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Microbe evolution virtually finished 2.5by ago

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With all the major evolution done so early, microbe evolution has been retired for a very long time. No wonder we can’t evolve new pathways in the lab!

From ScienceDaily

New research shows that for microbes, large-scale evolution was completed 2.5 billion years ago.

“For microbes, it appears that almost all of their major evolution took place before we have any record of them, way back in the dark mists of prehistory,” said Roger Buick, a University of Washington paleontologist and astrobiologist.

All living organisms need nitrogen, a basic component of amino acids and proteins. But for atmospheric nitrogen to be usable, it must be “fixed,” or converted to a biologically useful form. Some microbes turn atmospheric nitrogen into ammonia, a form in which the nitrogen can be easily absorbed by other organisms.

About 2.5 billion years ago some microbes evolved that could add oxygen to ammonia to produce nitrate. These microbes are on the last, or terminal, branches of the bacteria and archaea domains of the so-called tree of life, and they are the only microbes capable of carrying out the step of adding oxygen to ammonia. This indicates that large-scale evolution of bacteria and archaea was complete about 2.5 billion years ago, Buick said. “Countless bacteria and archaea species have evolved since then, but the major branches have held,”

“All microbes are amazing chemists compared to us.” Buick said.

Comments
A couple of comments on my last post. That should be while not why, and cop-out should have a strike through it. It showed up o.k. in the preview yet for some reason it didn't go through with the post. Oh well, no big deal.ShawnBoy
March 15, 2009
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What an absolutely phenomenal post by AussieID at #75. Bravo! The Ivy League professor's response? Pretend it never happened, copy and paste another questionable finding, and end his ranting with the child-like "I can do this all day". You're better than that Mr. MacNeill......I think. Darwinists, here's your problem - when you twist every finding in a way in which it's concluded to support Darwinism - even when it does not (Liars For Darwin) - it's not hard for the highly educated I.D. supporters to take you to school over it. Post #75 for example, or the majority of posts from DaveScot, BarryArrington, kairosfocus, and many, many more regular contributors here. Why I'm on the subject, why is it Darwin supporters are so reluctant to publicly debate IDists? The cop-out rational explanation I've seen most often is that they don't want the public to think there's a controversy. Here's my problem with that: according to a recent Gallup Poll, no less than 80% of the U.S. public supports I.D. (whether they know it or not) while just 14% agree with Darwinism. If you feel your argument is so strong that it's necessary to mercilessly insult anyone who disagrees with it, as Darwinists do, then surely you have enough confidence to publicly debate it, educate the "ignorant" public, and chip away at that 80%? I can't help but think there's another reason for your reluctance to publicly debate Darwinism vs I.D., and after studying said debate for the past year or so, I'm pretty sure I know what it is (think K.F.C.).ShawnBoy
March 15, 2009
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“…how can it be demonstrated that every mutation is an accident?”
There are several ways to do this. Probably the most effective way to do so is to compare the sequence in question with other sequences from organisms in which this sequences is either not present, or present in a different form. In almost all cases, such comparisons have shown that something like the “new” sequence (i.e. the mutation) is present in other organisms, but in a different form (i.e. some of the sequences are different):
But that doen't mean the new sequence occurred by accident.
• the mutant sequences have different bases in specific locations, which indicates that the mutation is a point mutation, such as a substitution, insertion, or deletion
OK I will grant that point mutations can be attributed to a genetic accident. But insertions and deletions are another matter.
• the mutant sequences are in a different order, indicating that the sequence was inverted during replication
Still doesn't make it an accident. I would expect individuals to be different because individuals are affected by different epigenetic events.
• the mutant sequences include relatively long sequences that can be correlated with similar sequences located elsewhere in the genome, indicating that retrotransposition, translocation, or viral transduction has taken place.
