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Future Risk Assessment in the Genome

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I found the following research quite intriguing. It has far reaching implications of interest to IDists. One implication requires a front-loading IDist to appreciate. Basically what the researchers found is that there are risk assessments in the promoter regions of genes. If a gene is critical and random mutations to it would be bad news it is marked as high risk and isn’t subject to mutation. If it’s not so critical it is marked low risk and exposed to experimentation.

How does this apply to front-loading? A major problem for front-loading is no known mechanism for conservation of genomic information other than natural selection. Information stored for a distant future that isn’t used in the present is ostensibly destroyed by deep time and random mutation. Other research we’ve blogged here showed compelling evidence that a mechanism for conserving unexpressed information exists. This is even more compelling – tags saying “conserve this”. Now all we need to find is the enhanced error detection and correction mechanism that is employed to conserve information tagged for conservation and there’s our mechanism for presevation of front-loaded genomic information over deep time.

Evolution: When Are Genes ‘Adventurous’ And When Are They Conservative?

ScienceDaily (Nov. 8, 2007) — Taking a chance on an experiment – this is one of the impulses that drive evolution. Living cells are, from this angle, great subjects for experimentation: Changes in one molecule can have all sorts of interesting consequences for many other molecules in the cell. Such experiments on genes and proteins have led the cell, and indeed all life, on a long and fascinating evolutionary journey.

Prof. Naama Barkai of the Weizmann Institute’s Molecular Genetics Department recently took a look at gene expression – the process in which the encoded instructions are translated into proteins – and the evolution of mechanisms in the cell for controlling that expression. Changes in genes, and thus in protein structure, are a double-edged sword: They can give cells new abilities or advantages for survival, but they can also spell disease or death for the organism. Not all genes evolve at the same rate. Indeed, some have been conserved through long stretches of evolution: Similar versions of some genes are found in yeast, plants, worms, flies, and humans.

When do cells hold on to specific gene sequences, and when do they allow evolution to experiment with them? Clearly, highly conserved genes fulfill some basic, universal function for all life, and changes in their sequences have drastic consequences, involving death or the inability to multiply. How does evolution “decide” which genes need to be conserved, and which it can change freely? What keeps these genes safe from the ongoing experimentation that’s constantly carried out on other genes?

Barkai and her team discovered a sort of “risk distribution law” for evolution. They found that a genetic “phrase” that regularly shows up in the promoter region of genes (the bit of genetic code responsible for activating the gene) contains a key to gene conservation: The expression of a gene that contains the sequence TATA in its promoter is more likely to have evolved than that of a gene that does not have TATA in its promoter.

In other words, the level of risk appears to written in the gene code, in a way that’s similar to financial risk analysis: When the cost of error is high, an investor’s willingness to chance the risk is low, but if the cost of a mistake is negligible, even if the chance of making one is high, the possibility of gain may make the risk worthwhile. Evolution, it seems, discovered this principle millions of years before Wall Street.

Read the rest of the article at the source here

Comments
bornagain77 -
Even if there were totally neutral mutations, which is highly unlikely given the overwhelming interrelated complexity of the genome,
What about synonymous substitutions? I'm also curious if you're read this article. If not, I can try and get a copy to email you. BobBob O'H
November 12, 2007
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DaveScot and all, You may find this study interesting; Protein stability imposes limits on organism complexity and speed of molecular evolution Konstantin B. Zeldovich, Peiqiu Chen, and Eugene I. Shakhnovich http://www.pnas.org/cgi/content/abstract/104/41/16152 of special note: Here we study population dynamics in a where fitness can be inferred from physical properties of proteins under a physiological assumption that loss of stability of any protein encoded by an essential gene confers a lethal phenotype..... It establishes a universal speed limit on rate of molecular evolution by predicting that populations go extinct (via lethal mutagenesis) when mutation rate exceeds approximately six mutations per essential part of genome per replication for mesophilic organisms and one to two mutations per genome per replication for thermophilic ones. Although I don't know the details yet, this seems that evolutionists are themselves in the foot again, since evolutionists are required to have rapid speciation events that occur within 5 to 50,000 years to explain the gaps in the fossil record. Thus on one hand, because of the fossil record, they must have a certain rate of rapid speciation, yet on the other hand, because of functional properties of proteins, they are limited to the amount of change they can incur per generation.. Though the study is technically a bit beyond me right now...I do smell another rat in evolutionary thinking with this particular study!bornagain77
