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Nobel Prize winner HJ Muller, unwitting pioneer of genetic entropy theories

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hj muller

Muller received the Nobel Prize for “for the discovery that mutations can be induced by x-rays”. He studied the effects of mutation on populations, and indirectly spawned ideas which were elaborated in the book Genetic Entropy by Cornell geneticist John Sanford.

The theory of genetic entropy has the potential to overturn Darwinism on empirical grounds alone. Darwinism argues for inevitable progress, genetic entropy argues the opposite.

The thesis of genetic entropy can be explored by considering the amount of mutation in the human genome at present. Muller offers his thoughts:

it would in the end be far easier and more sensible to manufacture a complete man de novo, out of appropriately chosen raw materials, than to try to fashion into human form those pitiful relics which remained…

it is evident that the natural rate of mutation of man is so high, and his natural rate of reproduction so low, that not a great deal of margin is left for selection…

it becomes perfectly evident that the present number of children per couple cannot be great enough to allow selection to keep pace with a mutation rate of 0.1..if, to make matters worse, u should be anything like as high as 0.5…, our present reproductive practices would be utterly out of line with human requirements.

Hermann Muller quoted by John Sanford
Appendix 1, Genetic Entropy

“u” is the mutation rate. As John Sanford observes, Darwinian selection cannot keep pace with reality. Deterioration of the genome seems to be in evidence, and the efficacy of Darwinian mechanisms has been essentially falsified with respect to the human genome. Here is an excerpt of Sanford commenting on Muller’s work:

Muller calculated that the human fertility rate of that time (1950) could not deal with a mutation rate of 0.1. Since that time, we have learned that the mutation rate is a least 1,000-fold higher than he thought. Furthermore, fertility rates have declined sharply since then.

John Sanford

Walter ReMine was kind enough to point me to a more modern day version of Muller’s concerns: Why have we not died 100 times over? by Kondrashov (also from Cornell).

It is well known that when s, the selection coefficient against a deleterious mutation, is below 1/4 ~ Ne , where Ne is the effective population size, the expected frequency of this mutation is ~ 0.5, if forward and backward mutation rates are similar. Thus, if the genome size, G, in nucleotides substantially exceeds the Ne of the whole species, there is a dangerous range of selection coefficients, 1/ G less than s less than 1/4 N e . Mutations with s within this range are neutral enough to accumulate almost freely, but are still deleterious enough to make an impact at the level of the whole genome. In many vertebrates Ne ~ 10 , while G ~ 10 , so that the dangerous range includes more than four orders of magnitude. If substitutions at 10% of all nucleotide sites have selection coefficients within this range with the mean 10 , an average individual carries ~ 100 lethal equivalents. Some data suggest that a substantial fraction of nucleotides typical to a species may, indeed, be suboptimal.

Darwinian evolution doesn’t clean out all the bad in a population. Kondrashov’s observations discredit Darwin’s implicit claim of inevitable progess and the supposed survival of the fittest. The problem is that if genetic entropy is true, the ancestors are the fittest not the decendants. In that sense, the fittest don’t survive. To use Muller’s words, what remains in the end are not the fittest, but “pitiful relics”.

Kondrashov offers a supposed “fix” to the paradoxes so as to bolster Darwin’s failing theory. His fix is an appeal to “synergistic epsitasis”, but Sanford responds to this supposed “fix”:

one will encounter the term “synergistic epistasis”. When I first encountered this phrase I was very impressed. In fact, I was intimidated. It seemed to speak of a very deep understanding, a deep knowledge, which I did not possess. As I have seen it used more, and have understood these issues better, I believe I understand the term better. It is a sophisticated-sounding expression, signifying nothing. It has all the appearance of deliberate obfuscation. Literally translated, synergistic epistasis means “interactive interaction.”

Genetic Entropy by John C. Sanford is available at Amazon. I wrote a little bit about Sanford 2 years ago here: Respected Cornell geneticist rejects Darwinism.

