Future Risk Assessment in the Genome

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. Bob Bob O'H

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

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

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

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

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

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

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

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

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

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

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

"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

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

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

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

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

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

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

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

bornagain77 - how does Sanford explain away synonymous mutations as not being neutral? Bob O'H

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

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

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

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 Exploding DaveScot

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

"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

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

BA77, The Gerrish and Lenski paper is available directly here: http://myxo.css.msu.edu/lenski/pdf/1998,%20Genetica,%20Gerrish%20&%20Lenski.pdf getawitness

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

I guess I'm on the modpile, unless something's wrong with my machine. Oh well. Forgive the multiple submissions of one comment. getawitness

bFast: You mean "dissent." Your "wow," however, is exactly right. In fact I'd call the paragraph you cite a concession of historic proportions. I can see Dawkin's head, about now, doing 360s as airborne spirals of pea soup erupt out of his mouth. It's a good thing the Doc's got tenure. He may end up, before all is said and done, needing it. jstanley01

Professor MacNeill you stated, As for macroevolution, I agree that at the present time we have little or no formal theory predicting the observed patterns of change in deep evolutionary time. This is one reason why I have asserted that the so-called “modern evolutionary synthesis” of the mid-20th century is “dead” – it’s theoretical predictions have either been superceded (e.g. by evo-devo) or shown to be inadequate. Professor Macneill, the evidence evolutionary theory is currently having so much trouble with, and is constantly being surprised with, lines up perfectly with the ID/Genetic Entropy that has come forth from foundational ID thought,,,Unlike you and other evolutionists, IDers are never severely "surprised" by recent discoveries in evidence (need I mention ENCODE), other than being "surprised" at how well everything falls into the ID/Genetic Entropy framework established by Dembski, Gitt, Behe, and Sanford. Getawitness you stated; In other words, 1 million: 1 is their estimate of total mutations:beneficial mutations. The quote is from Dr. Sanford's book "Genetic Entropy". He is a head and shoulders above his peers in his particular field of genetics (He invented the biolistic "Gene Gun" process as well as numerous other breakthroughs). Thus I am positive he meant exactly what he wrote since it was crucial to the main thesis of his book. bornagain77

Dr. MacNeill:

As for macroevolution, I agree that at the present time we have little or no formal theory predicting the observed patterns of change in deep evolutionary time. This is one reason why I have asserted that the so-called “modern evolutionary synthesis” of the mid-20th century is “dead” – it’s theoretical predictions have either been superceded (e.g. by evo-devo) or shown to be inadequate.

Wow, that's an amazingly ID-postive statement! Is it inappropriate quotemining to attribute this paragraph, stand-alone, to you? As for evo-devo, I have found the science to be an intriguing topic that carries very loud echos of the front-loading hypothesis.

this only means that we do not currently have a comprehensive theoretical understanding of how macroevolution has occurred. What we do have is an immense and exponentially expanding body of evidence strongly supporting the inference that macroevolution has indeed happened. ... the argument is not about whether, but rather about how.

As far as I can see, this is the beginning and end of the ID evolutionist's perspective (as opposed to the ID creationists, those who do not hold to common descent.) I agree with you that speciation is reasonably well explained by RV (with all of your variety) and NS. I am fully comfortable with suggesting that the variety within the feline family, for instance, are the product of these forces. Yet science not having a well-worked theory to explain the big changes, the real macro-evolution, is no small issue. In light of your view as stated in post #42 above, I invite you to sign the "Discent from Darwinism" document. It would seem that you would agree, possibly in a soft way, with the discent: “We are skeptical of claims for the ability of random mutation and natural selection to account for [all of] the complexity of life. Careful examination of the evidence for Darwinian theory should be encouraged.” bFast

BA77, I don't want to speak for the Darwinists in general (or for Prof. MacNeill in particular). I think, thought, that one reason for the silence is that CSI is not a widely used concept in biology (or for that matter in mathematics). It remains a kind of "specialist" term. getawitness

Prof. Macneill, Sorry for the SHOUT. But, again, where is your evidence for CSI generation i.e. the mutational studies that will back up your claims for your (new) theory? bornagain77

Whoops! Reverse the terms in what I wrote above. In other words, 1 million: 1 is their estimate of total mutations:beneficial mutations. getawitness

As for macroevolution, I agree that at the present time we have little or no formal theory predicting the observed patterns of change in deep evolutionary time. This is one reason why I have asserted that the so-called "modern evolutionary synthesis" of the mid-20th century is "dead" – it's theoretical predictions have either been superceded (e.g. by evo-devo) or shown to be inadequate. However, this only means that we do not currently have a comprehensive theoretical understanding of how macroevolution has occurred. What we do have is an immense and exponentially expanding body of evidence strongly supporting the inference that macroevolution has indeed happened. This is the inference that both Michael Behe and William Dembski (and my friend and colleague, Hannah Maxson) have agreed with on numerous occasions. the argument is not about whether, but rather about how. One approach to answering the question of how has macroevolution occurred is to analyze the previously mentioned mountain of empirical evidence with respect to any patterns that it might yield. This is precisely what Eldredge and Gould did in the 1970s, and what evolutionary biologists studying macroevolution have been doing right along. That is, you look at the data and try to see if it suggests mechanisms. What you don't do is decide a priori on the basis of some questionable mathematical models that such a search is both pointless and counterproductive (as Michael Behe and William Dembski have both done on several occasions). 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. Allen_MacNeill

BA77, You write, "Gerrish and Lenski estimate the rate of harmful to beneficial mutations at 1 million:1." I don't think that statement is correct. Rather, that's s their estimate of beneficial to total mutations. getawitness

"Contamination of the genome by very slightly deleterious mutations: Why have we not died 100 times over? J. Theor. Biol. 175:583-594. “accumulation of VSDMs in a lineage … acts like a timebomb … the existence of vertebrate lineages … should be limited to 10^6 to 10^7 generations.” A. S. Kondrashov. 1995." I worked with Alexei when he was at Cornell. The specific problem he was discussing in this paper is Tomoko Ohta's theory of "Nearly Neutral Mutations," according to which sequences in the genome that are not maintained by selection can slowly drift as the result of mutations with almost no effect on survival and reproduction. However, this quote most emphatically does not apply to sequences that are under selection, as any significant changes in such sequences are almost immediately eliminated as the result of lowered fitness. 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. As I posted earlier, one must be careful to distinguish between sequences in the genome that are changing randomly as a result of genetic drift (i.e. the founder effect and genetic bottlenecks) and those that are changing as a result of selection. The former show no regular patterns of change, whereas the latter conform quite nicely to the patterns predicted by evolutionary theory. Allen_MacNeill

bornagain77: I do not respond to people who SHOUT, nor to people who use rhetorical tricks to score points with the members of one's own side in debates (e.g. "Is that to [sic] hard Prof. Macneill?). Allen_MacNeill