That still doesn't make it an accident. Dr. Spetner discussing transposons:
A transposon has in it sections of DNA that encode two of the enzymes it needs to carry out its job. The cell itself contributes the other necessary enzumes. The motion of these genetic elements to produce the above mutations has been found to a complex process and we probably haven’t yet discovered all the complexity. But because no one knows why they occur, many geneticists have assumed they occur only by chance. I find it hard to believe that a process as precise and well controlled as the transposition of genetic elements happens only by chance. Some scientists tend to call a mechanism random before we learn what it really does. If the source of the variation for evolution were point mutations, we could say the variation is random. But if the source of the variation is the complex process of transposition, then there is no justification for saying that evolution is based on random events.
And BTW the way evolutionary biologists define macro-evolution not even YECs dispute it. Also it carries an ambiguity- that of "species". 1- You are using something that NO ONE disputes to try to settle a dispute. 2- Even your use is ambiguous because "species" is ambiguous.Joseph
March 10, 2009
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Allen: I await your response to my post above [51].PaV
March 9, 2009
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Allen_MacNeill:
In almost all cases, such comparisons have shown that something like the “new” sequence (i.e. the mutation) is present in other organisms, but in a different form (i.e. some of the sequences are different)
Would you say that is also the same with the human HAR1F gene. It differs by a mere 18 nucleotides, but is mutated compared to the ultra-stability found in all other vertibrates. Experiments done with bacteria seem to support Behe's suggestion that even three simultaneous mutations simply won't happen by chance. Eighteen non-contiguous mutations is far more than chance can account for. The ultra-stability of the gene should be very strong evidence that any one point mutation will be deleterious.bFast
March 9, 2009
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"would you also please include the mechanisms by which the Intelligent Designer has brought about the examples that you have provided? Thank you!" Allen, I already answered this. Se #83 on synthetic biology. Allen, I have told you in #52, we are your choir. Nothing you present to us has ever undermined ID. And we continually thank you for your examples and references. The book by Vrba and Eldredge so far has supported ID even though it is on macro evolution because there is no hard evidence in it on how macro evolution took place, only speculation. The book by Jablonka and Lamb also heavily supported ID because they could not provide any information on macro evolution either. Lots of stuff on micro evolution and it was good stuff. So we thank you for all these references supporting ID. Every time you fail to provide empirical evidence for macro evolution (what we call macro evolution or call it mega evolution if you wish) it is support for ID. The logic is inescapable. Either a study supports ID, is neutral to ID, or undermines ID. So far all of your examples have been the first two and mostly the first. The one above by Brookfield supports ID.jerry
March 9, 2009
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In #88 Joseph asked: "...how can it be demonstrated that every mutation is an accident?" There are several ways to do this. Probably the most effective way to do so is to compare the sequence in question with other sequences from organisms in which this sequences is either not present, or present in a different form. In almost all cases, such comparisons have shown that something like the "new" sequence (i.e. the mutation) is present in other organisms, but in a different form (i.e. some of the sequences are different): • the mutant sequences have different bases in specific locations, which indicates that the mutation is a point mutation, such as a substitution, insertion, or deletion • the mutant sequences are in a different order, indicating that the sequence was inverted during replication • the mutant sequences include relatively long sequences that can be correlated with similar sequences located elsewhere in the genome, indicating that retrotransposition, translocation, or viral transduction has taken place. All of these can be verified using statistical analysis, as developed by evolutionary geneticists over the past few decades. If you are interested, I could provide some references to textbooks in which these methods are explained and their uses (including their advantages and shortcomings) are discussed.Allen_MacNeill
March 9, 2009
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In #87 aussieD wrote:
"Evolutionary theory claims that life arose by a process which is ultimately creative, and virtually without limits."
The first half of this assertion is correct, but the second half is not. On the contrary, evolutionary theory is quite clear that there are multiple limits on what can be accomplished via the various mechanisms that produce phenotypic change. Indeed, this is the crux of the argument that evolution (and especially macroevolution) is an historically contingent process. There are many examples in evolutionary biology of cases in which "you can't get there from here". That is, the particular genetic and/or phenotypic resources of a population do not include a characteristic that would allow for the exploitation of a new adaptive zone, so that no matter how beneficial a particular change might be, it simply doesn't happen. This is clearly the case with the example you cited of Drosophila birchii. Indeed, the example you chose illustrates the point I just made quite well (and undermines yours). As you pointed out,
"...the Drosophila flies from intermediate (less humid) environments, D. melanogaster, D. simulans, and D. serrata, still contain sufficient genetic variation to enable the population to adapt to drier conditions."