Comments
jerry The estimated average tenure of vertebrates in the fossil record is about 10 million years. There are about 50,000 different ones alive today. If you bother to do the math it means we should expect to see one vertebrate species go extinct every 200 years. We're seeing far more than that in recent history not all of which can be attributed to catastrophic environmental stress (man-made or otherwise). Individual vertebrates, if they don't get killed by an accident, eventually die of old age. Vertebrate species are no different - if not an accident they just get old and die too.DaveScot
June 16, 2008
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Dave, "Millions and millions of extinctions in the fossil record and hundreds in recorded history are evidence of genetic entropy." I don't think your conclusion follows. Micro evolution could lead to the same phenomena of extinctions. Each sub population is more limited and so is the overall population if the environment changes dramatically. Each culls the gene pool so when a new environmental change happens the species is even more subject to extinction. I would have no problem with genetic entropy if it could be showed it is actually happening. This is not some thing in the deep past but hypothesized to fill all life currently on the planet. We are within a few years of developing the data bases to investigate genetic entropy. We are also within a few years of investigating the structure of all the species around and verifying or falsifying that nearly all appeared by micro evolutionary processes. One thing that could frustrate Sanford's hypothesis is that most of the genome is useful and not subject to too much mutation and thus preserved. So the nearly neutral mutations are not that neutral at all but in reality harmful. Also if genetic entropy was the cause of all the past extinctions then why did it stop. There is no evidence that any or many of the recent extinctions has to do with genetic deterioration, Thus, as macro evolution has seemed to disappear from the planet so has these mass extinction events. This is not a finding that is consistent with the continual battering of the genome hypothesized by Sanford. We should see a constant parade of extinctions and also some very sick current genomes ready to go belly up.jerry
June 16, 2008
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jerry Millions and millions of extinctions in the fossil record and hundreds in recorded history are evidence of genetic entropy. The real question is why do an exceedingly small percentage of germ lines in higher plants and animals avoid extinction for hundreds of millions of years when almost all their peers go belly up in a comparatively short amount of time? My money says that we'll eventually discover that the answer is anticipated in intelligent designs created by human agency - some form of highly protected core code. The beetle example is poorly thought out. The smaller the genome the less susceptable it is to genetic entropy and/or the larger the number of progeny the less susceptable it is to genetic entropy. This is because the number of individuals whose genome is a flawless copy of its parents' genome rises in proportion with both those factors. Nearly neutral mutations don't accumulate as quickly, if at all, in that case. This explains why P.falciparum is still here and unchanged even after undergoing more replications every year for the last 50 years than all the mammals that ever lived. I calculated that 95% of them are flawless copies of their parents. But they're such prodigious replicators that the other 5% allows them to quickly adapt if needed (within The Edge of Evolution, of course) to a wide range of environmental insults. It also explains the recent finding of why 250mya bacteria are virtually identical at the genetic level to modern descendents (BA77 has been pointing this out repeatedly recently). Beetles, on average, have much smaller genomes than mammals and reproduce in much larger numbers. DaveScot
June 16, 2008
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Off topic: In mulling over the law of "Conservation of Information" I believe the final "Conservation of Information" law may look something like this, All information that can exist does exist completely separate of the physical realm in the transcendent realm and cannot be created or destroyed in the physical realm, but can only be "borrowed" and/or imprinted from the transcendent realm. --- The key for me in this deduction, to the law, is "transcendent information's domin^ation of energy" (telling energy what to be/do) in Zeilinger's teleportation experiments. Since the first law states energy can be neither created nor destroyed, anything having dominion over energy must, of necessity, possess even greater qualities than energy. Therefore information, in the least, cannot be created or destroyed either. This inference to the "Conservation of Information" warrants even further reference to the "Mind of God" when the foundation of the created universe, we are living in, is shown not to be a "dead" chaotic foundation of "chance", but is shown, and now known, to be a exceedingly stable transcendent foundation that exhibits intent, purpose and foresight. Thus since we can deduce intent, purpose and foresight in the foundation of the universe, This means the transcendent information is "alive". --- Now it is fair to say this: Since transcendent information can not be created nor destroyed, and since "information" exhibits dominion and purposeful control of the "material realm", then we may now say that all "information" that can possibly be "known" is already "known" by the "infinite mind of God".bornagain77