Allen_MacNeill, Thanks for the response and courtesy, now to reiterate a question that is pertinent to this thread: Please list your source for CSI (complex specified information) generation i.e. What genetic mutational study lays the foundational framework for your latter assertions? i.e. Why should your any part of your (new) hypothesis be considered viable, when you have no mutational study backing you up in the first place that says you can generate CSI you must have? While evolution “must” have beneficial mutations, almost all recorded mutations are harmful. Gerrish and Lenski estimate the rate of harmful to beneficial mutations at 1 million:1 Gerrish, P.J. & R. Lenski, 1998. Theh fate of competing beneficial mutations in an asexual population. Genetica 102/103: 127-144. " Bergman (2004) has studied the topic of beneficial mutations. Among other things, he did a simple literature search via Biological Abstracts and Medline. He found 453,732 "mutation" hits, but among these only 186 mentioned the word "beneficial" (about 4 in 10,000). When those 186 references were reviewed, almost all the presumed "beneficial mutations" were only beneficial in a very narrow sense- but each mutation consistently involved loss of function changes-hence loss of information." One of the world's leading information scientists, Dr Werner Gitt from Germany's Federal Institute of Physics and Technology in Braunschweig, says, 'There is no known natural law through which matter can give rise to information, neither is any physical process or material phenomenon known that can do this.' His challenge to scientifically falsify this statement has remained unanswered since first published. Even those mutations which give a survival benefit are seen to be losses of information, not creating the sorely needed new material upon which natural selection can then go to work. “But in all the reading I’ve done in the life-sciences literature, I’ve never found a mutation that added information… All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not increase it.” Lee Spetner (Ph.D. Physics – MIT, taught information and communications at Johns Hopkins University), Not By Chance, 1997, pp. 131, 138 Contamination of the genome by very slightly deleterious mutations: Why have we not died 100 times over? J. Theor. Biol. 175:583-594. “accumulation of VSDMs in a lineage … acts like a timebomb … the existence of vertebrate lineages … should be limited to 10^6 to 10^7 generations.” A. S. Kondrashov. 1995. M. W. Nachman & S.L. Crowell 2000. Estimate of the mutation rate per nucleotide in humans. Genetics 156:297-304. “The human diploid genome … about 175 new mutations per generation. The high deleterious mutation rate in humans presents a paradox. If mutations interact multiplicatively, the genetic load associated with such high U would be intolerable in species with a low rate of reproduction …” etc..etc...etc... On and on I could go citing studies Prof. Macneill. The point being where are your foundational studies backing your claim of novel information generation? As well I want to point out all available evidence I can find conforms to the Principle of Genetic Entropy and fails to validate evolution: For a few studies I've collected: “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.” 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. Also, In this study for ancient Australian (Mungo Man) DNA we have clear evidence of Genetic Entropy being obeyed!: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=33358 Of special note: Adcock et al. (7) clearly demonstrate the actual extinction of an ancient mtDNA lineage belonging to an anatomically modern human, because this lineage is not found in living Australians. Although the fossil evidence provides evidence of the continuity of modern humans over the past 60,000 years, the ancient mtDNA clearly does not, providing an excellent example of why the history of any particular locus or DNA sequence does not necessarily represent the history of a population. Adcock These following genetic studies of sheep are interesting: Single male and female sheep maintain genetic diversity. A mouflon (The parent sheep population) population, bred over dozens of generations from a single male and female pair transplanted to Haute Island from a Parisian zoo, has maintained the genetic diversity of its founding parents. This finding challenges the widely accepted theory of genetic drift, which states the genetic diversity of an inbred population will decrease over time. “What is amazing is that mo^dels of genetic drift predict the genetic diversity of these animals should have been lost over time, but we’ve found that it has been maintained,” said Dr. David Coltman, an evolutionary geneticist at the University of Alberta. http://www.sciencedaily.com/releases/2007/03/070309103157.htm This is exactly what the Theistic ID/Genetic Entropy position would have postulated! Whereas sub-species of sheep always have problems with inbreeding: Heredity - Diversity and evolution of the Mhc-DRB1 gene in the two … Low levels of genetic variation were detected in both subspecies, ….. Is the decline of desert bighorn sheep from infectious disease the result of low MHC … http://www.nature.com/hdy/journal/v99/n4/full/6801016a.html Thus conforming to Genetic Entropy. AS well I wanted to point out that evolution has no foundational principles of science on which to lay its assertions (Indeed it has to pollute the second law to the nth degree and blatantly ignore everything that is known about information theory1)! Whereas ID/Genetic Entropy can rest its assertions directly on the foundations of the second law of thermodynamics as well as the law of conservation of information (Dembski; Gitt)! That is why I (and every other IDer who is worth his salt) will always press you for experimental proof of generation of CSI, for it is proven impossible for totally material processes to generate CSI in this universe…and thus you will always fail to provide substantial proof that will not fall apart upon examination! If you are trying to prove evolution true, You will always be trying to prove something akin to the perpetual motion machine or the philosopher's stone…the simple fact is you will never do it! You just don't have, nor will you ever have, the physical evidence to conclusively prove your theory, for lo and behold Prof. Macneill, THERE REALLY IS A GOD AND YOU AIN'T HIM! (Neither am I for that matter!) "Perhaps the most obvious challenge is to demonstrate evolution empirically. There are, arguably, some 2 to 10 million species on earth. The fossil record shows that most species survive somewhere between 3 and 5 million years. In that case, we ought to be seeing small but significant numbers of originations (new species) ... every decade." Keith Stewart Thomson, Professor of Biology and Dean of the Graduate School, Yale University (Nov. -Dec. American Scientist, 1997 pg. 516) "The extreme rarity of transitional forms in the fossil record persists as the trade secret of paleontology." Stephen Jay Gould, Professor of Geology and Paleontology at Harvard University and the leading spokesman for evolutionary theory in America prior to his recent . “Almost without exception, bacteria isolated from ancient material have proven to closely resemble modern bacteria at both morphological and molecular levels.” Heather Maughan*, C. William Birky Jr., Wayne L. Nicholson, William D. Rosenzweig§ and Russell H. Vreeland ; (The Paradox of the "Ancient" Bacterium Which Contains "Modern" Protein-Coding Genes) http://mbe.oxfordjournals.org/cgi/content/full/19/9/1637 “Whatever we may try to do within a given species, we soon reach limits which we cannot break through. A wall exists on every side of each species. That wall is the DNA coding, which permits wide variety within it (within the gene pool, or the genotype of a species)—but no exit through that wall. Darwin's gradualism is bounded by internal constraints, beyond which selection is useless." R. Milner, Encyclopedia of Evolution (1990) "The new molecular based phylogeny has several important implications. Foremost among them is the disappearance of "intermediate" taxa between sponges, cnidarians, ctenophores, and the last common ancestor of bilaterians or "Urbilateria."...A corollary is that we have a major gap in the stem leading to the Urbilataria. We have lost the hope, so common in older evolutionary reasoning, of reconstructing the morphology of the "coelomate ancestor" through a scenario involving successive grades of increasing complexity based on the anatomy of extant "primitive" lineages." From an article published in the Proceedings of the National Academy of Sciences, USA, in 2000 In fact, it is commonly known that the further scientists deviate any particular bacteria type from its original state, the more unfit for survival the manipulated population will quickly become. As esteemed French scientist Pierre P. Grasse has stated “What is the use of their unceasing mutations, if they do not change? In sum, the mutations of bacteria and viruses are merely hereditary fluctuations around a median position; a swing to the right, a swing to the left, but no final evolutionary effect.” On and on and on I could go Prof. Macneill, but this is science we are talking about is it not,,,,now I grant you are quite the wordsmith but there comes a time, and the time is now to put your conclusive proof on the table! How about just showing us one species to come along since man suddenly appeared in the fossil record, that does not include trivial reproductive isolation that can be traced back to genetic entropy? How about showing us just on micro-organism that has been transmuted "evolved" into any other type of micro-organism? Is that to hard Prof. Macneill? OK, this one is real easy, how about showing us the peer reviewed work in which more than 2 protein/protein binding sites are generated by purely material processes, thus violating Dr. Behe's limit? I'm sure your a smart man from reading your post, but as honest as I can be I tell you the truth, YOU HAVE BEEN SUCKED INTO A LIE WITH EVOLUTION!!!! bornagain77

getawitness, I greatly appreciate Dr. MacNeill's knowledge and read his post here eagerly and only lament they are too infrequent. He is a fount of information and is certainly aware of what is current in evolutionary biology as much as anyone in the country. That does not mean I agree with all he says. But as he answers our questions, we learn the edge of evolution in a different way than Michael Behe has outlined. I have not found anything he has said that undermines ID. He may disagree but as of yet I have not seen it. I just wish he would come here more often because he is so well regarded in his field. jerry