Exactly; these three species had evolved in environments in which dessication stress was a periodic threat, and so they had either gained or retained the genetic ability to respond to it. This was not the case with Drosophila birchii, which either lost the ability to do so, or never had it to begin with (without a complete scan of its genome, it would be difficult if not impossible to say which). And so, faced with the validity of my example in response to your question (and recognizing that your own examples provide even more evidence for precisely the point I was making), you (like jerry) switch questions on the fly. Now the question is not "can natural selection (a microevolutionary process) produce new genetic information?" The answer, for which you have yourself provided evidence, is "yes". So, having given up that point, you switch to a completely different question: "Okay, so microevolution can produce new genetic information (and new phenotypic adaptations to environmental stresses, as pointed out in your examples). It still can't produce macroevolutionary changes." Note that this is an assertion, not an argument. You have presented no evidence that macroevolution can't do this, nor have you presented evidence in support of an alternative explanation for macroevolution, nor have you attempted to provide any plausible (and empirically testable) mechanism by which this can occur. Rather than repost the same examples and evidence over and over again, I simply refer you to the link posted in comment #89, above. And, like jerry, would you be so kind as to provide us with examples of macroevolution that are unambiguously the result of “intelligent design”? And, so that we can all see the differences between what scientists do and what “intelligent design theorists” do, would you also please include the mechanisms by which the Intelligent Designer has brought about the examples that you have provided? Thank you!Allen_MacNeill
March 9, 2009
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In #85 jerry wrote:
"Remember we do not deny these changes take place and sometimes have some beneficial effects."
If "we" includes aussieD, then yes, you do. I was specifically asked to present evidence that natural selection (which, as I have pointed out, includes the various "engines of variation") can produce new genetic information. I did so, and apparently did so conclusively, as your tactic was to change the subject to macroevolution. On that subject, let me refer you to a recent post at my blog: http://evolutionlist.blogspot.com/2009/02/macroevolution-examples-and-evidence.html In it, I provide exactly what you are asking for: examples and mechanisms of macroevolution, as discovered and elucidated by evolutionary biologists. And yes, I use the definition of "macroevolution" used by scientists who do the research. So, please provide me with examples and macroevolution via "intelligent design", and so that we can all see the differences between what scientists do and what "intelligent design theorists" do, please include the mechanisms by which the Intelligent Designer has brought about the examples that you have provided. That way we can "play by the rules of science" in which evidence for mechanisms is part of the argument, rather than arguing via unsupported assertion.Allen_MacNeill
March 9, 2009
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The mechanism the designer may have used is spelled out in "Not By Chance" by Dr Lee Spetner: "Built-in responses to environmental cues". And as I have already stated the only way to demonstrate that is by actually learning to read the genetic programs. However to date the only genetic program readers are the organisms we observe. And exactly how is saying "genetic accident" in any way scientific? IOW how can it be demonstrated tat every mutation is an accident? That is besides our ignorance...Joseph
March 9, 2009
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Allen, "I can keep this up all day ..." ... and you do: without being able to give a real response to the question of 'new information'. Finding articles to support your 'idea' but that don't support the facts isn't what you need to show. Repeat to Allen ad nauseum: “Natural selection, though, adds no information.” Elephant hurling, Allen, only produces a lot of big excrement. Here is a parallel to your article: The rainforest fly Drosophila birchii likes living in, not surprisingly, rainforests, where the air is humid and everything is nice and moist. But Australia ’s pockets of tropical rainforest are becoming more fragmented by land clearing for roads, agriculture and urban development. Increasing penetration of drier air from outside alters the ‘microclimate’ inside the rainforest—particularly humidity. So scientists decided to test Drosophila birchii in the laboratory to see how quickly this rainforest fly would be able to adapt to a drier environment. They exposed flies to a dessication (drying) stress