Nachman’s Paradox Defeats Darwinism and Dawkins’ Weasel

_{Salvador Cordova

November 14, 2009

Creationism, Darwinism, Evolution, Intelligent Design, Video}

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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

Salvador,
Assuming a minimum of 1 is several standard deviations from the mean which covers 99.9999….% of the cases. You can thus have a minimum of 1 and that would be a minimum within 99.999..% of the cases in a Normal distribution. So the assumption by any standard is reasonable given the premises. I also pointed out, the outlier would be so improbable to be of no consequence.
Fair enough, if the mean is sufficiently high (in this case 100 mutations per offspring), a normal distribution is a good approximation to a poisson distribution. What strikes me as odd, though, is that you would choose 1 as the minimum number of mutations, rather than the more obvious choice of zero. I asked:
Next, in the model, how did the mutations affect viability and/or fecundity of the offspring?
and you answered
I pointed out they were not modeled because they were moot points. If you wish to provide a model that models moot points and numbers that deal with moot points you can provide them and post them here.
They are not moot points at all. The harmfulness of mutations determines how efficiently selection can remove them from the population.
The bottom line is based on the premis of 1 new mutation per new born, deterioration will happen. The issues of fecundity and viability will only affect the speed and severity.
I am not so sure about that. On any given locus, recombination creates offspring without mutations on that locus if both parents carry a single mutation on that locus. Then the spread of the mutation depends on the selective advantage of that offspring compared to offspring that do inherit the mutation. Look, Dawkins may have lost the source code of his original Weasel model, but I am sure you were not that careless and you can show us the source code of your model, so that we can check for ourselves if your conclusions are justified.jitsak_{November 14, 2009
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In comment #13, jitsak asked a crucial question. Specifically, it is of absolutely fundamental importance to know two things: 1) Are the organisms that we are considering diploid or haploid? Humans, like almost all animals, are diploid, but bacteria and all other prokaryotes (and many, but not all protists/protoctists) are haploid. 2) Are the mutations for which we are calculating coefficients of fitness dominant, recessive, or neutral (and if dominant, what is the degree of penetrance)? Without an answer to these questions, one literally cannot calculate anything having to do with the fitness of specific alleles. Here's why: Both Sanford's "genetic deterioration" model and the video presented in this thread assume that both beneficial and deleterious mutations will be “visible” to selection, and can therefore be subject to selection. However, in diploid organisms both beneficial and deleterious alleles can be "invisible" to selection if they are either recessive or if they are dominant, but lack complete penetrance. The opposite would the case for any genes located in the genomes of haploid organisms (bacteria, archaea, most protists, many fungi most of the time, the gametophyte generations of plants and multicellular algae, and even some animals, such as whiptail lizards). This would also be the case for alleles located in the y chromosomes of mammals and other non-paired non-homologous chromosomes. In all of these latter cases, dominance does not exist and all genes are immediately "visible" to selection. As far as I can tell, it is only genes like these that are subject to the effects modeled by Sanford and others, and which could (at least theoretically) lead to some kind of "genetic deterioration". Furthermore, as Motoo Kimura (and Jukes and Crow independently) pointed out, neutral mutations (i.e. mutations that are neither beneficial nor deleterious) are not "visible" to selection and can therefore persist in populations indefinitely. Even severely deleterious mutations will not be visible at all unless they are dominant (or at least exhibit some dominant “penetrance”). If they are recessive (and/or show no penetrance), then they will not be eliminated from populations except when they appear in homozygous recessives. For example, consider the empirical fact that the allele for cystic fibrosis (call it "f") is extraordinarily deleterious and recessive, whereas the F allele is both normal and dominant with virtually 100% penetrance. The f allele almost always results in death when homozygous (usually in childhood), but has no immediately obvious phenotypic effect when heterozygous. I know this for a fact, as my wife is heterozygous for the cystic fibrosis allele (i.e. she is Ff, whereas I am FF, yet she shows absolutely no phenotypic signs of having any of the symptoms of cystic fibrosis). We know (as the result of molecular genetic analysis) that the f allele has the effect of disabling the chloride protein ion channels in animal cell membranes. People