Dr. MacNeill, In your long post, #31, there is nothing in it relative to selection that is not basic. So there isn't anything to object to and most of us here will not object. It make common sense. As an aside, there tends to be an emphasis on traits where there is a distribution and not a on/off distribution. Height, beak size or other physical characteristics often appear in gradations when it is possible that some traits may exist or not exist in an organism. There is nothing here I object to and only wondered how it affected such traits and how many traits are like that. Natural selection and its different manifestations is really not of interest to me and a lot of ID because it is not the real issue. What really interests me is the source of variation and this seemed to get passed over in your discussion. What confused me is how you seem to blithely integrate the various types of selection with the origin of variation or how much variation can occur or will be allowed to occur. However, I do object to your brief discussion of macro evolution and whether it is controversial or not. It seems to imply that ID is not interested in things other than OOL issues which is not true. Macro evolution covers a lot of ground and I am not sure there is good evidence to support all of what is called macro evolution. For example, I would not call most IC systems macro evolution since a lot of it is pre Cambriian or only showed up in the Cambrian. I tend to refer to macro evolution as that which occurred after the Cambrian. After the Cambrian there is a lot of macro evolution which is purely speculation on how it occurred. Most of the debate in the popular press is how did one species arise from another species when there are substantial functional differences between them. This is the major league of macro evolution. How did insects, birds and bats get wings to fly, how did land creatures develop oxygen breathing systems or how did man get such a big brain and why such a long time for children to develop and where did consciousness come from. How did 4 chamber hearts and warm vs. cold blooded arise. How did birds develop their unique oxygen transport system. There is a lot more but this gets to the issue. There is lots of speculation but no evidence, only as series of "just so" stories. An occasional fossil is brought up to show the progression ignoring the fact that there had to be tens of thousands of other steps for these progressions of which only a handful have been found. There is another part of this discussion which I call macro-evolution light or the minors. This is how did a lot of the orders and families develop? For example, within Carnivora how did all the families arise? ID seldom cares about this area but evolutionary biology does. I don’t think ID would care much if someone showed how all the family canidae or felidae arose by gradualistic approaches but yet the evolutionary biologists would claim that would be a major verification of their theory. So I am not sure Behe or Dembski would buy your assessment of macro evolution and you conflate the macro evolution light with all macro evolution and in no way touch the systems that must have been present at origin of the phyla during the Cambrian. jerry

Therefore (and as we concluded last summer), the only real areas of dispute between evolutionary biologists and the major theorists and supporters of intelligent design is the origin of life from non-living material (“abiogenesis”) and the origin of a small number of complex biochemical mechanisms and pathways (including the bacterial flagellum, selected components of the vertebrate immune system, and the mammalian blood clotting cascade, to which Behe has now added the evolution of chloroquine resistance in Plasmodium falciparum).

#31 dodges the issues entirely by pretending we don't understand the subject matter and espousing on matters that have long been understood as uncontroversial. Did you really just say SMALL number of complex biochemical mechanisms and pathways? Those are just the highlights, chosen for their relative simplicity that allows us to discuss them without getting too lost in the details. If I remember aright Mike chose the flagellum not only because we--referring to all scientists again--understood it well but partially because it could be readily compared to common objects (outboard motors) for easier comprehension. Despite agreeing about universal common descent, I doubt Mike would agree with your overall characterization of the situation. One of the focuses for ID proponents has always been--even 10+ years ago--to find whether there is positive evidence for Darwinian mechanisms being capable of macroevolution to the extent that everything we see since the OOL was created without any directed design involved. That is nowhere near a "small" disagreement. That's a gaping hole in evolutionary biology that you're attempting to fill in with a shotgun filled with pebbles (the list of purported mechanisms). We're just seeking one example. Every time a Darwinist claims there is an example it's either a trivial example we would not disagree with in the first place or they're playing connect-the-dots by comparing various creatures and presuming the mechanism works...which is the point under contention in the first place! Yet most Darwinists will never admit that examples have never been observed but are instead inferred to be real. Let's get real. There are real issues that both Darwinism and ID have trouble with. I'd be lying if I said that the ID movement has all its ducks in a row. The relatively low amount of ID research is one of them. It's a real problem even if there are a real life reasons such as persecution and the need to maintain day jobs that usually don't provide the opportunity for ID research. But increasing the amount of ID research is fixable, given enough support. Before you disappeared from UD a while back I called upon you to actively support finding decent funding and resources for conducting further ID research. Are you going to do so? getawitness,

but at least people should stop making the accusation that you don’t know what you’re talking about

I doubt anyone is claiming MacNeill lacks knowledge on this subject. In fact, I personally am very thankful to him for declaring that Neo-Darwinism is largely dead and a new "modern synthesis" must be formed. The debate has been centered around old ideas in evolutionary biology for far too long. Anyway, the real reason the others are irritated is because he's not answering the truly pertinent questions (although perhaps he has discussed them elsewhere in a blog...or he's preparing a book). Patrick

correction: for "jeery" read "jerry." I wasn't playing with his name, promise. getawitness

Dr. MacNeill, That is a very helpful explanation. I'm not sure what to make of it all, but at least people should stop making the accusation that you don't know what you're talking about, that your terms are "gibberish" and your view "esoteric" (jeery), or that you "pick and choose" among selection types (bornagain77). Whatever the merits of your views, these accusations should be laid to rest. BA77, I have to ask: what's with all the commas,,,in your comments? getawitness

Michael Behe has done no original empirical research into the evolution of chloroquine resistance in Plasmodium falciparum. On the contrary, all he has done is speculate on how this might have come about, using empirical data gathered by other scientists, nearly all of them professionally trained in the dynamics and consequences of evolutionary theory. Until a practicing scientist actually proposes a testable hypothesis about some aspect of intelligent design, tests that hypothesis with actual field and/or laboratory research which s/he has carried out, has analyzed the results using generally accepted methods of statistical analysis, and published such results, intelligent design is not even a hypothesis (i.e. something than can be empirically tested). It's just speculation, and therefore doesn't even begin to approach the threshold of what counts as science. Allen_MacNeill