until 80 to 90% had died, and then bred from the survivors. But the offspring were no better than their parents at surviving drier-than-normal conditions. With mounting surprise, the researchers repeated the process—for 30 cycles over 50 fly generations—but still no increase in dessication resistance. The astonished researchers thought something must have gone wrong with that particular batch of D. birchii flies. After all, when the lab tested other species of Drosophila from less humid environments—D. melanogaster, D. simulans and D. serrata—they saw a two- to five-fold increase in dessication resistance. Even after dry-stressing fresh batches of the flies from four separate rainforest populations, the researchers noted that ‘the most resistant population lacks the ability to evolve further resistance even after intense selection for over 30 generations’. As other evolutionists have commented, this was ‘a complete surprise’. For IDists, this is a classic example of the built-in limits to genetic variation. Evolutionary theory claims that life arose by a process which is ultimately creative, and virtually without limits. When researchers found that a rainforest fly was unable to adapt to drier conditions, it was ‘a complete surprise’: Natural selection eliminates genes, it does not create new information. This is most noticeable in extreme environments, e.g. in dry conditions, flies that lose body moisture too quickly will die out and, without offspring, their genes will be lost from that population. But in a wet rainforest environment, there’s no advantage in conserving body moisture; what’s needed is just the opposite—the ability to withstand high humidity and the rampant diseases which thrive in such conditions. Hence Drosophila birchii populations have become highly adapted to life in the rainforest, but it has come at a cost. The price paid for such specialisation is the permanent loss of genetic information useful for survival in a drier environment. In contrast, the Drosophila flies from intermediate (less humid) environments, D. melanogaster, D. simulans, and D. serrata, still contain sufficient genetic variation to enable the population to adapt to drier conditions. So, what we have here is not evolution, just natural selection. Not a creative, limitless process, but one of culling genes already in existence. As Jerry notes, you aren't able to answer the question asked: microchanges that aren't moving to macro. I am amazed that you - in a position of educating the future - is incable of registering this fact. Just give us one "of your thousands" that show us the pathway of macroevolution. I asked for your 'A' game. Where is it? Do we have to go through your "thousands" and still continue to show you that it is microevolutionary in nature; that the mechanisms of natural selection do not provide new information; and that your science is more about faith than evidence!AussieID
March 9, 2009
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uoflcard, I have tried to find out what the junk DNA is supposed to do. As far as I know the only thing they know is that it gets transcribed but not translated in any way. After that they are still at a lost as to why it is transcribed and what the function of the transcribed RNA has if any. If it has none, then it may be still junk and it will be a colossal waste of energy because the cell expends energy to transcribe. Most of the DNA are repetitive elements like ABABABABABAB etc. Does anyone have any different insight on this? A big deal was made of the ENCODE project but I have not seen any real substance out of it except the claim made by some that nearly all the genome has function.jerry
March 8, 2009
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Allen, You done it again. Thank you very much. We ask for major changes and we get back simple micro evolution which ID accepts. An interesting article. I admit I do not understand all that is being said but know enough to know that this is a minor change with positive results. Is it beneficial over all for the fruit fly or just locally because of DDT. Would the change persist in other areas with no insecticides or be selected against? It is still a fruit fly with a slight genomic change to add the insecticide resistance and it looks like it is the result of a jumping gene or something similar. I now know what a selective sweep is and will be on the look out for it in the future. Jumping genes or jumping beans. It is still a long way from true macro evolution. Remember we do not deny these changes take place and sometimes have some beneficial effects.jerry
March 8, 2009
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However, I would also like to hear how the alternative hypothesis – that adaptive changes are produced by the intervention of an Intelligent Designer – can be tested and either verified or falsified empirically, and by what mechanism(s) the Intelligent Designer accomplishes this.
