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Future Risk Assessment in the Genome

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

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

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

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

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

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

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

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

Read the rest of the article at the source here

Comments
I guess I'm on the modpile, unless something's wrong with my machine. Oh well. Forgive the multiple submissions of one comment.getawitness
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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Whoops! Reverse the terms in what I wrote above. In other words, 1 million: 1 is their estimate of total mutations:beneficial mutations.getawitness
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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"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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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correction: for "jeery" read "jerry." I wasn't playing with his name, promise.getawitness
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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
November 10, 2007
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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 TKIkairosfocus
November 9, 2007
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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
November 9, 2007
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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
November 9, 2007
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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
November 9, 2007
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