November 12, 2007
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getawitness, "I’m arguing for a good use of sources." I have been watching your debate with BA77, and agree with you that as the underdog we need to be particularly cautious to use sources carefully. Further, I agree that a source should be presente from the source's perspective, even if we then suggest that said perspective is in error. SR, if well adapted is confirmed by "billions of trillions" of replications, then the fact that humans have only replicated about ten billion times would indicate that we are not well adapted ;) Surely one would agree that if the organism replicates billions of times per acre per day -- which malaria does -- that if an otherwise fertile acre becomes toxic, and replication rates drop to near zero, those malaria find themselves in an environment for which they are not well adapted. As the microbe can reproduce more in an acre per year than there are humans in history, they should be able to make changes that somewhat match the difference between man and chimp -- at least 2% of DNA. Why have they made NO progressive mutational changes even in toxic environments?bFast
November 11, 2007
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bFast, how can something that's not well adapted to its environment go through, as DaveScot puts it, "billions of trillions" of replications?Stanton Rockwell
November 11, 2007
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bornagain77, The short answer is "I'm not sure," because in the paragraph beginning "I have seen estimates," I'm not sure what are your words and what are Sanford's. (It would be easier for me to tell if I had Sanford's book. I'll get a copy, though, and tell you when I find out.) Thanks for taking the objection seriously, however. As I mentioned before, I'm not arguing against genetic entropy or against Sanford: I'm arguing for a good use of sources.getawitness
November 11, 2007
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SR, "ToE doesn’t expect such changes in organisms well-adapted to their environments." Oh, I see what you are suggesting. The reason Behe points to p.falciparum's mutation rates is because it is not "well-adapted" to its environment. Man, in his wisdom, has done everything we can to make a toxic environment for malaria (p.falciparum). In doing so, we have created a situation where malaria should feel poorly adapted, and should adapt. That said, malaria has adapted somewhat, but always by lessening itself, rather than by becoming something greater. With more organisms being so challenged than there ever has been quadrupeds, one would think that the malaria should have been able to pull off at least one progressive (rather than regressive) mutation by now.bFast
November 11, 2007
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Getawitness, I've revised my study notes to reflect your objection, I would like to know if the revision passes your inspection: The primary thing that is crushing to the evolutionary theory is this fact. Of the random mutations that do occur, and have manifested traits in organisms that can be measured, at least 999,999 out of 1,000,000 (99.9999%) of these mutations to the DNA have been found to produce traits in organisms that are harmful and/or fa^tal to the life-form having the mutation! “I have seen estimates of the incidence of beneficial mutations which range from one in one thousand up to one in one million. The best estimates seem to be one in one million (Gerrish and Lenski, 1998) Since neutral mutations can be inferred to almost never occur in a genome, then the ratio of deleterious to beneficial mutations seems to be one million to one.” (Sanford; Genetic Entropy, page 38: Note: this statement has been revised to reflect the evolutionary belief of some totally neutral mutations of Gerrish and Lenski) http://myxo.css.msu.edu/lenski/pdf/1998,%20Genetica,%20Gerrish%20&%20Lenski.pdf Even if there were totally neutral mutations, which is highly unlikely given the overwhelming interrelated complexity of the genome, Gerrish and Lenski most likely used a incomplete measure of fitness/information in order to arrive at their one in a million number for beneficial mutations. I maintain that their, one in a million, estimate is flawed and that ALL mutations to a genome will be found to be harmful/fatal when using a correct measure of fitness/information. The following article points out this flaw, in measuring the total fitness/information of a organism, by evolutionary scientists and thus skewing the already crushing mutational studies: http://www.answersingenesis.org/docs2007/0131observation.asp In fact, from consistent findings such as these, it is increasingly apparent that Genetic Entropy is the overriding foundational rule for all of biology with no exceptions: The foundational rule for biology can be stated like this: All adaptations away from a parent species for a sub-species, which increase fitness to a particular environment, will always come at a loss of information from the parent species.bornagain77
November 11, 2007