First of all, not all of ID theory proposes miraculous interventions whenever some major evolution needs to happen. I am becoming more and more partial to front-loaded evolution, especially with what is beginning to be discovered about genomes, and "junk" DNA. If it is proven that some of "junk" DNA is basically programming that influences evolution (instead of random mutation/variation creating all information), I think ID's case becomes very strong. I need to learn more about the front-loaded theory, and we all need to learn more about "junk" DNA. But I have heard for years from front-loaded theorists that our genomes could be programmed for evolution. It was easily rejected by neo-Darwinists because they were thoroughly engulfed in the dogmatic acceptance of "junk" DNA being worthless evolutionary artifacts. But now it appears there is much more to the genome than what has been unquestionably accepted for decades. If it turns out to be true, the evolutionary "warehouse" of DNA (a.k.a. "junk") would be a possible mechanism.uoflcard
March 8, 2009
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"by what mechanism(s) the Intelligent Designer accomplishes this." Allen, there is a whole area of study called Synthetic Biology which I am sure you are aware of. Maybe it was one of the ways they are thinking of using. But I bet it was more advanced than anything they are currently using so you may have to wait awhile.jerry
March 8, 2009
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However, I would also like to hear how the alternative hypothesis – that adaptive changes are produced by the intervention of an Intelligent Designer – can be tested and either verified or falsified empirically, and by what mechanism(s) the Intelligent Designer accomplishes this.
Not only that, but can A) The amount of FSCI B) The change in the amount of FSCI C) The final amount of FSCI As defined by Kariosfocus be shown for the adaptive changes detailed in Allen's post? If not, what is needed in order to be able to do so? DNA sequences? What? I'd really like to know what would be needed to work it out. Does anybody know?George L Farquhar
March 8, 2009
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Here's another one, much more recent (2004). I'm copying the entire article from an online scientific journal that is not available to people without a subscription. I can get it for free through my university library gateway. ARTICLE CITATION: Brookfield, J. F. Y. (2004) Evolutionary genetics: Mobile DNAs as sources of adaptive change? Current Biology, Volume 14, Issue 9, Pages R344 to R345. Available online 3 May 2004. ABSTRACT: Mobile DNAs are potent sources of mutation in wild populations, but seem only rarely to have been used in adaptive evolution. A new study has revealed a mobile DNA insertion in Drosophila simulans that is associated with an apparent selective sweep and an elevation in expression level of an adjacent gene which creates insecticide resistance. FULL TEXT: The neo-Darwinian paradigm of evolutionary change assumes that mutations occur independently of any natural selection that will subsequently act on them. While such independence has been challenged in some descriptions of adaptive mutation in bacteria [1], it is still generally accepted to apply in multicellular organisms. It follows that, were one to examine simultaneously the process of mutation and the process of evolution, the kinds of mutational change that one would see should not be different in kind from the sorts of changes one sees occurring over evolutionary time, unless different types of mutation had systematically different phenotypic consequences: only selection can create a systematic difference between mutational and evolutionary changes. A lack of agreement between mutation and evolutionary change was first noted in the context of dominance. In the 1920s, when the neo-Darwinian synthesis was being created, it was seen that mutations in Drosophila melanogaster are usually recessive to the wild-type allele. The paradox was that if genes are evolving, then the current wild-type allele would have been a mutant when it first arose, spreading to become the wild-type because of its advantageous phenotypic effect. Why should advantageous mutations generally be dominant, when their advantageousness depends on the particular environments that they will encounter? R.A. Fisher [2] and [3] suggested that the solution to this conundrum was that dominance evolves – an advantageous mutation is only co-dominant when it first arises, but, as it spreads through the population as a result of selection, evolutionary changes at other, ‘modifier’ loci cause the mutation to be dominant by the time it is fixed in the population. For Sewell Wright [4] and [5], however, the explanation was that the Drosophila mutations are recessive because they inactivate genes, so that their recessivity has a physiological, rather than an evolutionary, cause. Wright's prediction, subsequently abundantly confirmed, implies that, at the molecular level, there is no symmetry between typical major mutations studied in laboratories and the