In light of such problems Kondrashov posed the rhetorical question, Why have we not died 100 times over?. Kondrashov attempted to answer the question, but I don’t think the problem has been solved. The animation expresses my skepticism of the long term benefit of “synergistic epistasis”.

And if the conclusion symbolized by the animation is true, then on what grounds can we believe Darwinism is true?

The animation was inspired by a paper by Nachman and Crowell. Two years ago I wrote: Nachman’s U-Paradox. This animation helps illustrate the problem of Nachman’s paradox.

I recommend we should build a non-partitioned WEASEL to feature how Nachman’s paradox will trump Dawkins conclusions that somehow Darwin found the answer to appeance of design. One can get an idea of what it would look like given the animation.

[ Admins, I can’t seem to embed the video, can you embed it for me? I think embedded video requires higher privilege than my account has.]

Notes:

1. We could have done the drawings differently to emphasize the mutations are unique and novel and different for each ginger kid, but I save that work for later (including audio).

2. There is a refinement to the animation that is in order based on Nachman’s calculation of average removal rates of harmful mutations assumng trucation selection, “U”=3, and a conservative reproduction rate for humans, but I didn’t get around to it. That is yet another modification for future animations. We’ll need also some technical research on the matter.

Comments
scordova at 107,
I’d really like to understand your underlying model, possibly to the extent of being able to implement it in software.
Haploids: 1 new harmful per new born Try implementing that. Are you having problems counting up to 1?
Ah, it could be worse, I could be having problems demonstrating common courtesy. Zachriel at 101 politely detailed the additional information required to understand your model: Is that the average mutations per individual? What is the distribution of effects of the harmful mutations? How often do reversions occur? How frequent are beneficial mutations and what is their distribution? What is the population? The size of the genome? What about recombination which is common in haploid organisms? Without knowing those kinds of parameters, it is not possible to replicate your model. I am more than willing to go to the effort of doing so; I hope you are willing to provide the additional information.Mustela Nivalis
December 3, 2009
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I’d really like to understand your underlying model, possibly to the extent of being able to implement it in software.
Haploids: 1 new harmful per new born Try implementing that. Are you having problems counting up to 1?scordova
December 3, 2009
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scordova at 102, "Is that the average mutations per individual?" Minimum. See the discussion above. How about trying to model it with the other parameters to your choosing. Feel free to report the results. Now you're just teasing. Why so coy? I'd really like to understand your underlying model, possibly to the extent of being able to implement it in software. Could you please describe it at the level of detail suggested by Zachriel?Mustela Nivalis
November 23, 2009
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Mung, It wasn't in this thread, it was 2 years ago here at UD.
Sal, this is not a model.
Baloney. Look at the animation. The seleciton model doesn't matter. Who gets killed doesn't matter. With haploids, the number of offspring doesn't matter. The model is minimally simple to drive home the theme: if there are enough harmfuls mutations, no model of selection can prevail against deterioration. Therefore with respect to haploids,the other details are moot. Do you understand what the word "moot" means.
Care to comment?
I just did. Do you understand what the word moot means with respect to the matter at hand. Hint: moot means with respect to any other possible modeling parameters or details, the parameters and details don't affect the final outcome. Thus it doesn't add anything to the clarity of the model.
Perhaps you mean to model the case of haploid organisms who experience 1 new harmful mutation per newborn.
Look at the friggin animation!!!! It illustrates visually what will happen!!!! Sheesh. Zach has yet to run it with those specifications. He's been running the diploid model. I've objected, and Zach, who's been quick to provide sim work, has been noticably quiet to run the simulation that is consistent the animation. Why the silence?scordova
November 23, 2009
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Model: Haploids, 1 new harmful per newborn.