June 16, 2008
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scordova: I may have misunderstood, I don't know. I believe the ratio of male to female births is 1.06 to 1. Apparently there's been a drop in that the last few decades, but I don't suspect that's "genetic entropy" kicking into high gear. This y chromosome problem will be manifest once we start seeing like 45% males to 55 females in the general population with that ratio continually decreasing, I guess. I'll just lurk for a while.JunkyardTornado
June 16, 2008
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There are some DNA repair mechanism on the human Y-chromosome. Nevertheless: Oxford geneticist Bryan Sykes in the UK Gaurdian: Do we need men
Of all our chromosomes, it is the only one that is permanently locked into the germ cells of men, where the frenzy of cell division and error-prone DNA copying required to keep up the daily output of 150m sperm creates the ideal conditions for mutation. And it shows. Seven per cent of men are infertile or sub-fertile and in roughly a quarter of cases the problem is traceable to new Y-chromosome mutations, not present in their fathers, which disable one or other of the few remaining genes. This is an astonishigly high figure, and there is no reason to think things will improve in the future - quite the reverse in fact. One by one, Y-chromosomes will disappear, eliminated by the relentless onslaught of irreparable mutation, until only one is left. When that chromosome finally succumbs, men will become extinct. But when? I estimate that, at the current rate, male fertility caused by Y-chromosome decay will decline to 1% of its present level within 5,000 generations - roughly 125,000 years. Not exactly the day after tomorrow - but equally, not an unimaginably long time ahead. Unless something changes in the way we breed, women will vanish too and Homo sapiens will disappear in the next 1-200,000 years. But is extinction inevitable? Plenty of species a lot older than our own are still going, so how is it that they are not vulnerable to extinction by the same process of Y-chromosome decay? They will all eventually face the same challenge and I suspect that many species have already gone under for this very reason. Some, however, have found a way round their death sentence. One strategy is to recruit genes on other chromosomes to take over the job of male development. It is a race against time. Can a species get all the genes it needs off the Y-chromosome, or recreate them elsewhere, before the chromosome finally vanishes? Always the last gene to go will be SRY, the male master switch itself. We know it is capable of smuggling itself onto another chromosome - the evidence lies in the rare cases of males who have no Y-chromosome. Lots of species may have tried variations on this theme to avoid extinction, but it seemed that none succeeded until, in 1995, researchers found a mammal that had managed to escape this fate. When they looked at the chromosomes of a small burrowing rodent called the mole vole, Ellobius lutescens, which lives in the foothills of the Caucasus mountains, they discovered that the male voles didn't have a Y-chromosome. Neither, it transpired, did they have a master SRY gene either. This inconspicuous little rodent has managed to activate a gene relay one or two stages down the line from SRY. And only just in time. The mole vole Y-chromosome has now completely disappeared. The vole is now safe from Y-chromosome-driven extinction, the only mammal species known to have succeeded in getting itself out of danger.
Regarding the Y-chromosome in other species. Also Decoding offers view of humans and hairier cousins
The 16 X-related genes are present in only single copies. Page and his colleagues thought the chimpanzee genome might show how they were protected. To their surprise, they report in Nature, the protection was not there. The chimp Y chromosome has lost the use of five of its 16 X-related genes. The genes are there, but have been inactivated by mutation. David Page
and Rodent Y chromosome TSPY gene is functional in rat and non-functional in mouse
Recombination is believed to prevent genetic deterioration in sexual populations because it allows conservation of functional genotypes by removing deleterious mutations. Moreover, evidence that non-recombining segments of a genome deteriorate is provided by genetic experiments in Drosophila and yeast. Y chromosomes generally do not recombine along most of their length, and thus Y chromosome genes, despite having been selectively maintained for their function, could be lost from the genome. Here we present definitive evidence that functional Y genes can be lost from the mammalian genome.
scordova
June 16, 2008