who are homozygous FF and Ff can make all the normal (i.e. functional) chloride channels they need. Only ff individuals cannot do this, and hence cannot regulate the transport of chloride ions across cell membranes. Despite the fact that homozygous ff individuals virtually always die, usually in childhood, the frequency of the f allele among people whose ancestors are from Europe (i.e. Caucasians) is approximately one in twenty (or about 5%). Given that the ff homozygous condition is literally as deleterious as it can be, how quickly should the cystic fibrosis allele be removed from the human population, and is there some equilibrium value at which the frequency of the cystic fibrosis allele is so low that it only ever appears in heterozygotes (i.e. its frequency is so low that the probability of two heterozygotes interbreeding and having 1/4 of their offspring expressing cystic fibrosis is effectively zero)? The answer always surprises my students: let's take just Europeans. Even though the allele is present in 5% of the population, the probability that two people who carry the allele will mate and produce children is only 1/20 X 1/20 = 1/400. Furthermore, the probability that two heterozygotes will have a child that has cycstic fibrosis is only 1/4 (i.e. 1/4 of their children will be homozygous normal and 1/2 = 2/4 will be heterozygous carriers). Ergo, the probability that two Europeans (chosen at random) will have a child that has cystic fibrosis is 1/20 X 1/20 X 1/4 = 1/1,600. This is why the majority of cases of cystic fibrosis in the United States are the very first appearance of this condition among either of the families of the parents of the affected child. But that's the theoretical calculation. What is the actual frequency of cystic fibrosis? In 1997, about 1 in 3,300 Caucasian children in the United States was born with cystic fibrosis. In contrast, only 1 in 15,000 African American children suffered from cystic fibrosis, and in Asian Americans the rate was even lower at 1 in 32,000. Why is the actual frequency of cystic fibrosis so much lower than the predicted frequency? One reason is that the actual frequency of the cystic fibrosis allele varies from subpopulation to subpopulation. Indeed, if one does a calculation based on the assumption that the f allele is a complete recessive, but completely lethal allele, and the F allele is both completely dominant and has no deleterious effects, then the frequency of the f allele should be less than 1/10,000, and therefore the actual rate of appearance of cystic fibrosis should be 1/400,000,000 (i.e. 1/10,000 X 1/10,000 X 1/4). This calculation is based on the assumption that every single individual who is ff dies before reproducing, whereas every single individual who is FF and Ff dies of something else (i.e. unrelated to the presence or absence of the F allele). So the interesting question is not “why is the frequency of the f allele not zero”, but rather “why is the frequency of the f allele so anomalously high among Europeans (but not African Americans or Asians, who still exhibit a frequency of the f allele that is slightly higher than that calculated on first principles alone). The answer seems to be that, like the allele for sickle-cell anemia, the allele for cystic fibrosis increases the fitness of heterozygotes, relative to homozygous normal FF. Using standard population genetics calculations, it is possible to calculate the degree of this increased fitness and then factor it into the forgoing calculations. Physiological and developmental research is now being conducted to determine precisely how the anomalously high frequency of the f allele is being maintained in some (but not all) human populations. Four hypotheses have been advanced for this, all based on the assumption that being Ff confers some resistance to at least one of the following diseases: • Cholera: With the discovery that cholera toxin requires normal host chloride transport proteins to function properly, it was hypothesized that carriers of the mutant f allele benefited from resistance to cholera and other causes of diarrhea. Further studies have not confirmed this hypothesis. • Typhoid: Normal chloride transport proteins are also essential for the entry of Salmonella typhi into cells, suggesting that carriers of mutant chloride transport genes might be resistant to typhoid fever. No in vivo study has yet confirmed this. In both cases, the low level of cystic fibrosis outside of Europe, in places where both cholera and typhoid fever are endemic, is not immediately explicable. • Diarrhea: It has also been hypothesized that the prevalence of cystic fibrosis in Europe might be connected with the development of cattle domestication. In this hypothesis, carriers of a single mutant chloride transport chromosome had some protection from diarrhea caused by lactose intolerance, prior to the appearance of the mutations that caused lactose tolerance. • Tuberculosis: Poolman and Galvani from Yale University have added another possible explanation – that carriers of the f allele have some resistance to TB. My money is on the diarrhea hypothesis, as there is good evidence that the f allele