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getawitness, Since, Gerrish and Lenski most likely used a incomplete measure of fitness, I maintain that their, one in a million, estimate is skewed. I maintain that when taking into account a complete picture of fitness for mutated e-coli (loss of information from original strain as well as compared complete robustness to original strain), there will NEVER be a beneficial mutation that will both increase fitness and information at the same time. Thus holding to the foundational principle of Genetic Entropy: The rule can somewhat be stated like this: All adaptations away from a parent species for a sub-species, which increase fitness to a particular environment, will always come at a loss of information from the original parent species. This overriding principle, drawn directly from Genetic Entropy, is substantiated for all adaptations I have looked at from "simple" micro-organisms to complex higher organisms. It is a solid inference, all the way down to the second law and the conservation of information. Thus it most likely is a rule that will hold across the board for all of biological life forms!bornagain77
November 11, 2007
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Pantrog you stated, I also note Gerrish and Lenski do witness a series of fitness improvements in the evolving E. coli they study? Where is the entropic decay in this ? I guess your referring to this statement: Based on three sudden fitness increases during  1400 natural generations (Lenski & Travisano, 1994), I think this paper has part of the answer: http://www.answersingenesis.org/docs2007/0131observation.asp Of special note: "Scientists used the MG1655 strain of E. coli K-12 bacteria that has been cultured in the lab environment for approximately 80 years. This strain has adapted well to the lab setting of growing on rich media full of carbon sources (unlike that found in natural environments). MG1655 was grown in a minimal medium containing the sole carbon source glycerol for a period of 44 days. The strain already has the pathway to catabolize (breakdown) glycerol so the “evolution” that occurred did not originate the pathway to utilize glycerol. MG1655 did not utilize glycerol well initially (as evidenced by a slow growth rate) but it was found that mutant strains developed that could utilize glycerol better (faster growth rate) than the original strain over time. The entire genome (all the DNA) from these strains was sequenced to observe mutations that led to the better utilization of glycerol. Do these mutations provide evidence that the bacteria evolved? One strain had a mutation in a gene for the enzyme glycerol kinase which is important in the first step of glycerol breakdown. This mutation reduced the ability of glycerol kinase to be inhibited by fructose-1,6-bisphosphate (FBP). FBP is important in limiting the rate at which glycerol is catabolized. This is important since a side reaction during glycerol breakdown results in the production of a metabolite which is toxic at high concentrations. No gain of information took place as required by evolution, only loss leading to dysregulation of this pathway. In the wild, versus the rather comfy lab environment, this could be extremely detrimental." This study is typical of every study I've looked claiming fitness increase Pantrog, Thus they can claim fitness increase while ignoring the fact that they have really broken something in the e-coli, and have in fact created a e-coli that would be "less fit" in the wild and would soon be out-competed into oblivion by the original e-coli. Are you beginning to get the picture at how foundational Genetic Entropy truly is to biology Pantrog?bornagain77
November 11, 2007
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BFast, I'm not sure how what you are saying answered the question, which was directed to DaveScot's contention that in "billions of trillions" of replications, we should see significantly more change than we do in p.falciparum. My point was (and I'm a neophyte, don't forget) that ToE doesn't expect such changes in organisms well-adapted to their environments. Once again, I'm not making any claims of my own here, I'm just trying to understand the argument and hoping that those here who have more experience and knowledge than I do can help me along.Stanton Rockwell
November 11, 2007
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Pantrog, In my suggested revision, Sanford does not attribute the absence of neutral mutations to Gerrish and Lenski. That's pretty clearly Sanford's claim.getawitness
November 11, 2007
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bornagain77, Thank you for sharing some aspects of your life with me; that was very touching. I'm sure not going to take that bet even if I were a betting person! You should know that I agree with you on more than you may think, including the fundamentally Theistic implications of ID. Sorry if I sound like a old hen with a ruler sometimes. I want ID to make the best case possible!getawitness
November 11, 2007
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"Since neutral mutations almost never occur, then the ratio of deleterious to beneficial mutations seems to be one million to one." To be fair to Gerrish and Lenski they never say they think "neutral mutations almost never occur", given that they cite Kiumra so heavily I suspect they would say many mutations are neutral. I also note Gerrish and Lenski do witness a series of fitness improvements in the evolving E. coli they study? Where is the entropic decay in this model?Pantrog
November 11, 2007
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SR:
doesn’t ToE predict that we shouldn’t necessarily see the kind of changes you’re looking for in organisms that are successful in a given environment?