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ba77: "As well it should be noted that the ancient lineages of cichlids upon closer examination had something like 7 different types of photoreceptor cells while all younger species had lost the use of some, Thus the younger lineages of cichlids are severely constrained in their ability to radiate while the most ancient line retains its ability." The only way genetic entropy would be demonstrated is if the ancient lines were losing abilities as well. scordova (#108): So in the past 150 years the world population has been increasing geometrically, while the fertility rate has been decreasing 0.1% every twenty years. If a male's Y chromosone is defective, it takes whatever genes he has out of the gene pool. But it opens a niche for someone else, with no necessary loss in population at all. Don't know how the 100,000 years figure was derived, but it seems a decrease in fertility could only have an adverse affect indirectly, by increasing the homogeniety of the gene pool (extremely gradually), thus making it susceptible to a catastrophic event. (Or is that what you were saying). It seems ultimately you could have a world of disease-free identical clones.JunkyardTornado
June 16, 2008
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I gave this earlier of a present day example of the Genetic entropy mo^del being obeyed. African cichlid fish: a model system in adaptive radiation research of special note: Interestingly, ecological opportunity (the availability of an unoccupied adaptive zone), though explaining rates of diversification in radiating lineages, is alone not sufficient to predict whether a radiation occurs. The available data suggest that the propensity to undergo adaptive radiation in lakes evolved sequentially along one branch in the phylogenetic tree of African cichlids, but is completely absent in other lineages. Instead of attributing the propensity for intralacustrine speciation to morphological or behavioural innovations, it is tempting to speculate that the propensity is explained by genomic properties that reflect a history of repeated episodes of lacustrine radiation: the propensity to radiate was significantly higher in lineages whose precursors emerged from more ancient adaptive radiations than in other lineages. As well it should be noted that the ancient lineages of cichlids upon closer examination had something like 7 different types of photoreceptor cells while all younger species had lost the use of some, Thus the younger lineages of cichlids are severely constrained in their ability to radiate while the most ancient line retains its ability. This fits perfectly with the previously stated model in post 104, I point out that it shows both loss of genetic diversity as well as a tangible, undeniable loss of morphological variability that does not have to be deduced such as human skin color does..bornagain77
June 16, 2008
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"A reasonable question is why are we still alive in light of these considerations?" A reasonable answer is that there is something wrong with the theory. We are looking at man in a lot of our examples but the 300,000 beetle species seem to be doing fine except where man encroaches. What species are deteriorating out of existence due to genetic problems? What are examples or counter examples? So far all I have seen are Sanford's arguments.jerry
June 16, 2008
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Oxford Geneticist Bryan Sykes
Male infertility is on the increase. Under the microscope a high proportion of human sperm from what we would consider a normal human male are already visibly deformed. Sperm counts are falling dramatically though there are other contributory causes as well as Y-chromosome decay. The Y-chromosome has been decaying for a very long time and will continue to do so; and we have to expect a progressive decline in male fertility as these injuries accumulate. One by one Y-chromosomes will disappear and eventually only one remains. when that chromosome finally succumbs, men will become extinct. page 293 Adam's Curse
'But when?' I hear you ask. Before I answer that question -- before I even attempt an estimate -- I must urge you not to confuse what I see as the inevitability of the process with my confidence producing an accurate figure. So here goes. For the purpose of this estimate, I am going to assume that nothing else come into it other than the rate at which we already know Y-chromosomes are deaying at the present time. Let us begin with the figure of 7 per cent for the proportion of infertile men, and take it that 1 per cent of all men are infertile because of a Y-chromosome muation. These mutations must have occurred in the fathers of these men, since by definition their fathers were not infertile. So these mutations are the last straw as far as that particular Y-chromosome is concerned. It cannot be saved except by artificial means. Lots of other, less serious, mutations that decrease, but do not eliminate, male fertility will also have occurred in all men. In wartime, casualty lists always include more wounded than dead, and genes under attack from mutation are no different. For the sake of simplicity, I will also take 1 per cent as the rate at which wounding Y-chromosome mutations occur in male germline cells. When passed on to their sons, these mutations make them not clinically infertile but less fertile than their father. Taking these figures, and in the absence of any other influence, the fertility of the whole population will decline by 0.1 per cent (1 percent of 10 per cent) in each generation owing to Y-chromosome decay alone. What effect does that progressive delcine have in the futhere? I won't bore you with the formula, but have a look at the graph in figure 6. Adam's Curse