first appeared among Europeans about 52,000 years ago (based on the neutral mutation rate of “silent” base-pairs in the f allele). In the context of this thread, cystic fibrosis is as lethal as a mutation gets, yet its frequency has neither caused humans (including Europeans) to go extinct, nor has it been removed from the collective human genome. How might this eventually occur? The probability of the f allele persisting in the human genome is an equilibrium between the rate of its removal (via both expression among homozygous ff individuals and pure, random accidental disappearance as the result of heterozygotes failing to pass on the allele for reasons unrelated to its phenotypic effect) and the rate of its preservation as the result of the increase fitness of heterozygotes. It is virtually impossible for the f allele to cause humans to go extinct nor for the allele to completely disappear as long as the effective breeding population of humans remains relatively high (this also calculable using standard population genetics, but I won’t go into it here). However, if the effective breeding population declines enough, then inbreeding effects begin to cause the f allele to appear much more often as ff homozygotes. However, this has the effect of removing the f allele from the population, and if the population is small enough, it can completely disappear (this is the so-called “Sewall Wright effect”, which is now usually referred to as “genetic drift”). Ergo, if effective breeding populations fluctuate in size enough that they get so small that deleterious alleles can disappear from them by accident as the result of genetic drift, then the Muller/Kondrashov/Sanford problem of “genetic load” (i.e. the accumulation of deleterious alleles, which appear only in heterozygotes) goes away.Allen_MacNeill_{November 14, 2009
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No reason to get upset. Just asking some questions here. The technical problem is, the domain of a normal distribution ranges from minus infinity to plus infinity, so it cannot have a minimum of 1
No you mis-interpret again. Assuming a minimum of 1 is several standard deviations from the mean which covers 99.9999....% of the cases. You can thus have a minimum of 1 and that would be a minimum within 99.999..% of the cases in a Normal distribution. So the assumption by any standard is reasonable given the premises. I also pointed out, the outlier would be so improbable to be of no consequence.
Next, in the model, how did the mutations affect viability and/or fecundity of the offspring?
I pointed out they were not modeled because they were moot points. If you wish to provide a model that models moot points and numbers that deal with moot points you can provide them and post them here. The animation depicts the simplifying assumption that the removal rate is zero, but a more accurate depiction would have a removal rate between zero and one, and I pointed out a future animation will account for non-zero removal rates. I alluded to the calculation by Nachman. For this animation, the assumption was whatever fecundity or viability will result in zero removal rates. This was a simplifying depiction for the first go around. For future animations, we can have a removal rate between zero and one assuming any conceivable viability and fecundity that can support that number. No value of viability or fecundity will affect the basic point of deterioration if the removal rate of harmfuls on average is less than 1. Fecundity and viability would affect the removal rate number, but by assumption, it cannot be greater than one given the premise put forward. A removal rate greater than one is not possible (given the premises), and a removable rate of 1 is not realistic. Thus removal rates would have to be less than 1. But a removal rate of less than 1 guarnatee deterioration. The way to resolve the question of course is not by theoretical modeling but to track things like the actual increase in single nucleotide polymorphisms. If Sternberg's hypothesis that 90-99% of the genome is functional, then an unabated rise in the number of polymorphisms would imply an unabated rise in the number of harmfuls, which imply the removal rate is closer to zero than to one, which would underscore the claim issues with fecundity and viability are moot points. You are welcome to post what you think the removal rate should be based on any reasonable value of viability or fecundity that you desire, so long as the constraint of 1 new harmful per new born is modeled. With respect to fecundity, Nachman mentioned human females having 40 kids each. I think that is a bit much! The bottom line is based on the premis of 1 new mutation per new born, deterioration will happen. The issues of fecundity and viability will only affect the speed and severity. I leave the question of speed and severity for others to investigate.scordova_{November 14, 2009
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Salvador,
Apparently you missed that I said 1 was minimum and was presumed several standard deviation from the mean of 100. Invoking the phrase “standard deviation” conventially means a NORMAL distribution.