One of the basic principles of Darwinian evolutionary theory is that there must be sufficient inter-individual variation to allow for phenotypic change over time. Darwin himself pointed this out in the first chapter of the Origin of Species. This concept was further elaborated by Ronald Aylmer Fisher in his book, The Genetical Theory of Natural Selection, now considered to be one of the foundational texts for the neo-Darwinian synthesis of the 1930s and 40s. Fisher's "Fundamental Theorem of Natural Selection" is still considered to be the basis for all scientific explorations of adaptive evolution, which along with Sewall Wright's concept of genetic drift, Motoo Kimura's "Neutral Theory of Molecular Evolution", and Tomoko Ohta's "Nearly Neutral Theory of Molecular Evolution" form the basis of virtually all of current microevolutionary theory. Central to this concept is the observation that all naturally occurring populations exhibit what Fisher called continuous variation. That is, a range of variation in various traits that, when plotted in cartesian coordinates, approximates a normal distribution (i.e. a so-called "bell-shaped curve"). In a trait that exhibits continuous variation, most of the individuals exhibit the trait at a value reasonably close to the mean, with a relatively small number of individuals exhibiting relatively large or relatively small values for that triat. An example is height in humans, which is often illustrated in introductory biology texts with a group of students (or sometimes military cadets) arranged along a football sideline in order of height. There are a few very short and a few very tall people, but the vast majority form a bulge in the middle of the curve. Given a population that exhibits continuous variation for a trait, there are three different patterns of natural selection that can result: Stabilizing selection, in which individuals from both extreme "tails" of the normal distribution are not preserved over time (i.e. they do not have as many offspring that survive to reproduction), compared with those in the middle bulge of the curve. Under such conditions, the mean value for the trait does not change over time (hence the term "stabilizing selection"). In our example of height, stabilizing selection would be the result if individuals of average height had the most surviving and reproducing offspring (assuming that height is heritable from parents to offspring, of course). Directional selection, in which individuals from one (but not the other) extreme "tail" of the normal distribution are not preserved over time (i.e. they do not have as many offspring that survive to reproduction), compared with those in the middle bulge of the curve. Under such conditions, the mean value for the trait changes over time, shifting toward the tail of the curve that includes the surviving individuals (hence the term "directional selection"). Diversifying selection, in which individuals from the middle of the range (but not either extreme "tail") of the normal distribution are not preserved over time (i.e. they do not have as many offspring that survive to reproduction), compared with those at the extreme tails of the curve. Under such conditions, the mean value splits and becomes bimodal, with two new mean values increasing in frequency, and the old mean value disappearing. This process would eventually (depending on the intensity of selection) produce two phenotypically different populations where one had previously existed (hence the term "diversifying selection"). All three types of selection have been observed in nature. By far the most common type is stabilizing selection; that is, most populations appear to be in rough selective equilibrium within their environments, an outcome that was predicted by Eldredge and Gould in their 1972 paper on punctuated equilibrium. Directional selection has also been observed in nature, and is usually correlated with fairly dramatic changes in ecological conditions, such as major ecological disruption correlated with a mass extinction event. Directional selection has also been observed in nature; an example is bimodal divergence in mean beak in African seedcrackers (a finch-like bird), in which seedcrackers with small and large beaks have higher reproductive success than those with average sized beaks. And so, rather than being a “just-so story” that is finagled to fit the data, these three modes of natural selection, which were first outlined by Theodosious Dobzhansky (one of the founders of the neo-Darwinian evolutionary synthesis and a devout Eastern Orthodox Christian), comprise a comprehensive theory of natural selection that has been repeatedly verified by comparison with data collected in the field by evolutionary biologists and ecologists. Notice, please, that none of these types of selection contradict the others in any way. Indeed, they all depend on the same underlying process that Darwin proposed in 1859: unequal, non-random survival and reproduction among populations of living organisms having continuously variable, heritable traits. Notice also that the underlying source of new traits is the “engines of variation,” not natural selection, which merely preserves those traits that are carried by those individuals that survive and reproduce. Natural selection, as John Endler and Will Provine have repeatedly pointed out, is not itself a “mechanism,” it is an outcome of the operation of three “mechanisms:” • variation between individuals in populations • inheritance of such variations • reproduction which together have the effect of producing • non-random, unequal survival and reproduction which has the effect of producing • non-random preservation of particular individuals with particular heritable traits (i.e. adaptations). So well supported is the foregoing with repeated empirical field and laboratory research that even Michael Behe and William Dembski do not dispute any of it, as evidenced by the fact that they (like most creationists) accept microevolution (i.e. natural selection, sexual selection, and genetic drift) as a strongly supported theory. In my evolution/design seminar last summer, in which Hannah Maxson (founder of the the Cornell IDEA Club) was an invited co-presenter, every participant (i.e. both supporters of evolutionary biology and intelligent design) agreed that there was no rational dispute over the facts or theory of microevolution. Furthermore, Michael Behe (like all but one of our seminar participants) also publicly accepts that macroevolution (defined as the descent with modification of higher taxa from common ancestors) is strongly supported by multiple lines of empirical evidence. Therefore (and as we concluded last summer), the only real areas of dispute between evolutionary biologists and the major theorists and supporters of intelligent design is the origin of life from non-living material (“abiogenesis”) and the origin of a small number of complex biochemical mechanisms and pathways (including the bacterial flagellum, selected components of the vertebrate immune system, and the mammalian blood clotting cascade, to which Behe has now added the evolution of chloroquine resistance in Plasmodium falciparum). As anyone who has actually read the Origin of Species knows, this leaves absolutely all of Darwin’s original theory untouched and unchallenged, as Darwin never published any theory concerning the origin of life, nor the origin of any biochemical pathway. Furthermore, it leaves virtually all of evolutionary biology untouched, because evolutionary biology is about living organisms (i.e. not the origin of life). Quod erat disputandem? ********************************* Allen D. MacNeill, Senior Lecturer The Biology Learning Skills Center G-24 Stimson Hall, Cornell University Ithaca, New York 14853 ********************************* phone: 607-255-3357 (Allen's office) email: adm6@cornell.edu website: http://evolutionlist.blogspot.com/ ********************************* "I had at last got a theory by which to work" -The Autobiography of Charles Darwin ********************************* Allen_MacNeill

Has anyone found the primary paper yet? It would be good to look at the exact methods - at the moment were going on a description from Prof. Barkai to a Weizmann Institute PR person, to a ScienceDaily journalist. bFast "I am trying hard envision the inevitable “just so story” that fits this phenomenon into the RV*+NS hypothesis." Coming up - a “just so story” just for you. It looks like TATA sequences are not placed behind house-keeping genes. This maybe because TATA promoters induce gene expression in a pattern which is ineffective for the genes' physiological role (e.g. inducible to environmental stimuli rather than constant low level operation). House keeping genes are critical - hence subject to intense conservation. Genes which are involved in reacting to external stimuli - are subject to adaptation. TATA is therefore more commonly infront of genes undergoing adaptation. It is a correlation rather than a cause. Experiment: Put in or take out TATA promoters infront of genes in yeast, and see whether gene mutation rates change. If the hypothesis (aka just-so-story) is correct then we expect inserted-TATA sequences to be lost, and those that were deleted will probably mutate back. Selection for fitness is driving the position of TATAs, rather than the poition of TATAs driving adaptation. Cost: ~$30,000 I imagine the DI could stump up the cash for that? and I suspect they could find at least one motivated grad student who could do this type of work. Pantrog

Jerry, His theory is unfalsifiable ...period. Whereas the ID/Genetic Entropy are clearly falsifiable and fit the evidence to perfection from the preliminary evidence I have gathered,,,In fact if variability were seen to increase instead of decrease once the parent species has reached maximuim diversification then this would falisify the Genetic Entropy postulation of Sanford. What does the fossil evidence consistently show,,,. 1. Abrupt Appearance 2. Rapid diversification 3. Long term Stability with no new variability introduced. 4. Loss of specific variability within sub-species types as well as loss of actual number of sub-species to gradual extinction of (most?) all sub species. This is a perfect conformation to ID/Genetic Entropy hypothesis to its foundational principles(Concervation of Information married to Second Law), Yet evolution cannot explain this to its foundation principles, even though Professor MacNeill obfuscates to the nth degree and pretends it does. bornagain77

Allen MacNeill want to be the one to have developed the new "punk eek." Or rather how punk eek really works and then put himself alongside Gould and Eldredge or maybe a little ahead of them. I have a little bit of trouble understanding all the gibberish about directional and stabilizing selection. Shouldn't a variation that is superior to the current stable genome always have a place at the table. After all it will start producing more offspring. And his engines are constantly churning out all these good variations amongst the bad so why should the superior variations be selected against. I am a little confused. Maybe it would be helpful to dissect MacNeill's speculations. They seem esoteric but are they really self contradictory. jerry

correction the statement in post should read: Let’s get this straight, natural selection does not drive evolution,,,when you don’t want it to (second statement),,,yet when you want it to (first statement), natural selection can not only be directional (when you want it to fit the evidence) it can also be stabilizing (when you want it to fit the evidence) bornagain77