The graph in figure 6 is a simple exponential decay.
On this estimate, the fertility caused by Y-chromosome decay drops to 1 per cent of its present level within 5,000 gemerations.
Hence extinction happens in 100,000 years. The uncomfortable conclusion of genetic entropy is not a happy one if ture. But what are the facts independent of our biases? It appears Muller's ratchet applies to the Y-chromosome. A reasonable question is why are we still alive in light of these considerations?scordova
June 16, 2008
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Dave, My question had nothing to do with Sanford or his ideas. I was just interested in what recombination does and how it works and how it might affect a gamete. After reading Sanford and watching the dialogue here, I am not too big a fan of genetic entropy. That could change if someone presented evidence of the deterioration that Sanford predicts. This should come in the near future as Salvador and Bob say, the mapping of genomes gets cheaper and faster.jerry
June 16, 2008
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jerry asked: "It would seem a random recombination has a potential for causing havoc in the zygote." bob answers: "Random recombination causing havoc may not be too big a problem, as long as the havoc is caused early enough, so that the embryo dies very early on in development." The question and answer are irrelevant to Sanford's genetic entropy hypothesis. Don't confuse people. Sanford's "genetic entropy" is the accumulation of nearly neutral mutations which are by definition individually invisible to natural selection. As these accumulate the reproductive population becomes weaker and weaker until something happens (a new predator, climate change, etcetera) that the weakened species can no longer survive and booya -they become quickly extinct, disappearing from the fossil record in an eyeblink of geologic time.DaveScot
June 16, 2008
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I forgot the last part of Genetic Entropy, d. eventual extinction of all species of the kind from "genetic meltdown".bornagain77
June 16, 2008
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Well scordova, again the way I am using Genetic Entropy is consistent with Theism in that a. Special creation of a optimal genome for a undetermined parent species (Kind) (This satisfies Conservation of Information requirement) b. A fairly rapid unfolding of "front-loaded" diversity and variability that would stay within the overriding principle of Genetic Entropy by decreasing "meaningful" genetic diversity (information) of parent species genome. i.e. (any decrease from a less than optimal genome, from any method, is still within the overriding principle of Genetic Entropy) c. a long slow decline in within species, and within kind, variability and diversity. (This also stays within the overriding principle of Genetic Entropy, but the main mechanism for this is the actual decay of the genome from deterioration of its integrity. So do our mo^dels mesh now scordova?bornagain77
June 16, 2008
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scordova, as far as the divergence of races in humans we have fairly good overall evidence that this is the result of Genetic Entropy (culling of preexisting information) and not the result of information being added.
I'm reluctant at this time to presume genetic entropy is the cause of all evolutionary events. Personally, and this is a speculation, the correct model of evolution, imho: 1. Special Creation 2. Front Loaded Events 3. Genetic Entropy For example, creationists think that Dogs, Foxes, Jackals, Wolves, etc. descended from a common ancestor. Are these varieties the result of genetic entropy or front loading. I'd argue they are the result of front loading. Genetic entropy is not the appropriate model for how these varieties came about. That's my opinion at this time, I could of course be wrong. I just don't see that the emergence of Dogs, Foxes, Wolves, and Jackals is the result of a disasterous set of genomic mistakes.... What will be important is whether the genomes suggest punctuated explosion of alleles which was not repeated ever since. This would confirm front-loading of alleles.... The more general Front-Loaded evolution which some subscribe to (like Mike Gene, DaveScot, possibly Mike Behe...) involves the front loading of major body plans or big divisions of biology. My focus is on a more recent front loaded event of alleles, not majro body plans.... I would be interested in how we can test the hypothesis of allele front loadiing followed by genetic entropy after the alleles de-repressed (to use John Davison's terminology) into the populations...I think the Y-chromosomal data in humans and comparable studies in animals will accord with allele front-loading followed by gradual increase in genetic entropy.scordova