No reason to get upset. Just asking some questions here. The technical problem is, the domain of a normal distribution ranges from minus infinity to plus infinity, so it cannot have a minimum of 1. Moreover, number of mutations is a discrete variable, while a normal distribution applies to continuous variables. Maybe that's nit picking, but if I wanted to reconstruct your model, those details matter.
Ok jistak, let me spoon feed you. If the distribution is normal and the mean is 100 and standard deviation is 5, 1 would be several standard deviations from the mean in a normal distribution. Comprende?
Yo comprendo muy bien amigo, gracias. OK, so the mean number of mutations per offspring was 100 from a (truncated) normal distribution with SD=5. Thanks, that answers one of my questions. Next, in the model, how did the mutations affect viability and/or fecundity of the offspring?jitsak_{November 14, 2009
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1 is an assumed minimum. If the average number of new harmfuls per human is 100, several standard deviations from the mean would easily be a minimum of 1 per human if the standard deviation is say 5, and even if one were lucky enough to avoid getting a novel harmful mutation, on balance I think it would be of too little help.
Ok jistak, let me spoon feed you. If the distribution is normal and the mean is 100 and standard deviation is 5, 1 would be several standard deviations from the mean in a normal distribution. Comprende?scordova_{November 14, 2009
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In the model, what is the distribution of harmful mutations among the offspring?
Apparently you missed that I said 1 was minimum and was presumed several standard deviation from the mean of 100. Invoking the phrase "standard deviation" conventially means a NORMAL distribution. Before accusing me of not answering the question, perhaps you should show a little more astuteness. I don't take kindly to such flimsy nit picking. It is you who didn't read and comprehend that I answered your question.
Please answer those questions. After all, you make some strong claims in the OP, so it seems only fair that you explain exactly how you arrived at those conclusions.
Please be more astute in recognizing that your question was answered. I have little patience for trolling.scordova_{November 14, 2009
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Salvador, you haven't answered my questions, which were very specific. Let me rephrase them, in case I was unclear. I am talking about the specifics of the model on which your animation is based. In the model, what is the distribution of harmful mutations among the offspring? In the model, exactly how harmful are individual mutations? Please answer those questions. After all, you make some strong claims in the OP, so it seems only fair that you explain exactly how you arrived at those conclusions.jitsak_{November 14, 2009
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I hinted about a future modification to the animation. It is possible for Dad to have a bad mutation and Mom to have a bad mutation and because of basic laws of inheritance, some of the kids may not have that mutation. Nachman discusses this issue in his paper if Mom and Dad have 3 mutations: Estimate of Mutation rate per nucleotide
For U = 3, the average fitness is reduced to 0.05, or put differently, each female would need to produce 40 offspring for 2 to survive and maintain the population at constant size. This assumes that all mortality is due to selection and so the actual number of offspring required to maintain a constant population size is probably higher.
So there is a removal rate on the generous assumption of truncation selection and every human females giving birth to 40 kids (OUCH!). The removal rate of harmfuls cannot be greater than 1 per human on average (recall the assumption 1 always being added), so any inefficiency (due to less than perfect truncation and/or less than need number of offspring) will result in net increase of harmfuls. I should mention, I suggested a mutation rate of 1 novel mutation per new born will lead to deterioration. Muller estimates even 0.1 would be intolerable. I don't think I'm stating anything that should be controversial.scordova_{November 14, 2009
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Incidentally, contingent S values are esentially the behavior of synergistic epistasis. That is, mutation A in and of itself has zero effect on reproductive fitness, mutation B in and of itself has zero effect on reproductive fitness, but the presence both simultaneously results in death. I tried to depict what would happen even if that were true with the last slide and selection based on synergistic epistasis. The issue is not one of seleciton coefficients, but rather the cost of purification. Walter has put forward the cost model of selection with a paper funded by the Discovery institute. I think the cost model would be very good for topics like purifying selection as it can be easily visualized (as evidenced by the animation).scordova_{November 14, 2009
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It’s great to see some modeling being done here, and congrats with the nice animation. However, it would be nice to have some more details, so us readers can check your results. Therefore I have a couple of questions: (1) You say there is one harmful mutation per offspring. Is that one on average from a poisson distribution, or do you give every single offspring exactly one harmful mutation?