Allen_MacNeill you state: "then stabilizing selection replaces directional selection" Yet in your blog you state: the primary "engine" of evolution has been considered to be natural selection. However, if one takes a closer look at this, it is clear that natural selection is not an "engine," it is an outcome. Let's get this straight, natural selection does not drive evolution,,,when you don't want it to (first statement),,,yet when you want it to (second statement), natural selection can not only be directional (when you want it to fit the evidence) it can also be stabilizing (when you want it to fit the evidence) Even if your highly unlikely niche theory were to be true, What in the world is going to tell the Random Variation part of your theory to stop searching variability within a species to fill any random niche that would happen along,,,This is absolutely ludicrous for you to pick and choose what parts of your highly flexible theory you want to operate when you want them to operate. Your theory is clearly an imaginary conjecture that has no foundation nor place in the scientific method! bornagain77

Allen_MacNeill (8): [T]his is relatively easily explained as a consequence of stabilizing selection.... [O]nce an evolving population reaches a state in which the mean phenotypic type has the highest relative fitness, then stabilizing selection replaces directional selection and the population stops changing significantly. This stasis then persists as long as the ecological niche of the stable population doesn’t change significantly. Under such conditions, any mechanism that might increase the stability of the evolved phenotype in a stable ecological niche would have a higher relative fitness than one that was continually producing new variations at a rate equivalent to that during the evolutionary transition to the new stable state. Therefore, modifications of the promoters to the genes undergoing selection would be selected for in organisms that have undergone one or more periods of evolutionary stasis... According to your hypothesis, the genes without the TATA sequence in their promoters correspond to those for traits that have undergone substantial directional selection and then required stabilization once a stable state was achieved. Presumably, since periods of stasis, followed by periods of change, have occurred repeatedly through time, the longevity of such genes will be fully variable. However, in the article, it's implied that the genes without the TATA sequence in their promoters correspond to those for traits that "fulfill some basic, universal function for all life, and changes in their sequences have drastic consequences, involving death or the inability to multiply" and therefore "have been conserved through long stretches of evolution". These are not the same thing. j

Professor MacNeill you stated: Is this version of macroevolutionary theory non-falsifiable? On the contrary, it could easily be falsified by showing (in the fossil record) that intra-taxonomic diversification increases steadily over deep evolutionary time. This finding would verify the gradual diversification that Eldredge and Gould called “phlogenetic gradualism” and falsify their alternative hypothesis of “punctuated equilibrium.” However, as more and more evidence has accumulated about the adaptive radiation of various taxa following major extinctions, it is clear that Eldredge and Gould’s has more empirical evidence supporting it. This is what I mean by unfalsifiable, to restate your very own words: "This finding would verify the gradual diversification that Eldredge and Gould called “phlogenetic gradualism” and falsify their alternative hypothesis of “punctuated equilibrium.” You are saying, "If we find variation through deep time for a branch of species (which we categorically don't) we have a evolutionary theory. Yet if we don't find a branch of species developing variability then we also have a (punctuated) evolutionary theory. Thus heads I win tails you lose! How in the world does this allow evolution to be falsified Professor MacNeill? My few words to you on the audacity of it all can barely contain my displeasure for how you mistreat the scientific method! bornagain77

Professor MacNeill While I have no desire to keep the thread off-track, I find it important to put in a corrective. For, you have unfortunately materially misrepresented Dr Gonzalez's academic record [he GREATLY exceeded the academic productivity requirements [68 papers (well beyond the 15 stipulated), providing the basis for discovery of two new planets, etc etc], and was in an environment where some 90% of applicants were granted tenure and one in which the man who led a wit^ch-hunt^ing campaign against him (and whose own academic track record has some very dubious "contributions" in it) was rewarded by the university], AND what has come out about why he was denied tenure. That those who support the denial of tenure cannot frankly face the evident and material facts that have manifestly come out -- including right here in this blog -- is all too telling. IDNet.Au and Patrick are right to highlight the NCSE's indefensible agenda: publish or perish, but if you publish we will persecute the Editor of the Journal [Rick Sternberg] and we will deny tenure [Gonzalez], or drive you out of "our" institutions [Dembski]. And, as a matter of fact, there is in spite of all this, a growing body of relevant empirical research, peer reviewed, peer edited, and more to the point, out there for us to look at and weigh up for our selves. (In a wit^ch-hunt^ing environment, so-called peer review rapidly becomes simply worthless as a criterion of excellence.) Behe's Edge of Evolution and the point it shows empirically on the limitations of random variation and natural [as opposed to artificial] selection to create complex novelty, is only the latest and in some ways the most telling. So, BA's point that the evidence strongly points to loss of variability and functionality through this process is relevant. So is the point highlighted by Meyer in that paper that cost Rick Sternberg so much to have the courage to publish:

. . . In order to explain the origin of the Cambrian animals, one must account not only for new proteins and cell types, but also for the origin of new body plans . . . Mutations in genes that are expressed late in the development of an organism will not affect the body plan. Mutations expressed early in development, however, could conceivably produce significant morphological change (Arthur 1997:21) . . . [but] processes of development are tightly integrated spatially and temporally such that changes early in development will require a host of other coordinated changes in separate but functionally interrelated developmental processes downstream. For this reason, mutations will be much more likely to be deadly if they disrupt a functionally deeply-embedded structure such as a spinal column than if they affect more isolated anatomical features such as fingers (Kauffman 1995:200) . . . McDonald notes that genes that are observed to vary within natural populations do not lead to major adaptive changes, while genes that could cause major changes--the very stuff of macroevolution--apparently do not vary. In other words, mutations of the kind that macroevolution doesn't need (namely, viable genetic mutations in DNA expressed late in development) do occur, but those that it does need (namely, beneficial body plan mutations expressed early in development) apparently don't occur.6

That is the challenge to be answered, and so far as I can see, it has not been answered -- apart from red herrings leading out to strawmen that have been burned to cloud and poison the atmosphere, and then are backed up by the appeal to the stick. FOR SHAME! GEM of TKI kairosfocus