As far as the theory of evolution "predicting", well, Darwin formally predicted that we would see a multitude of transitional forms. However, the modern theory makes allowance for holes in the rock record. However, there are other records to contend with, most noteably the record of the DNA. Haldane, a noted evolutionist, presented the dilemma that man has many more mutations compared to chimps than can possibly be accounted for by means of RV+NS. This is a sore spot in the tale of ToE. For ToE to be validated, it must be able to account for the reasonable statistical possibility of all changes in DNA. Currently it is far from being able to do so. SR:
Even if we grant Darwinists’ claims of knowledge regarding mechanisms, we know that materialism has barred the door marked “Cause.”
I would suggest that cause and effect are both subject to modern science. The only issue of "cause" that is barred is the issue of "first cause". The ToE presents a formula of causation, namely RV+NS. These two mechanisms -- variations in DNA from replication errors, damage etc., plus variation in environment caused by unrelated phenomenon (asteroids, etc.) and interaction of organisms filtered through the great "if it works" mechanism of selection. The ID hypothesis seeks to "detect evidence of design". As such, the ID hypothesis, at least within biology, does not suggest that that the designer(s) be "super-natural." If the designer(s) are not super-natural, then, by definition, their effects can be detected and studied by a fully materialistic science. If the effects of a non-supernatural designer can be studied by a fully non-materialistic science, then the effects of a designer supernatural or not should by no means be beyond the scope of science.bFast
November 11, 2007
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getawitness, For me to even discuss such high level matters on the web is extremely humorous to the highest degree, for I was a homeless alcoholic for over 12 years, before I managed, with a lot of help from the Lord, to turn my life around. What is extremely funny is that even though, I should not be able to so easily refute such high level critics of ID, I do so (albeit as you have pointed out, rather clumsily) with relative ease. Hopefully I am getting better in my use of sources and appreciate your constructive criticism. But the main point being that my faith in God has not been compromised in the least by these high level debates but has been rewarded and strengthened remarkably. Shoot, I am even confident enough to make this following prediction for the Theistic position of ID. Further deciphering of the human genome will reveal 100% functionality with severe polyfunctionality revealed throughout the entire genome. As well I predict the complexity of the genome will severely stress if not exceed man's ability to completely understand it. If you are a betting man, That is sure money the way I see things getawitness!bornagain77
November 11, 2007
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bornagain77, Please calm down. I'm not attacking Dr. Sanford. In fact, I thought I was just offering a minor and friendly correction to you, since your original comment gave the impression that you'd read Gerrish and Lenski yourself. Now I realize that you were citing that paper secondhand, from Dr. Sanford's book. First, however, let me correct something you wrote about me. You wrote: "This reflects your belief that some mutations are not deleterious but could be neutral and as such have some hypothetical future beneficial effect." I said no such thing. I've said nothing about my beliefs regarding mutation but only about the claims of Gerrish and Lenski. They're the ones who assume not all mutations are negative. Frankly, you're assuming a lot about me. Let me explain why I think Dr. Sanford uses the source wrongly. It has nothing to do with intuition or what Dr. Sanford knows to be true; it has to do with treating sources fairly. That's the first rule of citation. Imagine that Gerrish and Lenski cite Sanford's book, and they say "Sanford has argued that most or all mutations are neutral or deleterious." Sanford would be hopping mad at such a misuse of his book, and rightly so! Such a statement claims that Sanford believes in neutral mutations, when he clearly does not! The proper way to disagree with Sanford would be to write, "Sanford has argued that most or all mutations are deleterious, but he should consider neutral mutations more carefully." So my point is simply that Sanford gives the false impression that Gerrish and Lenski were intending to estimate the rate of bad to good mutations. What Sanford should have said was something like this: “I have seen estimates of the incidence of beneficial mutations which range from one in one thousand up to one in one million. The best estimates seem to be one in one million (Gerrish and Lenski, 1998) Since neutral mutations almost never occur, then the ratio of deleterious to beneficial mutations seems to be one million to one.” That would be a fair use of the source. Finally, let me offer again a suggestion, in all friendship: You should not give the impression that you've read a primary source when you've gotten that material through a secondary source.getawitness
November 11, 2007
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bFast:
I don’t believe that this is Behe and Dembski’s view. I think that they are suggesting that the search include areas that are currently off-limits — searching for the kinds of evidences that we would see from intellignet causation. Further, I think that Behe and Dembski are doing a magnificent job of at least getting respectible scientists like yourself to publicly state that science hasn’t come near to the end of its exploration of the mechanism of evolution.