1 is an assumed minimum. If the average number of new harmfuls per human is 100, several standard deviations from the mean would easily be a minimum of 1 per human if the standard deviation is say 5, and even if one were lucky enough to avoid getting a novel harmful mutation, on balance I think it would be of too little help. I do not know off hand what the standard deviation is or whether anyone on the planet has a figure. I presume the figures from the Y-chromosme study would result in a 2-sigma mutation rate of at least 100 per individual, at least that is how I read their paper. Anyone with a better guess or a correction to that figure is more than welcome to post their estimate here are UD.
(2) What is the viability of mutant offspring? (s=0.99, s=0.9, what?)
The viability is not specified (not to mention even in field practice would be almost impossible to directly determine short of a high death rate) and the animation attempts to show that the viability is a moot point! If the viability is 1.00 (meaning the mutation is harmful but does not reduce immediate reproductive fitness), then that's bad, the mutation persists. If the viability is 0, well the individual dies. But the last image of the animation shows, that with the presumption of 1 new harmful per new born, it doesn't matter who is killed off. A note about viability being 1.0 and the mutation being harmful. I have taken issue with characterizing something as "fit" based on reproductive benefit. See: Survival of the sickest, why we need disease. Also, it is a bit suspect to characterize S values that are contingent. You can see the problem in characterizing S based on immediate fitness. See the quotation of Lawrence Hurst here: Airplane Magnetos, Contingency Designs, and Reasons ID will Prevail. If the S-value is contingent on other mutations, this makes traditional analysis difficult if not impossible. We can sometimes put some sort of estimate if we have recessives and a degree of inbreeding, but for other contingent situations, it is hard. However from an analytical standpoint, if we are not tracking the behavior of specific mutations but rather the net increase in harmfuls, one sees that it doesn't matter if S=1.00 or S=0. If S=1.00 for all every bad mutation, then the bad persists (a comparable example would be blind cave fish that have functionally bad mutation, but reproductively fit mutation that caused blindness). If all S values were zero, there is extinction. Thus, this shows there does not exist any conceivable value of viability that can arrest deterioration. Importantly, the general hypothesis or related hypotheses can be tested empirically with the advent of Solexa and Illumina technology and large bio-informatic systems. That is if we're willing to shell out the money and resources for such an enterprise.scordova_{November 14, 2009
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Thanks, born. I read the recent Current Biology paper about the mutation rate at a stretch of the human Y chromosome. But what I am interested in here are the details of Salvador's model.jitsak_{November 14, 2009
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It is overwhelming likely that most mutations on earth that have occurred have been reproductively neutral. For instance, humans average about 130 new mutations per sexual generation. And I'm doing fine.Mack_{November 14, 2009
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jistak, This following study confirmed the "detrimental" mutation rate for humans, of 100 to 300, estimated by John Sanford in his book "Genetic Entropy" in 2005: Human mutation rate revealed: August 2009 Every time human DNA is passed from one generation to the next it accumulates 100–200 new mutations, according to a DNA-sequencing analysis of the Y chromosome. (Of note: this number is derived after "compensatory mutations") http://www.nature.com/news/2009/090827/full/news.2009.864.html Professional evolutionary biologists are hard-pressed to cite even one clear-cut example of evolution through a beneficial mutation to the DNA of humans which would violate the principle of genetic entropy. Although a materialist may try to claim the lactase persistence mutation as a lonely example of a "truly" beneficial mutation in humans, lactase persistence is actually a loss of a instruction in the genome to turn the lactase enzyme off, so the mutation clearly does not violate Genetic Entropy. Yet at the same time, the evidence for the detrimental nature of mutations in humans is overwhelming for doctors have already cited over 3500 mutational disorders (Dr. Gary Parker). "Mutations" by Dr. Gary Parker Excerpt: human beings are now subject to over 3500 mutational disorders. http://www.answersingenesis.org/home/area/cfol/ch2-mutations.asp