Sal, this is not a model. Perhaps you mean to model the case of haploid organisms who experience 1 new harmful mutation per newborn. If that is the case, you need to develop such a model. Let us say that each newborn dies, as a result of the harmful mutation. GREAT! Now that is something we can actually model. For each newborn that enters the population, add one harmful mutation to that individual. For each harmful mutation in an individual in the population, remove that individual from the population. Are we making progress yet? Well, to answer that, we need to ask how well our model tracks with observations of actual organisms. Care to comment?Mung
November 23, 2009
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I do express my thanks that you’ve tried to stick to the topics at hand and you’ve never attacked me personally despite the fact that I’ve not always been so nice to you.
Unlike myself, who has apparently expressed a revulsion for Salvador that can only be expressed as contempt and repugnance. Now I've been charged of making the claim here at UD that I find Sal repugnant, even though I cannot recall the occasion. See my response to Sal here: http://telicthoughts.com/mutations-fitness-and-more/#comment-248736 I repeat what I said there: Sal, If I called you repugnant, I apologise. I can't find anyplace in this thread where I have done so.Mung
November 23, 2009
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Is that the average mutations per individual?
Minimum. See the discussion above. How about trying to model it with the other parameters to your choosing. Feel free to report the results. :-) Do you think that Jistak's provisional agreement with me is generally well founded regarding 1 harmful per newborn in haploids?
You still didn’t point to any such study. What specific research has Sternberg done to support the claim?
See the Evolution and News Report for a bibliography. Disagree with Rick? Do you needed peer-reviewed by Darwinists before you can even consider the conclusions. Feel free to express on what grounds specifically Sternberg is wrong. We'll know in the coming decades if junk DNA is junk. PS I do express my thanks that you've tried to stick to the topics at hand and you've never attacked me personally despite the fact that I've not always been so nice to you. For that I salute you.scordova
November 22, 2009
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scordova: Model: Haploids, 1 new harmful per newborn.
Is that the average mutations per individual? What is the distribution of effects of the harmful mutations? How often do reversions occur? How frequent are beneficial mutations and what is their distribution? What is the population? The size of the genome? What about recombination which is common in haploid organisms?
scordova: Sternberg said about 90% functional.
You still didn't point to any such study. What specific research has Sternberg done to support the claim?Zachriel
November 21, 2009
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What recent study indicates that deleterious mutations are that high in humans?
I made the inference several times in this thread. The nature paper said about 100 new mutations. Sternberg said about 90% functional. This would strongly suggest U = some number around 100. Whether this leads to meltdown is another story. The issue is whether selection can police these functional regions. Which it obviously does not (in light Kimura's work). Ergo: Selection doesn't create most of the function in the genome.scordova
November 21, 2009
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Analogous Diploid case: Mentioned in the OP at UD. U=3, 3 harmfuls per newborn Result: Kid gets about 1 or more harmfuls from each parent. Kid gets 3 additional. Why is this. With 40 kids, 2 might have no mutations from parents carrying 3 mutations. If parents have fewer than 40 kids, then, it's likely all the kids have 1 mutation or more! See the resemblance now to the haploid model. Did I get the chance to make these clarifications? Maybe, but I was so distracted by the strawmen and derailments being put forward I didn't get the chance to add these. I make amends now. But the data was right there in Nachman's paper. Comprende?scordova
November 21, 2009
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Everyone knows that gingerbread people include gingerbread men, gingerbread women and gingerbread children. You didn’t provide a model.
You keep repeating falsehoods zach. Model: Haploids, 1 new harmful per newborn.scordova
November 21, 2009
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scordova: And you don’t think statements like the following by Nachman aren’t handwaving by the same standard?
we estimate that the genomic deleterious mutation rate (U) is at least 3. This high rate is difficult to reconcile with multiplicative fitness effects of individual mutations and suggests that synergistic epistasis among harmful mutations may be common. … However, many mutations are unconditionally deleterious and it is improbable that the reproductive potential on average for human females can approach 40 zygotes. This problem can be overcome if most deleterious mutations exhibit synergistic epistasis; that is, if each additional mutation leads to a larger decrease in relative fitness
There are several differences. Nachman isn't trying to "prove evolution." It's already well-established, hence he is interpreting his finding in the light of the known facts, and in the light of plausible mechanisms. In addition, he's not claiming to have demonstrated synergistic epistasis, but suggesting it as an avenue of additional research.
scordova: Nachman’s number of U=3 (U=number of mutations per individual).