Allen_MacNeill, thanks for the response, now to reiterate a question that is pertinent to this thread: Please list your source for CSI (complex specified information) generation i.e. What genetic mutational study lays the foundational framework for your latter assertions? i.e. Why should your any part of your hypothesis be considered viable, when you have no mutational study backing you up in the first place that says you can generate CSI in any genome? Now back to our discussion: Thanks also for listing the work of Niles Eldredge and Stephen Jay Gould. Now let's try to fit the unbiased evidence into the ID/Genetic Entropy framework, and see how much better of a fit we have than the evolutionary scenario does for it. First you state: the general pattern for the evolution of diversity (as shown by the fossil record) follows precisely this pattern: a burst of rapid diversity following a major ecological change, and then a gradual decline in diversity over relatively long periods of time. Thus the Theistic prediction for ID/Genetic Entropy finds validation in this work you cite. Now let's see if I got it right: A fossil (parent species) suddenly appears in the fossil record, with no solid evidence of transmutation from any other fossil form,,, "... Every paleontologist knows that most new species, genera, and families, and that nearly all categories above the level of family appear in the record suddenly and are not led up to by known, gradual, completely continuous transitional sequences.” George Gaylord Simpson (evolutionist), The Major Features of Evolution, New York, Columbia University Press, 1953 p. 360. What can be considered to be a parent species, then, rapidly diversifies while sub-species maintain basic morphological robustness of parent species (Am I correct so far?), Then, stability ensues for a while with no new variability ever being found ever again in the sub-species (correct?), Then over longer periods of time, the fossil diversity of sub-species (and even diversity within specific sub-species fossil types) shrinks until most all lineages of the parent species go into extinction. (Correct?). This fits perfectly with loss of Genetic Diversity studies (i.e. Genetic Entropy)! And is completely contrary to the evidence evolution absolutely needs to be considered viable! Evolution given long periods of time is losing diversity! It is not searching every nook and cranny for a new niche to fill! To drive the nail further in the coffin, preliminary genetic diversity studies are backing up ID? Genetic Entropy!: "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." 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. Also, In this study for ancient Australian (Mungo Man) DNA we have clear evidence of Genetic Entropy being obeyed!: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=33358 Of special note: Adcock et al. (7) clearly demonstrate the actual extinction of an ancient mtDNA lineage belonging to an anatomically modern human, because this lineage is not found in living Australians. Although the fossil evidence provides evidence of the continuity of modern humans over the past 60,000 years, the ancient mtDNA clearly does not, providing an excellent example of why the history of any particular locus or DNA sequence does not necessarily represent the history of a population. Adcock et al.’s (7 As well, Here is a Paper that has confirmation of dogs and grey wolves staying within principle of Genetic Entropy. http://jhered.oxfordjournals.org/cgi/reprint/90/1/71.pdf of special note: Some sequences found in dogs were identical to those in wolves… The sequence divergence within (breeds of) dogs was surprisingly large: the mean sequence divergence in dogs 2.06 + or - 0.07% was almost identical to the 2.10 + or - 0.04% (sequence divergence) found within wolves. (notice that sequence divergence is slightly smaller for dogs than for wolves) Coupled with the diverse morphology of domesticated dogs and known hazards of dog breeding, this evidence strongly indicates “front loaded adaptations” at a loss of information from parent species. Thus, this is genetic confirmation of the principle of Genetic Entropy for dogs from wolves! This overall pattern of evidence (morphology and genetic diversity) conforms strongly to the evidence supporting the principle of Genetic Entropy found for humans. These following genetic studies of sheep are interesting: Single male and female sheep maintain genetic diversity. A mouflon (The parent sheep population) population, bred over dozens of generations from a single male and female pair transplanted to Haute Island from a Parisian zoo, has maintained the genetic diversity of its founding parents. This finding challenges the widely accepted theory of genetic drift, which states the genetic diversity of an inbred population will decrease over time. "What is amazing is that s of genetic drift predict the genetic diversity of these animals should have been lost over time, but we've found that it has been maintained," said Dr. David Coltman, an evolutionary geneticist at the University of Alberta. http://www.sciencedaily.com/releases/2007/03/070309103157.htm This is exactly what the Theistic ID position would have postulated! Whereas sub-species of sheep always have problems with inbreeding: Heredity - Diversity and evolution of the Mhc-DRB1 gene in the two ... Low levels of genetic variation were detected in both subspecies, ..... Is the decline of desert bighorn sheep from infectious disease the result of low MHC ... www.nature.com/hdy/journal/v99/n4/full/6801016a.html Thus conforming to Genetic Entropy. AS well I wanted to point out that evolution has no foundational princip[les of science in which to build its conjectures! Whereas Genetic Entropy can rest its conjectures on the foundation of the second law of thermodynamics as well as the law of conservation of information! That is why I will always press you for experimental proof of generation of CSI, for it is impossible for totally material processes to generate CSI in this universe... If you are trying to prove evolution true, You will always be trying to prove something akin to the perpetual motion machine...the simple fact is you will never do it! bornagain77

This thread seems to have wandered badly off of its initial track. I am finding the orignal report to be intriguing. I am trying hard envision the inevitable "just so story" that fits this phenomenon into the RV*+NS hypothesis. *Where a some of the sources and characteristics of variation are so aptly provided by Dr. MacNeill (see link in #8 above.) bFast

Having participated in tenure decisions on numerous occasions over the past thirty years (including my own, of course), I can honestly say that what makes the difference is – surprise! – money (and to a lesser extent, "collegiality"). If Gonzales had published major papers in the peer-reviewed journals in his field, brought in major grant money to his university, had trained and graduated a growing cadre of graduate students, and had actively participated in the advancement and management of his department, he almost certainly would have been granted tenure. That's precisely what the public record shows he did not do, and that squares with my experience in academia. Allen_MacNeill

In response to comment #16 by bornagain77: As Niles Eldredge and Stephen Jay Gould pointed out almost three decades ago, the general pattern for the evolution of diversity (as shown by the fossil record) follows precisely this pattern: a burst of rapid diversity following a major ecological change, and then a gradual decline in diversity over relatively long periods of time. This is clearly the case among east African cichlid fish, such as those in Lake Malawi and Lake Victoria. As numerous studies have pointed out, Lake Victoria is only a little over 12,000 years old, while Lake Malawi is approximately 1.5 million years old. Lake Victoria has (or had, until the introduction of the Nile perch) over 600 species of cichlids, while Lake Malawi has many, many fewer (the exact numbers are not known, due to rapid species turnover and the difficulty of sampling fish species in these lakes). In other words, the older the lake, the lower the species diversity. This general pattern is also observable among the arthropod phyla in the "Cambrian explosion", the vertebrate tetrapod taxa following the Permian-Triassic mass extinction, and the mammalian phyla following the Cretaceous-Teritary mass extinction. This is precisely what macroevolutionary theory predicts: adaptive radiation, followed by species "pruning", caused mostly by increasing niche specialization and the squeezing out of marginally adaptive taxa. Over deep evolutionary time, however, species diversity has shown a steady increase: there are more species of animals alive today than at any time in the preceding 600 million years. That is, although species diversity declines within taxa, the overall number of higher taxa increases over time. This is because macroevolution includes a kind of "rachet": mass extinctions rarely if even eliminate an entire set of higher taxa. Even the Permian-Triassic mass extinction didn't kill all of the multicellular organisms on Earth (only about 99% of them). And then, as the surviving taxa rapidly diversified into the now-vacant adaptive zones, the new taxa were added to the survivors. Is this version of macroevolutionary theory non-falsifiable? On the contrary, it could easily be falsified by showing (in the fossil record) that intra-taxonomic diversification increases steadily over deep evolutionary time. This finding would verify the gradual diversification model that Eldredge and Gould called "phlogenetic gradualism" and falsify their alternative hypothesis of "punctuated equilibrium." However, as more and more evidence has accumulated about the adaptive radiation of various taxa following major extinctions, it is clear that Eldredge and Gould's model has more empirical evidence supporting it. Now, just how much empirical evidence has ID going for it? The only published books and papers that I'm aware of (and I've read almost all of them, and assigned them as required reading in my evolution/design seminar last summer) are theoretical models and alternative interpretations of already existing evidence, virtually all of it collected and published by evolutionary biologists. Until IDers start doing actual empirical science of their own, their "theories" will remain untested hypotheses, and their ideas will consist virtually entirely of airy speculation. Want to have your ideas respected by other scientists? Get your hands dirty... Allen_MacNeill

Adam Rutherford, (the "impartial" reviewer of the NOVA PBS production "Judgement Day" in Nature http://www.nature.com/nature/journal/v450/n7167/full/450170a.html ), can perhaps help enlighten us on why not much overt ID research gets done in our universities. "Guillermo Gonzalez has been denied a physics post by his university. Quite right: you cannot believe in ID and call yourself a scientist. So farewell, I hope, to the scientific career of Guillermo Gonzalez. ... I know that, were I in a position to offer Guillermo Gonzalez tenure, I would deny it for the precise reason that his, yes, religious views about purpose in the universe explicitly mean he is a crap scientist, regardless of his ability to generate valid data. ... As a vocal supporter of the demonstrably unscientific guff that is intelligent design, Gonzalez displays ignorance of the scientific process, and appears to wilfully [sic] defy it. And for that reason, he neither deserves the use of the facilities of a university to conduct scientific research, nor the privilege of teaching the next generation of scientists." http://commentisfree.guardian.co.uk/adam_rutherford/2007/07/wrong_by_design.html idnet.com.au

Who is the “we” that Patrick refers to?