As well the slow accumulation of "slightly detrimental mutations" in humans, which are far below the power of natural selection to remove from our genomes, is revealed by this following fact: “When first cousins marry, their children have a reduction of life expectancy of nearly 10 years. Why is this? It is because inbreeding exposes the genetic mistakes within the genome (slightly detrimental recessive mutations) that have not yet had time to “come to the surface”. Inbreeding is like a sneak preview, or foreshadowing, of where we are going to be genetically as a whole as a species in the future. The reduced life expectancy of inbred children reflects the overall aging of the genome that has accumulated thus far, and reveals the hidden reservoir of genetic damage that have been accumulating in our genomes." - Sanford; Genetic Entropy; page 147bornagain77_{November 14, 2009
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It's great to see some modeling being done here, and congrats with the nice animation. However, it would be nice to have some more details, so us readers can check your results. Therefore I have a couple of questions: (1) You say there is one harmful mutation per offspring. Is that one on average from a poisson distribution, or do you give every single offspring exactly one harmful mutation? (2) What is the viability of mutant offspring? (s=0.99, s=0.9, what?) I have many more questions, but those will do for the moment.jitsak_{November 14, 2009
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Well I'm waiting to hear from the geneticists whether my heart defect (ARVC+CHF) is genetic i.e. caused by a mutant gene, either passed to me or a new one of my own as it were. So could I be one of the proof's that could overturn darwin? If so then praise the lord & pass the ammunition!My-opathy_{November 14, 2009
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Hi Scordova interesting topic, I have a bit of a off topic question though, Have you heard any word on the progress of Dr. Sanford's work down in the "salt mines"?bornagain77_{November 14, 2009
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I speculate there will be keen interest in this topic not becaue of the creation/evolution debate but because genetic deterioration has significance to medical understanding. The medical community is ramping up its ability to track sincle nucleotide polymorphisms. I mentioned at UD in 2006: Solexa: a development which may lead to measuring claims of ID
Some of the claims by ID proponents have not been adequately explored because of the cost issues involved in doing large-scale whole-genome sequencing of numerous individuals. Not even Warren Buffet has the trillions of dollars needed to accomplish such a massive amount of gene sequencing. At least not today, but maybe in the future! The human genome project took 3 billion dollars and 13 years to complete. By comparison, Solexa might be able to do a comparable job for a few thousand dollars per person (ideally even less) and in a much shorter time frame. (See the UD sidebar on Solexa Genomics.) Solexa might be viewed as an unwitting research partner of the ID movement. The fine work of two important ID proponents, Cornell geneticist John Sanford and independent researcher Walter ReMine, might finally get slam dunk empirical confirmation if Solexa succeeds in its grand quest. For example, a fundamental consequence of Sanford’s Genetic Entropy thesis is that there will be an unabated rise in Single Nucleotide Polymorphisms (SNPs) per generation per individual. If confirmed, this data will be more nails in Darwin’s coffin, and then Darwin Day might have to be renamed Darwin Bashing Day (or something else, how about Abe Lincoln Day?). Solexa, Inc. is developing and commercializing the Solexa Genome Analysis System, which is being used to perform a range of analyses including whole genome resequencing, gene expression analysis and small RNA analysis. Solexa expects its first-generation instrument, the 1G Genome Analyzer, to generate over a billion bases of DNA sequence per run and to enable human genome resequencing below $100,000 per sample, making it the first platform to reach this important milestone. Solexa’s longer-term goal is to reduce the cost of human re-sequencing to a few thousand dollars for use in a wide range of applications from basic research through clinical diagnostics. For further information, please visit www.solexa.com. Update: I should add, Solexa’s technology is poised to provide data which will overturn the prevailing ideas about molecular clocks (See: Molecular Clocks: Michael Denton continues to be vindicated). I will elaborate in the comment section if anyone is interested. In brief, we do not have accurate measurements of molecular evolution to the degree needed to overturn certain hypotheses. The increased accuracy provided by Solexa technology could permanently shatter the prevailing molecular clock hypothesis and vindicate various claims of ID proponents. Update: Solexa’s technology will also aid in the ID quest of steganography in biology. If the key to rapidly understanding the steganography in junkDNA is through comparative sequencing of various creatures, Solexa’s technology is a welcome friend. I would like to also acknowledge again the fine work of Dr. Pellionisz on JunkDNA. I expect he will be delighted by the work of Solexa. Here is the latest from Dr. Pellionisz comment 87430