That's Nachman's number of deleterious mutations. The total number of mutations is much higher. What recent study indicates that deleterious mutations are that high in humans?Zachriel
November 20, 2009
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For the readers' benefit, not all designs need to be "functional" in the sense of reproductive success. In the world of human affairs, if one came across a configuration of coins that were all heads, or like the configurations (where H=heads, T=tails):
HTTTT HTTTT HTTTT HTTTT HTTTT
or
HHH HTHTTT HHH THTTHT HHH .....
etc. These are recongizable linguistic type designs. Whether they have function or not, they are recognizable designs. The ENCODE project discovered comparable linguistic architectures in the genome. When I examined some of the sequences myself using data mining tools, the design was astonishing, definitely non-random (the above coin examples were non-random). These designs are especially found in the regions often thought to be expendable junk, hence not subject to selection (like those ultra conserved sequences). These designs are subject to deterioration. If they are non-functional, they will be especially immune to the mechanisms of selection to purge them even if we assume sexual recombination mechanisms. The haploid animation that I put forward can then be modified to deal with the diploid case, and it can be seen that selection will not arrest the deterioration of these designs. So these linguistic designs could be powerful designs that can't be attributed to selection, if there is a rise of SNP's in these regions in the present day, real time. Also, even on the assumption these are regions not subject to selection (from the prejudicial view that they were Junk DNA), how then do they have linguistic structure? Linguistic structures are recognizable designs. I gave some illustration with coins what linguistic designs could look like. Now, what would be especailly bad for the Blindwatchmaker argument is if these linguistic regions are both functional and invisible to selection. I've provided arguments above why I think that is the case based on Kimura and Sternberg. Further, testing of the real-time rise of SNP's in these regions would be empirical confirmation that selection is mostly impotent save a few exceptional cases. The animation would thus be materially correct provided it were modified to illustrate the diploid case and say Nachman's number of U=3 (U=number of mutations per individual). The work published in 2009 on human mutation rates using solexa technology suggests U = 100.scordova
November 19, 2009
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What would your prediction be, specifically, of the number you’d expect to find to confirm ID and the number you’d find and then conclude that ID was disconfirmed? Unless you are specific now, in advance, you’ll be accused of making a postdiction.
Prediction: The ultra "conserved" regions will experience an unabated rise of SNP's (single nucleotide polymorphisms). This will be inconsistent with the claim purifying selection (the purging of "bad" mutations") has been operating on the genome of mice and men for the last 100 million years.
BERKELEY, CA — Three years ago, "ultraconserved elements" were discovered in the genomes of mice, rats, and humans. These are DNA sequences 200 base pairs in length or longer — some are over 700 base pairs long — showing 100-percent identity among the three species. They have been perfectly conserved since the last common ancestor of mice, rats, and humans, which lived some 85 million years ago. These and other highly conserved sequences are thought to have persisted with little or no change because they are indispensable, performing functions vital for viability or reproduction. Scientists in the Genomics Division of the Department of Energy's Lawrence Berkeley National Laboratory and DOE's Joint Genome Institute set out to test this hypothesis by engineering four different "knockout" mice, each lacking one selected ultraconserved element. If truly indispensable, mice lacking an ultraconserved element should either die or be unable to produce viable offspring. Remarkably, as the researchers report in the September, 2007 issue of PLoS Biology, the knockout mice in this study showed almost no ill effects at all.