I was referring to all scientists, whatever their personal stance on this issue may be. Personally I'd love to see Darwinists and ID proponents working together. The major problem is procuring funding. I hate to see it when Darwinists are demanding that ID proponents produce more research and then at the same time advocating closing any potential avenues for this research to take place. If they want to be consistent and if they take these questions seriously they should be helping ID proponents receive a decent level of funding even if they do believe in general that ID is a waste of time. At the very least these research projects may discover the limitations of certain mechanisms and in the process discover information that could advance medical technology. Who knows, maybe it would be an ID proponent who does the actual gruntwork and manages to find positive evidence for some Darwinian mechanisms being capable of producing CSI. Patrick

Allen_MacNeill you stated: However, the only way to answer this question is to do the relevant empirical research, testing falsifiable hypotheses that distinguish clearly between the two. So far this has not been done, especially by IDers. I take issue with that statement. Since Patrick already pointed to Dr. Behe's work, in which malaria was subjected to extreme pressure to evolve complexity and failed to generate even one novel protein/protein binding site. I will refer you to my post on #7, it is one of many studies verifying the principle of Genetic Entropy (the marriage of the second law with conservation of information) (The exact opposite of the evolutionary theory). This study is unique in that it clearly demonstrates loss of variability over approximately 250 million years for trilobites: I maintain that over 250 million years severe environmental pressure would have been introduced at some time for the trilobites to evolve more complexity not less! Thus your assertions are found wanting in only this first study I've collected for long time span analysis of a species! http://www.terradaily.com/reports/The_Cambrian_Many_Forms_999.html Of special note: So for his Science study, Webster combed through 68 previously published studies of trilobites, searching for descriptions of evolving characteristics that could be incorporated into his analysis. After eliminating studies that were inappropriate for inclusion, 49 still remained. He focused on actively evolving characteristics. The trilobite head alone, for example, displays many such characteristics. These include differences in ornamentation, number and placement of spines, and the shape of head segments. His findings: Overall, approximately 35 percent of the 982 trilobite species exhibited some variation in some aspect of their appearance that was evolving. But more than 70 percent of early and middle Cambrian species exhibited variation, while only 13 percent of later trilobite species did so. “There’s hardly any variation in the post-Cambrian,” he said. “Even the presence or absence or the kind of ornamentation on the head shield varies within these Cambrian trilobites and doesn’t vary in the post-Cambrian trilobites.” Allen_MacNeill, what do you want to bet that every long term analysis of a species I can get my hands on will fall into this loss of variability category, thus conforming to Genetic Entropy,,,,Thus, I am making a clear prediction that can clearly be falsified,,,Indeed if variability is found to increase over long periods of time in the fossil record then Genetic Entropy will be tentatively falsified...That is a lot more than I can say for evolution for, from what I've seen, evolution can never be falsified! bornagain77

Hi, I'm new here, and I find the information very enlightening. I've been confused a bit by one thing that Patrick brings up in #14 above, namely his statement that "...we should continue researching." While a believer myself, and being a strong adherent to the design inference, I'm troubled by what seems to be a dearth of actual research on the part of ID advocates. Who is the "we" that Patrick refers to? Stanton Rockwell

Do the currently identified mechanisms of genetic and phenotypic variation produce enough variation to get from there to here or not? the only way to answer this question is to do the relevant empirical research, testing falsifiable hypotheses that distinguish clearly between the two. So far this has not been done, especially by IDers.

I was under the impression that Behe's EoE was intended to analyze this exact question. My understanding is that, no, we do not have positive evidence these mechanisms are capable to the extent required for them to be responsible for everything since OOL but at the same time we should continue researching. Patrick

In case some of your readers might be interested in more on this topic, here is a link to a discussion of it on my blog. In that blogpost, I ask the following question: • Is the rate of generation of genetic and phenotypic variation a constant? I then point out that if the answer is "no," then a new question immediately follows: • Is the increased rate of generation of variations correlated with any identifiable factor in either the genetics/development or the environment of organisms in which such variable rates of variation are observed? If the answer to this question is "no," then we may safely assume that the underlying "engines of variation" are probably random, insofar as we can observe phenotypes changing randomly over time. However, if the answer is "yes" (and the research report that is the sutbject of this blogpost strongly suggests that it is), then this suggests another question: • Via what mechanism(s) is the increased rate of variation generated, and are the "triggers" for such increased variation endogenous, exogenous, or some combination of the two? According to the article, the answer is (not surprisingly) a combination of the two. That is, the TATA box provides a switch that responds to a signal from the environment; • If the environment is becoming more variable, the switch throttles up the rate of production of variation • If the environment is becoming more stable, the switch throttles down the rate of production of variation If evolutionary theory is a reasonable explanation for the origin of biological diversity, then the "engines of variation" are prodigious, as they have been able over time to modify something as simple as a mycoplasm into an oak tree or a blue whale. Some supporters of "intelligent design" (ID) would dispute this statement, of course, claiming (without any empirical evidence) that "you can't get here from there." However, as Michael Behe, MikeGene, and other ID supporters have clearly asserted, we have gotten here from there; the real question is "how?" There are logically at least two possibilities: • The processes by which the "engines of variation" have produced the necessary variation have operated endogenously by means of a prodigious (and undirected) "random variation generator," the products of which have been sorted over time by natural selection (i.e. the Darwinian hypothesis) or • The processed by which the "engines of variation" have produced the necessary variation have operated endogenously by means of a series of equally prodigious "non-random variation generators," the products of which have been sorted over time by natural selection (i.e. the ID hypothesis). Notice that in both cases, natural selection is what finally determines what exists and what doesn't. The intelligent designer of ID theory, in other words, works virtually exclusively through modification of variation, allowing natural selection to preserve those variations that it has intelligently designed. Noticing that the only difference between these two possibilities is the amount of variation and its source also immediately suggests a way of testing the two hypotheses: • Do the currently identified mechanisms of genetic and phenotypic variation produce enough variation to get from there to here or not? If the answer is "yes," then the ID hypothesis is unnecessary, and therefore irrelevent to science. If the answer is "no", then ID may have something very significant to contribute to science. However, the only way to answer this question is to do the relevant empirical research, testing falsifiable hypotheses that distinguish clearly between the two. So far this has not been done, especially by IDers. Therefore, it is clearly not yet time for either side to declare that this is a settled question. To declare otherwise is not science but propaganda. –Allen ********************************* Allen D. MacNeill, Senior Lecturer The Biology Learning Skills Center G-24 Stimson Hall, Cornell University Ithaca, New York 14853 ********************************* phone: 607-255-3357 (Allen’s office) email: adm6@cornell.edu website: http://evolutionlist.blogspot.com/ ********************************* “I had at last got a theory by which to work” -The Autobiography of Charles Darwin ********************************* Allen_MacNeill

"You don’t seem to get it even though people keeping correcting you…universal common descent does not add even one dark speck to “All complex biological systems are generated by intelligent agents.”" Feel free to pop back to the P.falciparum thread to discuss it. I'm just pointing out that comparison between closely related species of Plasmodium suggests hundreds of genes have appeared since divergence, with complex new functions associated with the genes. But this information (and the TATA stuff) is only valid if common descent is accepted. Pantrog

Allen_MacNeill, Please list your source for CSI (complex specified information) generation i.e. What genetic mutational study lays the foundational framework for your latter assertions? i.e. Why should your your hypothesis be considered viable as far as generating the required information (CSI) it absolutely needs exactly when it needs to when all mutational studies, I know of, rule out your scenario from first principles even in the most favorable of circumstances? bornagain77

This assumes common descent (…apply that approach to Plasmoidum vivax and Plasmodium falciparum - and one gets a few dark grey swans).