June 16, 2008
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scordova, as far as the divergence of races in humans we have fairly good overall evidence that this is the result of Genetic Entropy (culling of preexisting information) and not the result of information being added. see subtractive color mixing http://en.wikipedia.org/wiki/Subtractive_color as well as what can tentatively be called the loss of "front loaded" genetic diversity. Tishkoff; Andrew Clark, Penn State; Kenneth Kidd, Yale University; Giovanni Destro-Bisol, University “La Sapienza,” Rome, and Himla Soodyall and Trefor Jenkins, WITS University, South Africa, looked at three locations on DNA samples from 13 to 18 populations in Africa and 30 to 45 populations in the remainder of the world. “We found an enormous amount of diversity within and between the African populations, and we found much less diversity in non-African populations,” Tishkoff told attendees today (Jan. 22) at the annual meeting of the American Association for the Advancement of Science in Anaheim. “Only a small subset of the diversity in Africa is found in Europe and the Middle East, and an even narrower set is found in American Indians.”bornagain77
June 16, 2008
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With respect to recombination in animals, there are at least two ways to look at geneome evolution: 1. A front-loaded "explosion of diversity" followed by a stable period where few new alleles are introduced into the populations 2. a constant steady stream of new alleles into the population..... The creationist front-loaded hypotheses are represented by Spetner's NREH, or Ashcraft's homologous recombination. Aschraft supposes a spurt of homologous recombination. See: Evolution God's Greatest Creation. I'm not saying anyone is right, merely pointing out we might be able to falsify certain ideas with more sequences and data mining. The data appear to support a front-loaded "explosion of diversity" followed by a stable period. It would be a good area of investigation if the genomic data actually falsify a gradualist introduction of new alleles, versus a more punctuated evolution. Punctuated evolution would favor front loading.scordova
June 16, 2008
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Dave - nearly neutral mutations would not "cause havoc". Causing havoc is what jerry was asking about, and that's what I was responding to. BA77 - for a start the Muller's ratchet argument doesn't work with recombining DNA, and secondly the recent evolution of sex theory suggests a difference. And if you want empirical evidence, compare the deterioration of the y-chromosome with the autosomes. jerry - No need to apologise, you're asking decent questions! You're exactly right (even down to the "things could go horribly wrong. A deletion or insertion of a single base would usually nicely destroy the function of the gene). Sal -
Is this evidence of the persistence of linkage blocks in Y-chromosomes?
Yes. The lack of any evidence for recombination.Bob O'H
June 16, 2008
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With respect to my ideas about front-loading, I believe that a large number of critical mutations in the human lineage were non-random and happened in a punctuated sort of way over a few generations, and then stablized. I believe variety of various racial and other features arrived suddenly, after which there was relative stability and lack of major innovation thereafter. Front-loading (in the creationist sense, not in the more general sense like Mike Gene and others) for humans happened over limited time spans. That is my speculation, and I could of course be very wrong...I have been wrong in the past. That said, let us suppose we have persistence of linkage blocks after the front loaded event. That would make the detectability of things like the Cohen Haplotype feasible. But I should point out, a front loading over a short period of time would create a hierarchical structure in patriarchal lines. One patriarchal hierarchy that could be confirmed by studying Y-chromosomal linkage blocks and haplotypes would be the one outlined in The Table of Nations. We know that the top part of the hierarchy is today beyond dispute. We call the top part "Y-chromosomal Adam". Creationists believe "Y-chromosomal Adam" to be Noah. But let us suppose how the hierarchy plus limited front loading might by confirmed. "Y-Chromosomal Adam" should have 3 major lineages. Each of those 3 lineages has its own hierarchical charactersitcs, and those can be confirmed.... We will see. In the mean time, I would like to hear data about the persistence of linkage blocks in the Y-Chromosome.scordova
June 16, 2008
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Regarding the Y-chromosome, is there re-combination there? It would seem, that notwithstanding the issues of linkage blocks in other chomosomes, the Y-chromosome appears to stand out in terms of linkage block preservation. It would appear genetic entropy and Muller's ratchet must surely be present in Y-chromoses.
Bob OH: As far as I’m aware, the X chromosome can recombine. The Y chromosome can’t, which is probably why it’s so small and scrappy - it has suffered from genetic entropy. In some species, the Y chromosome (or its equivalent) is simply missing.