So much for synergistic epistasis. :-) Synergistic epistasis would predict instant death or ill effects. Hardly a dent eh? Maybe Nachman's "fix" to his own paradox is no fix at all, but rather circular reasoning refuted by hard nosed empiricism. If these ultra-conserved regions are not being purified and purged via purifying selection, then why does it seem they have been arranged like a bunch of coins oriented to all heads? These knockout experiments are prima facie evidence that selection can't see these regions, yet somehow they appear to be magically ordered like a bunch of coins oriented heads, or plagiarism, or (gasp) common design. Unabated rise of SNP's in this region would confirm selection has a hard time seeing these regions. Finally, Kimura showed by cost arguments (comparable to the ones presented in the animation), that 90% of molecular evolution is non-Darwinian. This is symboliized by the much celebrated and widely accepted "Neutral Theory of Molecular Evolution". If 90% of the molecules in the genome are functional, and 90% of the molecules are not subject ot selection, the implication is that most of the functioning in the genome was totatlly originated independent of Darwninian blindwatchmaker processes. This is not "argument from ignorance" but rather a brutal proof by contradiction. Thus we have found design and function not attributable to natural selection. Where then is the source of this design and function? Whatever the source, we can have good reason to remove Darwinism as a plausible explanation. Continued degeneration of function will be evidence selection can't arrest deterioration. If selection can't arrest deterioration, circumstantially speaking, it would cast doubt that it had anything to do with the creation of such function. And in light of Kimura's work and Sternberg's hypothesis, it should seem painfully evident that selection doesn't account for the creation of most function in the genome, and perhaps most of the rest of the human body.scordova
November 19, 2009
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Jistak wrote: Come on. That’s just hand waving. It’s obvious that with sufficiently high mutation rates, even recombination cannot rescue from mutational meltdown. But you need to use a diploid model with recombination to figure out what the likely conditions are for this to happen, and then you can compare those conditions with empirical data.
And you don't think statements like the following by Nachman aren't handwaving by the same standard?
we estimate that the genomic deleterious mutation rate (U) is at least 3. This high rate is difficult to reconcile with multiplicative fitness effects of individual mutations and suggests that synergistic epistasis among harmful mutations may be common. ... However, many mutations are unconditionally deleterious and it is improbable that the reproductive potential on average for human females can approach 40 zygotes. This problem can be overcome if most deleterious mutations exhibit synergistic epistasis; that is, if each additional mutation leads to a larger decrease in relative fitness While extreme truncation selection seems unrealistic, the results presented here indicate that some form of positive epistasis among deleterious mutations is likely.
Just invoke "synergistic epistasis" and mutations magically become damaging enough to weed it out the population. Just invoke "positive epistasis" and magically the bad mutations become good. This line of deduction is known as circular reasoning. No model for viability, selection coefficients, fecundity (all the complaints you and Mung lodge against me). Fine. But I will make a subsequent comment about this regarding ultra conserved sequences and the potential for an unabated rise in SNP's and the impotence of purifying selection. By the way, thank you for agreeing that there is likely a point where there are enough mutations when no amount of selection can be of help. Muller said for humans, 0.1, Nachman (if there is no Synergistic Epistasis), 3. I will argue reasons empirically why synergistic epistasis is unlikely based on results of ultra "conserved" sequences between mice and humans.scordova
November 19, 2009
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Victor Tussle: This sounds like a project that could be undertaken and provide some significant proof for a reasonable price. Will you commit to undertake the required work, now that the cost of sequencing is much much lower and certainly within the reach of organizations and people connected to the, for example, Discovery Institute. The most recent cost I saw was $350,000 but that was some time ago. Alot of money, sure, but if it were to prove ID then I’m sure somebody would pay. And I’m sure it’s cheaper today then it was yesterday.