To play devil's advocate for a moment (and perhaps the word "devil" is instructive here)it seems that while the Darwinist's search for the mechanism isn't the point, but certainly the search for a cause is. Even if we grant Darwinists' claims of knowledge regarding mechanisms, we know that materialism has barred the door marked "Cause." I think that even Dr. Dembski has said that ID is not a mechanistic theory, so why not give the Devil his due wrt mechanisms, and emphasize the dearth of research into cause?Stanton Rockwell
November 11, 2007
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Bob O'H, I hope this does not sound rude, as I am not face to face with you, but for the 5th time, please go get the book Bob. getawitness, I believe that Dr. Sanford, being a more than highly qualified, Geneticist, is interpreting the evidence, presented by Gerrish and Lenski, exactly as he sees it, and you, not being privy to what he knows intuitively to be true, interpret their evidence very differently from his highly educated and more qualified perspective. Thus, I stand by what he wrote and will not retract it.bornagain77
November 11, 2007
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DaveScot:
ID claims that even billions of trillions of replications are not enough to have any reasonable chance of observing significant biological complexity on the order of what separates reptiles from mammals.
I'm just getting myself up to speed on all of the details in this debate, but doesn't ToE predict that we shouldn't necessarily see the kind of changes you're looking for in organisms that are successful in a given environment? From what I've read so far, it seems that there have been significant changes that Behe didn't account for, although I readily admit that I don't have the kind of knowledge necessary to sort out these claims very effectively. That's one reason I was glad to find this site, where there seems to be a proper ID perspective on things.Stanton Rockwell
November 11, 2007
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Dr. MacNeill:
This “let’s stop looking” approach is not, has never been, and never will be part of the tradition of the natural sciences.
Dr., I would fully agree with this statement from a natural sciences perspective and a committment to methodological naturalism. I have stated repeatedly that I believe that "we don't know, we might never know, but we're exploring" is a perfectly valid scientific position. However, the natural sciences is hardly the beginning and end of life. Beyond the natural sciences we have philosophy of science. In this area there are loud voices declaring that methodological naturalims equates to philosophical naturalism -- that sciences is committed to philosophical naturalism. In general, man must conclude that until the day science does uncover a fully natural (non-intelligent) explanation for biogenesis, and macro-evolution, that the "intelligently caused" explanation is most likely correct. This at least removes the natural sciences as a barrier to the exploration of the possibility of God. Dr. MacNeill, feel free to "not give up", but please let the world know that the puzzle of evolution's cause has not been determined by natural science. Dr. MacNeill:
Their suggestion is that, since we don’t yet know if a mechanism exists, we should simply give up the search for one.
I don't believe that this is Behe and Dembski's view. I think that they are suggesting that the search include areas that are currently off-limits -- searching for the kinds of evidences that we would see from intellignet causation. Further, I think that Behe and Dembski are doing a magnificent job of at least getting respectible scientists like yourself to publicly state that science hasn't come near to the end of its exploration of the mechanism of evolution.bFast
November 11, 2007
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bornagain77 - how does Sanford explain away synonymous mutations as not being neutral?Bob O'H
November 11, 2007
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BA77, I'm not taking issue with Sanford's larger argument; I'm only saying that he's wrong in using that paper. Specifically, Sanford says this: "I have seen estimates of the ratio of deleterious to beneficial mutations which range from one thousand to one, up to one million to one. The best estimates seem to be one million to one (Gerrish and Lenski, 1998)." But that's not what Gerrish and Lenski say, so citing them in support of that contention is wrong. Go read the paper for yourself; I linked to the PDF above.getawitness
November 11, 2007
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Getawitness, To keep me from getting in trouble, I dug out my Genetic Entropy book and will quote Sanford verbatim. "I have seen estimates of the ratio of deleterious to beneficial mutations which range from one thousand to one, up to one million to one. The best estimates seem to be one million to one (Gerrish and Lenski, 1998). The actual rate of beneficial mutations is so extremely low as to thwart any actual measurement (Bataillon, 2000, Elena et al, 1998) The reason for the difference between your view and Dr. Sanford's view, getawitness, is that, I believe, he is looking at the entire genome more realistically than you are, and you are in fact clinging to some misguided belief that beneficial mutations must occur because you believe the overall evolutionary hypothesis