As an aside, there are an intersting questions about the Cohen Haplotype and Y-chromosomal Aaron. See: Y-chromosomal Aaron. Is this evidence of the persistence of linkage blocks in Y-chromosomes? Does it seem reasonable that linkage blocks exist and persist in Y-chromosomes?scordova
June 16, 2008
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Bob O'H, So just to clarify. If the recombination takes place in the middle of a gene it most often means that the new gene is viable but potentially different from either the mothers or fathers gene. It is just the combination of the parent's gene, the first part coming from one parent and the second part coming from the other. I can imagine all sorts of things going wrong but also this is possibly the creation of a new allele that has never existed before. Is this an accurate observation? Sorry to be a pest, but this is interesting.jerry
June 16, 2008
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Bob O'H you stated: Mainly because it doesn’t recombine. So mitochondria don’t get all the advantages of sex. Poor things. Bob you have not established your case for your disconnect in logic, since sequential DNA is supposedly foundational to diploid DNA in the evolutionary scenario. I have established that Genetic Entropy is currently detectable at the base level of DNA organization for ancient bacteria and for ancient human mtDNA and you have not provided any reason why this pattern cannot be extrapolated to diploid DNA other than to say "sex" is not involved.bornagain77
June 16, 2008
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Bob O'H re: "Random recombination causing havoc may not be too big a problem, as long as the havoc is caused early enough, so that the embryo dies very early on in development." I wondered why you were talking about genetic problems so severe as to cause the unlucky embryo to abort in the context of Sanford's book about genetic entropy. Anyone that read and understands what he wrote knows that genetic entropy is all about the accumulation of nearly neutral mutations that are invisible to natural selection. If you read the book then I apologize for insinuating you did not. It must instead be a failure to understand what you read.DaveScot
June 16, 2008
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Um, Dave, if you mean the Sanford book, I have read it. Would you like to be more specific in your criticism? He does mis-represent quite a bit of the literature, so it might be that you're relying on his representations to criticise me. BA77 -
Thus my question Bob, is if mtDNA is successfully being used to trace actual ancestral lineages, why is it not also sufficient evidence to establish the overall pattern of Genetic Entropy we may find in ancient DNA?
Mainly because it doesn't recombine. So mitochondria don't get all the advantages of sex. Poor things. jerry - if we could perfectly sequence the complete genomes from several parents and offspring, we would be able to see what mutations had occurred. But we're some way off this, particularly as genotyping errors will look like mutations. But then we would need to look at the fitness, which is going to be difficult. And then we would have to look at how these mutations are selected over several generations. a lot of the ideas about the genome being imperfect are well accepted. But a lot of the lethal mutants are rare and recessive, so we barely see them. If I was going to investigate Sanford's ideas, I wouldn't use humans, I would use something with a smaller generation time, and preferably something for which we have DNA from several generations. We have that for a few species, but the genotyping technology isn't good enough yet (too slow and too expensive), so I think we would have to keep on collecting DNA. Which some groups are doing anyway, because it's interesting for other reasons. To answer your other question - many recombination events are possible per chromosome (IIRC, the average is 1. I can't remember where I saw that, so you don't have to believe me). Recombination is always (or almost always) between homologous sites, i.e. the same place on the two copies of a chromosome. Sometimes it does go wrong, which can have unfortunate consequences if a vital gene is removed. If its duplicated, it might not have an adverse effect, and indeed might be the start of the evolution of a gene with a new function. Recombination is random: there could be more than one recombination event on chromosome. However, the rate of recombination does vary across a chromosome, so some parts tend to have more recombination events than others.Bob O'H
June 16, 2008
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Something tells me that, though investigating this subject, we will find that there is indeed an impressive amount of "information" juggling going on in the humans genome, that will be impossible for Darwinism to reconcile to the overall stability of the Genome yet at the same time it will beyond our ability to completely trace to totally natural mechanisms. Just a hunch that that is what will be found. Psalm 139:13 For you created my inmost being; you knit me together in my mother's womb.bornagain77