The project of tracking the rise of SNP's and other mutations is being done independent of ID. It is done because of the intense medical interest in tracking hereditary diseases. And unlike Darwinism which is quick to mislable something as "beneficial" so long as it makes more babies, the medical community is more inclined to view mutations as a bad thing. See my objection to characterizing things as "fit" when by any other standard, they are diseased: Survival of the Sickest, Why We need Disease. Consider: Number of Rare Genetic Conditions on the Rise
The number of people living with identified rare genetic diseases is on the rise in Australia, because more conditions are being recognised. It is thought that up to 1.5 million Australians are now living with unique, rare and often recently identified genetic conditions which go largely under the radar. "It isn't so much that the number of people affected are going up it's more that the number of diseases that we recognise is increasing," says University of Melbourne Professor of Medical Genetics Bob Williamson. "There are now seven or eight thousand different genetic diseases known to occur, although many of them only affect a handful of children."
Is this merely more recognition? We'll see. The enigma is, why have these diseases persisted (selection ain't working so well). Thousands upon thousands of hereditary diseases persisting for centuries. We'll see. In the mean time there is another area of research that could cast doubt on Darwinism, purifying selection, the enigma of Ultra Conserved Sequences. More in a subsequent comment on this thread.scordova
November 19, 2009
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Victor Tussle,
What would your prediction be, specifically, of the number you’d expect to find to confirm ID and the number you’d find and then conclude that ID was disconfirmed? Unless you are specific now, in advance, you’ll be accused of making a postdiction.
What's wrong with a postdiction? Is there anything different in that and a prediction, logically?Clive Hayden
November 19, 2009
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I think it's fair to call it an imaginative piece of work.Mung
November 19, 2009
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Sal
We simply need to look at DNA of great grand parents, grand parents, parents, and kids, to get some good estimates of the real-time rise in SNPs. It is heartening to see that Solexa and Illumina technology is helping to inform the debate (as I predicted it would a few years back here at UD).
This sounds like a project that could be undertaken and provide some significant proof for a reasonable price. Will you commit to undertake the required work, now that the cost of sequencing is much much lower and certainly within the reach of organizations and people connected to the, for example, Discovery Institute. The most recent cost I saw was $350,000 but that was some time ago. Alot of money, sure, but if it were to prove ID then I'm sure somebody would pay. And I'm sure it's cheaper today then it was yesterday.
to get some good estimates of the real-time rise in SNPs
What would your prediction be, specifically, of the number you'd expect to find to confirm ID and the number you'd find and then conclude that ID was disconfirmed? Unless you are specific now, in advance, you'll be accused of making a postdiction.Victor Tussle
November 19, 2009
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I think the darwinists jumping in with their nitpicking and asking for unreasonable levels of detail are utterly missing the point. scordova's work here is certainly a thought-provoking presentation, and can also be used as a platform for visualization of mutations spreading through populations. As well as rigorous mathematical and biological lab work the ID movement of course has to do public outreach and this visualization work can help with both.waterbear
November 19, 2009
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Salvador,
For starters, we have the Y-chromosome in humans and femail mitochondrial DNA (widely believed to be subject too little if not zero recombination).
Y chromosomes tend to degenerate, presumably because of lack of recombination. That fits nicely with Muller's ratchet. Also as expected, we don't see the same thing with autosomes. As for mitochondrial DNA, many mitochondria are transmitted by the mother to the egg, so there is a much smaller probability that deleterious mutations will get fixed. Also, much mitochondrial DNA has migrated to the nucleus over millions of years. Still, there are some interesting differences between the evolution of nuclear and mitochondrial DNA. I recently attended a lecture by Jerry Coyne, where he described the evolutionary genetics of speciation in a pair of sister species of Drosophila. Although there was little introgression between species at the level of nuclear DNA, there was enormous introgression at the level of mitochondrial DNA. It seems that the mitochondria of one species can easily spread in another species, even if hybridization occurs extremely rarely. An evolutionary puzzle!
And thirdly, their may be a point where the mutation selection equilibrium breaks down and can be approximated by the deterioration in the haploid model.