Solexa and Illumina were used in a recent relevatn article on human mutation: Human Y Chromosome Base-Substitution Mutation Rate Measured by Direct Sequencing in a Deep-Rooting Pedigree. If Rick Sternberg's thesis is correct that 90-100% of the human genome is functional, then we have to wonder what this mutation rate (as determined through solexa technology) means for genetic deterioration. It would (by my calculation) mean that we could be experiencing 100 harmful mutations per new born. That would be difficult to estimate because what constitutes harmful. I would suggest however, with respect to the question of design, we could compare the progress of Single Nucleotide Polymorphisms in comparing deeply "conserved" sequences. I postulate the results will eradicate any presumption that the "conservation" is due to selection whatsover. There will simply not be enough population resources to sustain the needed purification (as suggested by the animation). The benefit of this is that we bypass any need to define "fitness" or functionality. We can measure purifying selection (or lack thereof) without needing to identify these other issues. Furthermore, we can extend this line of inquiry to the architectural designs uncovered by the ENCODE project, but I save that discussion for later.scordova_{November 14, 2009
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Notes: 1. To be fair, I believe Nachman is a convinced evoulutionist and in way do I mean to suggest he is a creationist or ID proponent. But the paradox he put forward could (unwittingly) defeat the Darwinian evolution (often symbolized by Dawkins WEASEL). 2. There are other schools of evolutionary thought that are non-Darwinian such as the mutationists and the neturalists. ID proponents and creationists like Walter ReMine and John Sanford have relied heavily on the work of the neturalists (most notably Kimura). They also drew on the works of Kondrashov, Nachman, and Crowell. The animation was named after Nachman who was the co-author of the paper that inspired this animation. I wrote about Nachman and Crowell's work in Nachman's U-Paradox. Any of the following 3 areas of investigation could separately overturn the Dawkinsian view that life was created by a Blindwatchmaker:
1. Origin of Life (see the works of Thaxton, Bradely, Olsen, Kenyon, S. Meyer, Yockey, Voie, Trevors, Abel, Don Johnson many others) 2. Population Biology ( Walter ReMine, John Sanford) 3. Irreducible, Specified, Integrated, Functional Complexity, No Free Lunch (Shutzenberger, Eden, Behe, Dembski, Marks, Denton, others)
I bolded the Population Biology because to date it is an underempahsized and misunderstood field, partly owning to difficult technical issues. This animation was intended to help make clear the essential issues of population biology and how it may challenge the hypothesis of Darwinian evolution. A little known area of population biology research funded by the Discovery Institute was pursued by Walter ReMine. ReMine's work was inspirational to a later book by John Sanford, Genetic Entropy. I speculate that problems for Darwinism in population has only begun to be explored. It has sympathizers even from secular quarters (the neturalist and mutationist schools of evolution). See: Part of the Discovery Institute’s secret research program uncovered 4. I wish to thank Allen MacNeill of Cornell and Joe Felsenstein of WSU for their comments on my writings the last two years. They helped correct and improve my understanding immensely, and though they are on the opposing side of the debate, they have helped increase my appreciation for the hard work and research being done in the field. Thanks also to Dave Wisker for alerting me to Lynch and Estes papers and "Zachriel" of telic thoughts. Special thanks to Walter ReMine and John Sanford. My hope is Walter's contributions to the field of population biology will finally be recognized and appreciated by the rest of the world. He's paid the price for challenging the mainstream.scordova_{November 14, 2009
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