to be true on some level. When you state this: "that Gerrish and Lenski are clearly referring to overall mutations, not harmful mutations." This reflects your belief that some mutations are not deleterious but could be neutral and as such have some hypothetical future beneficial effect. In fact this belief, that you somewhat allude to, is deeply entrenched in current evolutionary thought,,,because, by golly, they have got to come up with some beneficial mutations somewhere to make evolution work. Well, on page 37, 38 and 39 of Genetic Entropy, Sanford sets about to destroy much of the evolutionary thought that has grown around this belief. "Of all these mutations - what percent are truly neutral? In the last few years there has been a dramatic shift in the perceived functionality of most components of the genome. The concept of "junk DNA" is quickly disappearing (completely dismantled by ENCODE in June 07). In fact, it is the "junk DNA" (non-protein-coding DNA), which appears to be key to encoding biological complexity (Taft and Mattick, 2003). The recent Taft and Mattick study strongly suggests that the more "junk" - the more advanced is the organism. So mutations within "junk DNA" can hardly be assumed to be neutral! Approximately 50% of the human genome is now known to be transcribed into RNA (Johnson et al., 2005) At least half of all this transcribing DNA appears to be transcribed in both directions (Yelin et al., 2003)! So all this DNA is not only functional it is doubly functional... Sanford goes on to show, on page 38 and 39, that every evolutionary assumption of the genome, that has been forced upon us (Pseudogenes, transposable elements etc.. etc..) have been overturned by recent studies (Chen et al. 2004)(Morrish, et al.,2002)(Shapiro and Sternberg, 2005)(GC rich areas-Vinogradov,2003) word patterns (Karlin, 1998) (Tachida, 1990)(Sandman et al.,2000) He closes his devastating critique of evolutionary presumptions for the genome by stating at the bottom of page 39. "It is becoming increasingly clear that most, or all, of the genome is functional. Therefore, most, or all, mutations in the genome MUST be deleterious". As well getawitness, I want to point out that the ENCODE findings heavily suggest 100% functionality for the whole genome,,,As such, since the genome is now known to be a "complex interwoven network".... http://www.genome.gov/25521554 BETHESDA, Md., Wed., June 13, 2007 - An international research consortium today published a set of papers that promise to reshape our understanding of how the human genome functions. The findings challenge the traditional view of our genetic blueprint as a tidy collection of independent genes, pointing instead to a complex network in which genes, along with regulatory elements and other types of DNA sequences that do not code for proteins, interact in overlapping ways not yet fully understood. .....This very well may make the genome itself irreducible complex, and as such, Dr. Behe's inferences for irreducibly complex molecular systems can be slightly modified to include these 100% functional higher systems. Whereas Dr. Behe's base definition for IC means that the system will fail to operate if any component of the system is damaged or removed, the slightly modified meaning of IC would state that the overall functionality (information content) of the system has been decreased by modifying it from its original form. As well I want to point out the hard evidence backs up this preliminary assertion. "Professional evolutionary biologists are hard-pressed to cite even one clear-cut example of evolution through a beneficial mutation to DNA that would violate the principle of genetic entropy. Although evolutionists try to claim the lactase persistence mutation as a lonely example of a 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 clearly overwhelming, for doctors have already cited over 3500 mutational disorders (Dr. Gary Parker)." No Sir, getawitness, I believe Dr. Sanford stated 1 million to 1 harmful to beneficial mutations, for a very precise and exact reason and is not wrong in his assertion at all!bornagain77
November 11, 2007
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Allen There's nothing further to "test" about intelligent design in the way of verfication. We already know that intelligent agents can modify genomes for explicit purposes and such modfiications are not constrained by that which limits unintelligent mechanisms of variation. The field of genetic engineering is the proof of concept for intelligent design. Nobody questions the notion that genetic engineers acting as intelligent agents can modify genome content for explicit purposes. We know this is possible. Rather what is required is falsifcation of the design hypothesis. This can be accomplished in principle by observing evolution creating biological novelty that ID claims is too improbable to ever observe. The problem of course is the counter-claim that evolution works too slowly to observe any significantly complex novelty emerging de novo. This claim was disputed by Behe using falciparum as an example. ID claims that even billions of trillions of replications are not enough to have any reasonable chance of observing significant biological complexity on the order of what separates reptiles from mammals. The observation of falciparum represents the grandest test which could have falsified the ID hypothesis and, as I wrote in a recent blog article - no black swan was observed.DaveScot