Come on. That's just hand waving. It's obvious that with sufficiently high mutation rates, even recombination cannot rescue from mutational meltdown. But you need to use a diploid model with recombination to figure out what the likely conditions are for this to happen, and then you can compare those conditions with empirical data. I suggest you get working on that and show us the results, and we'll give you some feedback. Perhaps, in the end, the results can be published in Evolution, one of my favorite journals! Keep up the good work.jitsak
November 19, 2009
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Mr Cordova, Microporidia didn’t go extinct, it just lost most of its functionality and was reduced to being a parasite. That is exchanging cause and effect. Better to say that because of its success in the niche of parasite, Microsporidia lost functionality it no longer needed (or even interfered with being a good parasite).Nakashima
November 19, 2009
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If you can find one, publish it as soon as possible!
Simulations are being done. God willing they will be published. Walter ReMine informs me 10 mutations with truncation selection will result in mutational meltdown in diploid population with comparable reproduction rates as humans. The enigma has not escaped Muller, Crow, Kondrashov, Nachman, Crowell. They assume sysnergistic epistasis (a form of truncation selection). To make the matter of synergistic epstasis moot, the simulation is run with truncation selection. The whole thing of arguing over fitness and function can be very amorphous and nebulous and speculative. As Lewontin points out, fitness is hard, if not impossible to define since it is context dependent (unlike mass in classical physics). So where can we determine if there is genetic deterioration without direct reference to fitness and function? Sternberg unwittingly hints of a fruitful area of research:
Another counterintuitive result of the ENCODE project and other comparative genomic analyses is that known functional sections of the mammalian genome such as protein-coding segments appear to be diverging without constraint, whereas a host of “junk” sequences are under some type of selective pressure—including most human “noncoding” DNA stretches. The same has been repeatedly detected for the fruit fly genome, where most nonprotein-coding sequences appear to be under functional constraint—with the species-specific differences having the statistical hallmarks of being “adaptive”. Even the Y chromosome of the fruit fly, long presented as “exhibit A” in the gallery of garbage DNA, has been shown to have diverse effects on the phenotype of this insect. Such results are exactly the opposite of what Orgel and Crick and Doolittle and Sapienza predicted. from How the junk DNA hypothesis has changed
If realtime SNP growth is unabated in these "conserved" regions then we have reason to believe natural selection had little to do with their orgination. If these "conserved" regions are functional, then an increase in the SNP in these regions in the current day (real time measurments in newborns today, and subsequent tracking) this would suggest selection had nothing to do with the orgination of these functions. It would also suggest whether selection can even select against these defects. I hypothesize, the directly measured increase of the SNP's will be inconsitent with accepted mainstream ideads. This implies genetic deterioration of some sort. We'll see. I have faith empirical results over time will help decide which ideas are closer to the truth. We simply need to look at DNA of great grand parents, grand parents, parents, and kids, to get some good estimates of the real-time rise in SNPs. It is heartening to see that Solexa and Illumina technology is helping to inform the debate (as I predicted it would a few years back here at UD). The study I referenced above estimates a rate of 100 mutations per individual per generation. If 90% of the genome is functional, it is hard to conceive that the human race could tolerate 90 functional defects per new born for very long without suffering. I'm not saying humans will go extinct. Microporidia didn't go extinct, it just lost most of its functionality and was reduced to being a parasite. We all might hope we don't live to see that day for humans.scordova
November 18, 2009
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Allen wrote:
Large linkage blocks” is just another term for chromosomes.
Thank you for your comment, and this important enough to clarify. I don't believe that is Sanford's usage. Another common term is Haplotype blocks.
The most obvious and extreme form of selection interference is when there is tight physical linkage between benefician and deleterious mutations. This results in an irreconcilable problem referred to as "Muller's Ratchet". One of the most obvious requirements of natural selection is the ability to separate good and bad mutations. This is not possible when good and bad mutations are physically linked. John Sanford, Genetic Entropy p. 81
and
Essentially all of the genome exists in large linkage blocks (Tishkoff and Verrelli, 2003) John Sanford page 81
The reference to Tishkoff and Verrelli is Patterns of human genetic diversity: implications for human evolutionary history and disease The say "low levels of linkage disequilibrium (LD)". I read that to mean high linkage. Anyone agree or disagree? Dr. Sanford interprets this to mean the genome is composed of large linkage blocks. I have seen medical papers that rely on the assumption of large linkage blocks to detect diseases. If they use a few Single Nucleotide Polymorphisms to identify the presence of a large linkage block. PS This study seems mildly relevant: Human Haplotype Block Sizes Are Negatively Correlated With Recombination Rates.scordova
November 18, 2009
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Sal in comment #82:
"The animation clearly depicts one gingerbreadman giving birth to two offspring each. That doesn’t look like asexual haploid reproduction to you?"