adaptive changes occurring over evolutionary time. Major mutations represent losses of gene function, a change not often used in adaptive evolution – we do not evolve by successively losing more and more of our gene functions, but rather by subtly altering the ways in which genes work. Similarly, what are the evolutionary consequences of mobile DNA insertions? It has been estimated that 80% of the spontaneous mutations seen in Drosophila genetics result from transposable elements [6]. Do mobile DNA insertions similarly create 80% of evolutionary changes in this species? Without question, they do not. The most revealing observation is the almost complete absence of fixed sites of mobile DNAs in D. melanogaster [7]. A mobile DNA insertion that created an advantageous phenotype would be expected to spread to fixation in the species by natural selection. This would create a site fixed for the element throughout the species. Such sites are very rare, although they have recently been detected for the S element family in heat shock protein genes [8]. Is this simply because transposable element insertions are different in kind from base substitutions, the typical outcome of the insertion of a mobile DNA into the coding sequence being a gene inactivation? Possibly, but one can easily imagine that an insertion of a mobile DNA near to a gene could leave the coding sequence intact but could create a subtle, and potentially advantageous, alteration in the gene's expression pattern. A recent study by Schlenke and Begun [9] has revealed an example of an adaptive change apparently created in Drosophila simulans by the insertion of a mobile DNA. These authors have shown that, in D. simulans, a mobile DNA insertion 5? to the cytochrome P450 gene Cyp6g1 has apparently created an adaptive phenotypic change, as a result of which it has spread to high frequency in a local population. The sign of an adaptive change first noted by the authors was a region of around 100kilobases with very low heterozygosity, but only in a D. simulans population sampled from California, and not in African samples. This appeared to be the sign of a ‘selective sweep’. A selective sweep occurs when a new advantageous mutation arises and rapidly spreads through the population. Because the mutation arises initially in a single chromosome, as it spreads, this chromosome also spreads through the population, eliminating the standing crop of genetic diversity in the region. The length of the chromosome affected by such a selective sweep depends on the relative sizes of the selective coefficient favouring the new mutation and the local recombination rate per base. There are, of course, difficulties in identifying, in a 100kilobase region that has undergone a selective sweep, the particular mutational change in the region that has been responsible for the selection (many variants will have recently spread from low to high frequency as a result of the sweep). The identification of the cause of the sweep in D. simulans is thus based on circumstantial evidence. Schlenke and Begun [9] noted that there is an insertion of the non-long-terminal repeat (LTR) retrotransposon Doc in the 5? flanking region of Cyp6g1, around 200 base pairs upstream from the start of transcription and absent in African D. simulans lines. While this gene is not at the centre of the chromosomal region affected by the sweep, cytochrome P450 genes are known to play a role in insecticide resistance, and thus Cyp6g1 is a candidate cause of the sweep. One remarkable property of the Doc insertion is that an extraneous 72 base pairs of DNA at its 5? end seems to have been translocated from a 5? flanking sequence of the mitochondrial P450 gene Cyp12c1, thereby possibly introducing new controlling regions to Cyp6g1. Certainly, the Californian lines bearing the Doc insert have a higher level of Cyp6g1 expression than African lines. There is also statistically significant evidence for enhanced resistance to the insecticide DDT in the Californian lines, although the high between-line variation in resistance among lines all with the Doc insertion implies that the presence or absence of the insertion is not the sole determinant of resistance. The size of the region affected by the selective sweep allows the estimation of the strength of selection at 2% per generation favouring the new advantaged haplotype. Further evidence that insertion of mobile DNAs creates an advantageous insecticide resistance at this locus comes from comparison with D. melanogaster populations. Remarkably, in a similar location 5? to Cyp6g1, Californian D. melanogaster have a high frequency insertion of the gypsy-like LTR retro-transposon Accord. This insertion occurs at a much lower frequency in other populations. Again there is evidence that this insertion is associated with DDT resistance and that a selective sweep has occurred, but one that is smaller in extent than in the D. simulans case and more tightly associated with the Cyp6g1 gene. If these apparent selective sweeps are indeed the result of mobile DNA sequence insertions, why are insertion mutations that alter the expression patterns of