November 11, 2007
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Allen This is a basic principle of modern evolutionary genomes, so basic that it is used by virtually all people in the field as a method for distinguishing between those sequences in the genome that are currently (or recently have been) undergoing selection. This principle has been contradicted. In fact I included a link in the article to the research which contradicted it. I'll highlight it again in this comment since you must not have clicked on it in the main article: The Sound of Circular Reasoning ExplodingDaveScot
November 11, 2007
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Allen I don't dispute the notion of stabilizing selection. I dispute the notion that there's any kind of selection other than stabilizing selection. Also its niche isn't anywhere near stable. You've essentially repeated what another commenter wrote - that falciparum didn't evolve because it didn't need to evolve. It has been and continues to be massively assaulted by various factors - some of which it successfully addressed and some it did not. Analyzing where it succeeded and where it failed was the whole point of Behe's book. It established the edge of evolution - what evolutionary mechanisms (other than ID) can and cannot do. Falciparum defeats the manmade drug atovaquone. which requires just a single point mutation, in at least one of three humans infected with a non-resistant strain. Far less frequently it mutates to defeat the drug chloroquine. Chloroquine resistance requires a few interdependent point mutations and it arises spontaneously a hundred million times less often. A human hemoglobin variant (sickle cell) has never been defeated by falciparum. The number of point mutations required for that is apparently beyond the capability of any evolutionary mechanism given billions of trillions of opportunities. Yet another notable instability in falciparum's niche is sensitivity to temperature. It can't survive in climates where the temperature drops below about 60 degrees for long. At the fringes of its climate-dictated range it's under intense selection pressure for any mutations which would allow it to extend its range into temperate climates. This too is evidently beyond the capability of evolutionary mechanisms in billions of trillions of opportunities. These are empirical observations of what evolutionary mechanisms can and cannot do. Yet in orders of magnitude fewer opportunities we're asked to take it as a matter of faith that the same mechanisms available to falciparum somehow managed to transform reptiles into mammals. Non sequitur. There is no reason to believe that what didn't work for falciparum somehow managed to produce, in far fewer opportunities, a far more complex and diverse suite of biological novelties which distinguish reptiles from mammals. The only way one can swallow this contradiction is by a belief in things not observed - the very definition of faith. DaveScot
November 11, 2007
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"In other words, 1 million: 1 is their estimate of total mutations:beneficial mutations" I've had a look at Gerrish & Lenski, 1998. Good to see you citing some old school population genetics. They base their calculations on beneficial mutation rates between 10^-4 and 10^-10, per capita, per generation. For a bacterial population size of 10^10 (e.g. in 2cm of human gut) - that would suggest the authors expect 1 or more beneficial mutations, population-wide, every generation (i.e. every 20 minutes at body temperature).Pantrog
November 11, 2007
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However, this only means that we do not currently have a comprehensive theoretical understanding of how macroevolution has occurred. .... Their suggestion is that, since we don’t yet know if a mechanism exists, we should simply give up the search for one. This “let’s stop looking” approach is not, has never been, and never will be part of the tradition of the natural sciences.
I don't see acknowledging ID as equating to "let's stop looking." Personally I've always interpreted Dembski and Behe to mean that while design is greatly involved chance is a real component of reality and that we should strive to research and discover what exactly are the abilities of such indirected, unintelligent mechanisms. If we eventually find out that Darwinism is correct, so be it. Perhaps the OOL itself is the only thing that requires design. Obviously I doubt that to be true but my main point is that even ID proponents should desire to see such research continued even if we believe there will be limits, an edge, to these mechanisms. My opinion, of course, and perhaps I'm misinterpreting Dembski and Behe.Patrick
November 10, 2007
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BA77, The Gerrish and Lenski paper is available directly here: http://myxo.css.msu.edu/lenski/pdf/1998,%20Genetica,%20Gerrish%20&%20Lenski.pdfgetawitness
November 10, 2007
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What I wanted to say before I got on the modpile is that Gerrish and Lenski are clearly referring to overall mutations, not harmful mutations. With all repsect to Dr. Sanford, if he says the Gerrish and Lenski paper was referring to harmful mutations, he is simply wrong.getawitness
November 10, 2007
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