Yes, it does, but it is just as clearly not sexual reproduction, unless one defines the horizontal genetic transfer and binary fission of bacteria as sexual reproduction. Once again, your simulation does not model sexual reproduction in diploid eukaryotes (and certainly not in humans), as there is no indication in the simulation that the mutations can be "hidden" by dominant, non-mutant alleles.
"Unless we find a comparable case that is approximated in diploid organisms."
As I have repeatedly pointed out, there is no comparable case in diploid organisms, except for alleles located in the Y chromosome of mammals (and some, but not all haploid eukaryotes, such as cellular slime molds and some fungi, and then only during part of the life cycles of those organisms).
Secondly, the issue of large linkage blocks (more on that later).
"Large linkage blocks" is just another term for chromosomes. When Müller described his "ratchet" in the late 1930s, it wasn't entirely clear that the "linkage groups" discovered by Bridges, Stephens, and Sturtevant were exactly the same thing as eukaryotic chromosomes. Now we know they are, and know that two processes (and perhaps more) eliminate the problem of Müller's Ratchet in eukaryotes: 1) sexual recombination (via independent assortment during metaphase I of meiosis, followed by gametic fertilization), and 2) chromosomal recombination (i.e. "crossing-over between homologous chromosomes during prophase I of meiosis, followed by first-division segregation of alleles in meiosis I). These two processes, combined with diploidy, completely eliminate Müller's Ratchet, which explains why Müller proposed it as the groundwork for his hypothesis for the evolution of sexual reproduction in eukaryotes.
"...their may be a point where the mutation selection equilibrium breaks down and can be approximated by the deterioration in the haploid model.
If you can find one, publish it as soon as possible! No one else has found one in nearly a century of population genetics research.
"...to begin with a haploid model that would convey the basic point. and then show it’s approximate analogy to relevant diploid cases.
As far as anyone has ever been able to determine (either theoretically or empirically), there is no analogy to relevant diploid cases.
"...does the haploid model presented in the animation remind you of Müller’s Ratchet?"
Of course it does. That's because Sanford's GE model is based on Müller’s Ratchet (as I have repeatedly pointed out), and is therefore not applicable to diploid eukaryotes (nor even to haploid organisms that can exchange genetic material horizontally...which appears to be almost all of them).Allen_MacNeill
November 18, 2009
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scordova: The animation clearly depicts one gingerbreadman giving birth to two offspring each. That doesn’t look like asexual haploid reproduction to you?
Hmm.
scordova: Nobel Prize winner HJ Muller (of Muller’s ratchet fame) suggested that the human race can’t even cope with a harmful rate of 0.1 per new born. The actual rate has been speculated to be on the order of 100-300. The animation uses a conservative harmful rate of 1 and argues (with some attempts at humor) that deterioration would thus be inevitable even with a harmful rate of 1 per new born.
You are extrapolating the animation to the human race.
scordova: And if the conclusion symbolized by the animation is true, then on what grounds can we believe Darwinism is true?
Indeed, extrapolating to all of life! As I mentioned, organisms that don't recombine tend to have small genomes, so most of their offspring are exact clones; and also have large populations, meaning fixation of nearly neutral mutations take a very long time.Zachriel
November 18, 2009
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I am a bit confused now. If you say that the animation was the asexual case, then that seems to imply there is an underlying model. I thought there isn’t.