June 16, 2008
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Bob O'H, Sanford uses the metaphor of a rusted out car to describe genetic entropy and each rusted out car has to be unique in its ping marks of rust and different from its neighbor because the ping marks are mostly the result of random processes. And according to Sanford we are well on our way to being completely rusted out. If the hapmap data showed an order to the data as opposed to a system wide large scale discrepancy of each genome from each other then this would tend to falsify Sanford's thesis. After reading Sanford, I get the impression that each genome will become a pop marked replica of the original genome hundreds of generations in the past but that each deterioration should be unique. Such a pattern of disarray should be discernible whether it is fit or not fit because of the random lack of similarity with other genomes. I am not sure how much fitness would affect it because the parent organism was there and theoretically fit because it reproduced and according to Sanford on its way to being rusted out. Such a pattern should show up as one compares genomes. But I am the amateur in this and have no experience with comparing genomes so have no ideas what the problems would be or what to look for or how much differences there are from one genome to the next of the same species. Essentially I am just trying to follow the logic of Sanford's thesis to some logical hypotheses and then look to see whether any real data either supports or falsifies his ideas. The hapmap looks like a convenient set of real data that should be relevant. Separate subject - the possible recombination in forming the gamete in humans has 23 opportunities for recombination. How many possible recombinations per chromosome is possible? Is there always recombination for each chromosome or is it random? I am just curious as to what is known?jerry
June 16, 2008
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Bob, I know mtDNA does not apply to the random evolutionary scenario you are trying to apply here, but as to the integrity of mtDNA as a measure for stability and the warranted inference to the Genetic Entropy we may find in the genome of of modern humans, when compared to ancient Human mtDNA, I found this following site very interesting: Ancient DNA (A compilation of DNA haplotypes extracted from ancient human remains) http://www.isogg.org/ancientdna.htm#Demasduit It is somewhat surprising to me that they are able to gather enough detail, to surmise exactly which race of humans belong to which mtDNA group thus tracing, with accuracy, the timing and geographic origination of each group. In fact they were able to debunk the recent "Jesus Tomb" with mtDNA analysis; mtDNA Sequences From "The Lost Tomb of Jesus" mtDNA extracted from human remains contained in two ossuaries recovered from the Talpiot tomb in Jerusalem; one ossuary labeled "Jesus" and the other labeled "Mariamene e Mara" provided conclusive evidence that the two individuals did not share a common maternal line ancestor. Name Haplo Haplotype Jesus ? 270G, 278T Mariamene e Mara ? 290G Thus my question Bob, is if mtDNA is successfully being used to trace actual ancestral lineages, why is it not also sufficient evidence to establish the overall pattern of Genetic Entropy we may find in ancient DNA? i.e. why should we infer a complete disconnect in the pattern of loss of complexity from ancient mtDNA since it is in fact such a reliable marker of human ancestry?bornagain77
June 16, 2008
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Bob O'H I know this is asking an awful lot of a person like you but I think it would be a good idea if you read the book before talking about what's in it.DaveScot
June 16, 2008
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jerry - I think the big problem with using the hapmap data to assess Sanford's ideas is that we would have to have measures of fitness as well. And we would have to have them in a common environment. Random recombination causing havoc may not be too big a problem, as long as the havoc is caused early enough, so that the embryo dies very early on in development.Bob O'H
June 15, 2008
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...it’s a little hard to believe there aren’t mechanisms that mark the beginning and end of blocks.
But there is no evidence that the blocks are "real". They were just areas where there was little or no observed recombination, but that doesn't mean that no recombination is possible in the blocks. The data sets used only cover a small proportion of human diversity (IIRC the only African data was the Yoruba data), and the blocks may well be split up in other populations.
We can’t just willy-nilly slap half a linkage block into the middle of another and expect this won’t result in disaster at some point….
That would be a translocation, and yes it often will lead to disaster. But in recombination, the block is being slapped into the middle of the same block - it replaces an almost identical sequence. This happens without any problems - it's the basis of gene mapping in eukaryotes. Indeed it's difficult to stop without killing the organism.Bob O'H
June 15, 2008
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