You don't seem to get it even though people keeping correcting you...universal common descent does not add even one dark speck to "All complex biological systems are generated by intelligent agents." Also:

I think a lot of folks get confused because they think that all events have to be assigned en masse to either the category of chance or to that of design. I disagree. We live in a universe containing both real chance and real design. Chance events do happen (and can be useful historical markers of common descent), but they don’t explain the background elegance and functional complexity of nature. That required design.

Patrick

I note from the rest of the article that Prof. Barkai is studying evolutionary events (such as genome doubling) by comparisons between distantly related species. This assumes common descent (...apply that approach to Plasmoidum vivax and Plasmodium falciparum - and one gets a few dark grey swans). The other key point is causality - there's an association between TATA binding sites in promoters and conservation of the gene, but does this just reflect the physiological role of TATA binding sites - e.g. not being infront of house-keeping genes and therefore not subject to purifying selection i.e. the presense of TATA is an epiphenomenon, rather than a cue for non-conservation. Thirdly this finding is associated with conservation (or not) of expressed genes - rather than a mechanism to conserve unused front-loaded information. Pantrog

Hi, Dave: As I pointed out on my own blog, this is relatively easily explained as a consequence of stabilizing selection. During a transition from one stable phenotype to another, the "engines of variation" (listed here) produce a population of individuals with a range of modified phenotypes, some of which survive and reproduce more often than others. The preservation and resulting increase in frequency of such modified individuals over time constitutes directional selection. However, once an evolving population reaches a state in which the mean phenotypic type has the highest relative fitness, then stabilizing selection replaces directional selection and the population stops changing significantly. This stasis then persists as long as the ecological niche of the stable population doesn't change significantly. Under such conditions, any mechanism that might increase the stability of the evolved phenotype in a stable ecological niche would have a higher relative fitness than one that was continually producing new variations at a rate equivalent to that during the evolutionary transition to the new stable state. Therefore, modifications of the promoters to the genes undergoing selection would be selected for in organisms that have undergone one or more periods of evolutionary stasis (as defined by Eldredge and Gould). Indeed, this finding strongly suggests that the "engines of variation" that I listed in my own blog have a throttle: that is, the amount of variation that can be produced in any given gene is not fixed (i.e. it is not really "random"), but rather can increase or decrease as the result of selection. This possibility presents the very exciting possibility that we will be able to explain the apparent bursts of variation that accompany major ecological changes, such as the major adaptive radiations that have accompanied the five major mass extinctions on Earth. Far from being a problem for evolutionary biology, this finding is in fact a potentially major advance in our understanding of what G. G. Simpson called "tempo and mode" in evolution. Allen_MacNeill

DaveScot off topic sort of: In regards to verifying Genetic Entropy, I found this research interesting: http://www.terradaily.com/reports/The_Cambrian_Many_Forms_999.html of special note: "That led me into thinking there's something weird about these very primitive Cambrian trilobites that you don't see in other (more recent) ones," he said. The only way to verify his hunch was to conduct an analysis that combined the data compiled in previously published reports. "It's too much for one person to look at a thousand trilobite species," Webster said. So for his Science study, Webster combed through 68 previously published studies of trilobites, searching for descriptions of evolving characteristics that could be incorporated into his analysis. After eliminating studies that were inappropriate for inclusion, 49 still remained. He focused on actively evolving characteristics. The trilobite head alone, for example, displays many such characteristics. These include differences in ornamentation, number and placement of spines, and the shape of head segments. His findings: Overall, approximately 35 percent of the 982 trilobite species exhibited some variation in some aspect of their appearance that was evolving. But more than 70 percent of early and middle Cambrian species exhibited variation, while only 13 percent of later trilobite species did so. "There's hardly any variation in the post-Cambrian," he said. "Even the presence or absence or the kind of ornamentation on the head shield varies within these Cambrian trilobites and doesn't vary in the post-Cambrian trilobites." Paleontologists have proposed two ideas to account for why variation within species declined through time. One is ecological. In the very early Cambrian seas, fewer organisms existed than today, which meant that they faced less competition for food. "You didn't really have to be tightly specialized to make a living in the Cambrian," Webster said. But as evolution gave rise to more varieties of organisms, ecological communities became more diverse. "You had to be very fine-tuned to your particular niche to make a living and to beat out competitors for a limited resource." The genomic hypothesis offers a second explanation for the decline of within-species variation over time. According to this idea, internal processes in the organism were the key factors. Various developmental processes interact with one another to control the growth and formation of body parts as any organism progresses from egg to . "It's been suggested that early on in evolutionary history, in the Cambrian Period, the degree to which these different developmental processes interacted with each other within the organism was a lot less," Webster said. "As a result, the constraints on what the final organism looked like were relatively low." Well Dave, what do you think? I bet this pattern will hold across the board for all species that have exceeding long spans in the fossil record, and I also think it is directly attributable to loss of genetic diversity and clearly conforming to the principle of Genetic Entropy. It is the most reasonable explanation. When I think about no matter how they dress it up it is in direct opposition to what evolutionary theory would predict...i.e. We see a culling of variety, not a searching for new pathways to take advantage of! bornagain77

This has deep implications for genetic entropy as well. If the core code of an organism is protected then the rest can carry a high mutation load. There's also an opportunity for a "reboot" if things get bad - the genome can be cleaned up and restored to a previously known working state. Stuff like this is hard to anticipate or imagine under the rubric of blind evolution but not so for intelligent design. Researchers wouldn't keep being so surprised by what they find if they just bit the bullet and worked under the assumption that life is here by design not by chance. DaveScot

(Slightly) off topic. Speaking about Specified Complexity, I just saw this remarkable documentary: "Rivers and Tides" (links at bottom). It is about artist Andy Goldsworthy who creates art works in nature using natural materials. For example, he might create a work in the forest using leaves. For this reason, his works are often (but not always) transient. What got my brain it a twist is that you could be walking in the forest, see a "thing" made out of the same things that the rest of the forest was made out of, but be able to immediately recognize it as "art": it had specified complexity whereas the rest of the forest does not (or at least has a different kind of specified complexity). It is reminiscent of the Mount Rushmore example, But that example only makes sense if you know what a human face looks like. That requirement is removed when viewing Andy Goldsworthy's art. You would say that it is both in nature and of nature. But it is not natural. It uses a more abstract level of specificity than, say, Mount Rushmore. I would heartily invite anyone who is thinking deeply about specified complexity to view this film. I think it will give you a whole new perspective. Here are some links: http://www.imdb.com/title/tt0307385/ http://www.amazon.com/Andy-Goldsworthys-Rivers-Tides-Goldsworthy/dp/B0002JL9N6 http://www.netflix.com/Movie/Rivers_and_Tides/60027273 EndoplasmicMessenger

DaveScot in regards to this, 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. Seems to me there is a huge amount of "insider trading" going on in the Genome in this scenario, as far as future information is concerned that would be of benefit to future life forms. And that's illegal in science as well as on Wall Street! bornagain77

You need this unprecedented level of protection against mutation in deep time. That is untill you realize that "deep time" is another one of the stories that was necessary for the Darwinists story to have any plausibility. Latemarch

It's surprising that this is not presented as a challenge to Darwinism in the article. Somebody has to do the marking; somebody has to say to this gene, "you need some bodacious TATAs." :-) getawitness

This is also yet another level of unexpected specified complexity to be explained. It is clear that random mutation is not as random as we thought. Why is this so? I do not think, in the standard model of evolution, the important genes need to be marked as important. Would it not be OK for natural selection to do the work of preserving the important genes? Even if they do need to be marked, who is there to mark them? No designer allowed, where does the marking come from? idnet.com.au