The animation clearly depicts one gingerbreadman giving birth to two offspring each. That doesn't look like asexual haploid reproduction to you?
If you say that the animation was the asexual case, then that seems to imply there is an underlying model. I thought there isn’t.
The underlying model 1 new harmful per new offspring. Dawkins model wans't substantially more detailed than mine, yet is has been celebrated and defended by Darwinists.
If there is zero recombination and every offspring has at least one new deleterious mutation and zero beneficial mutations, then yes that is correct I think.
Thank you!
But are these assumptions reasonable? I think not
Unless we find a comparable case that is approximated in diploid organisms. For starters, we have the Y-chromosome in humans and femail mitochondrial DNA (widely believed to be subject too little if not zero recombination). Secondly, the issue of large linkage blocks (more on that later). And thirdly, their may be a point where the mutation selection equilibrium breaks down and can be approximated by the deterioration in the haploid model. This was the original intent to begin with a haploid model that would convey the basic point. and then show it's approximate analogy to relevant diploid cases. More on these, in subsequent posts. By the way, does the haploid model presented in the animation remind you of Muller's Ratchet? :-)scordova
November 18, 2009
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Salvador,
Before we move forward on this, the animation was the haploid or asexual case. There are obvious analogs to the issue of Y-chromsomal heredity……
I am a bit confused now. If you say that the animation was the asexual case, then that seems to imply there is an underlying model. I thought there isn't.
Before moving to the diploid case, is it correct to say 1 harmful per offspring in that case will lead to deterioration, independent of viability or fecundity, or for that matter selection strength?
If there is zero recombination and every offspring has at least one new deleterious mutation and zero beneficial mutations, then yes that is correct I think. But are these assumptions reasonable? I think not.jitsak
November 18, 2009
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In comment #77, Zachriel wrote:
"...if your point is that bacteria are due for extinction, I think you might be mistaken."
Indeed, if Sanford's model is valid and (for the reasons discussed here) applies mostly (perhaps entirely) to haploid organisms such as bacteria, then the continued survival of bacteria is surprising. Unless, of course, one assumes (as Dr. Behe does, at least in the case of the malaria parasite) that some (and perhaps all) bacteria (and other haploid organisms) are favored by the Intelligent Designer, who continuously "tweaks" the genomes of every line of prokaryotes to remove the deleterious mutations that would otherwise lead to their eventual extinction. Indeed, it would seem that Dr. Sanford's GE model is contradicted by Dr. Behe's observation that the malaria parasite has remained virtually unchanged over many millions of generations. Why has the genome of Plasmodium falciparum not degenerated according to Sanford's model? Does the Intelligent Designer have a soft spot for Plasmodium falciparum, as Dr. Behe speculates in The Edge of Evolution? Or might natural selection actually provide a solution to what would otherwise be incommensurate paradoxes?Allen_MacNeill
November 18, 2009
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As I have pointed out in another thread (see https://uncommondescent.com/neuroscience/coffee-neuroscience-do-you-really-need-a-refrigerator-when-you-have-this/#comment-340238 ), sex (defined as the exchange of genetic material between individuals) was proposed as a solution to the problem of the accumulation of deleterious mutations in haploid organisms in the 1930s by Hermann Müller, the originator of "Müller's Ratchet", upon which Sanford's GE model is based. Müller argued that the ability to counteract the accumulation of mutations was the principle selective advantage that diploid sex provides, and therefore can explain its evolution (but not necessarily its origin). So, Salvador, if you can indeed extend Sanford's GE model (and, presumably, your gingerbread man simulation) to apply to diploid, sexually reproducing eukaryotes, I urge you to submit it to a peer-reviewed journal for evolutionary biology as soon as you have verified its validity. If the model can then be tested empirically using either field or lab observations, you would definitely be eligible for a Crafoord Prize (the "Nobel prize for biology"), as this topic (i.e. the evolutionary origins of sex) has been one of the hottest areas of debate among evolutionary biologists for a century and a half.Allen_MacNeill
November 18, 2009
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