adjacent genes in a selectively advantageous way not more common? Why do these so rarely seem to spread through the species as a whole? One can clearly create a model in which insertions are eventually followed by imprecise excisions, leaving behind a small fragment only of the inserted sequence, or causing the loss of all the insertion, along with some flanking host sequences. Such a change might still create the advantageous phenotype, and thus one can imagine that an advantageous insertion is replaced by its deleted derivative. A recent sweep generated by a insecticide resistance phenotype might not have had long enough for this secondary event to have occurred. The other, more disturbing, aspect of this study is that the species is responding to a very strong, man-made selective pressure, as is the case with many of our best examples of recent adaptive change in wild populations. Are these sudden man-made changes in environments typical of the environmental changes that wild populations encounter, and to which they respond through evolutionary change? Or do environments more usually change in such a gradual way that the adaptive response is qualitatively different at the molecular level. In other words, just as the mutations seen in laboratories are not typical of the mutational changes used in adaptive evolution, is it possible that the mutational changes used in adaptive evolution triggered by sudden mad-made environmental changes are not typical of the mutational changes used in adaptation to the more gradual environmental changes normally encountered by wild populations? REFERENCES: [1] B.G Hall, Adaptive mutagenesis: a process that generates almost exclusively beneficial mutations, Genetica 103 (2003), pp. 109–125. [2] R.A Fisher, The possible modification of the response of the wild-type to recurrent mutation, Am. Nat. 62 (1928), pp. 115–126. [3] R.A Fisher, Two further notes on the origin of dominance, Am. Nat. 62 (1928), pp. 571–574. [4] S Wright, Fisher's theory of dominance, Am. Nat. 63 (1929), pp. 274–279. [5] S Wright, The evolution of dominance, Am. Nat. 63 (1929), pp. 556–561. [6] M Ashburner, Drosophila, a laboratory handbook, Cold Spring Harbor Laboratory Press, Cold Spring Harbor, New York (1992). [7] B Charlesworth and C.H Langley, The population genetics of Drosophila transposable elements, Annu. Rev. Genet. 23 (1989), pp. 251–287. [8] X Maside, C Bartolome and B Charlesworth, S-element insertions are associated with the evolution of the HSP70 genes in Drosophila melanogaster, Curr. Biol. 12 (2002), pp. 1686–1691. [9] T.A Schlenke and D.J Begun, Strong selective sweep associated with a transposon insertion in Drosophila simulans, Proc. Natl. Acad. Sci. USA 101 (2004), pp. 1626–1631. AUTHOR'S INFORMATION: Institute of Genetics, University of Nottingham, Queens Medical Centre, Nottingham, NG7 2UH, UK COMMENTARY: The transposon-mediated adaptive changes cited in this article are exactly the kinds of changes I cited in my earlier post (#71, above). Furthermore, the transposon-mediated changes cited here do not involve plasmids (which eukaryotes rarely if ever have). On the contrary, they involve the random insertion of transposable elements which, upon examination and correlation with frequency in different populations, have been shown to have become more common over time. This is the definition of adaptive evolution: an accidental genetic change (which in its original position in the genome had no detectable adaptive value) increases in frequency in a population because the individuals carrying this change survive and reproduce more often than individuals who do not carry it. Now, of course, someone could go on and argue that the Intelligent Designer somehow "guided" the insertion of this transposon by some entirely unspecified mechanism, but that assertion cannot be shown to be the case using any conceivable empirical method. Ergo, it's not science and should not be included in a scientific explanation. I can keep this up all day, so long as I have access to Google Scholar and the Cornell University Library Gateway. However, I would also like to hear how the alternative hypothesis – that adaptive changes are produced by the intervention of an Intelligent Designer – can be tested and either verified or falsified empirically, and by what mechanism(s) the Intelligent Designer accomplishes this.Allen_MacNeill
March 8, 2009
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George, If you write to Answers in Genesis- be nice and cordial- most likely they will answer you. However they may say just what the heck has this feature arising by accident advanced? BTW my "cause" is to get to the reality behind our existence and the existence of what we observe.Joseph
March 8, 2009
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Joseph, As that was published in 2003 are you aware of any follow ups in regard to
Further research will, I expect, show that there is a sophisticated, irreducibly complex, molecular system involved in plasmid-based adaptation
Has there been further research then? Has it shown that these systems are IC?
This system will once again, as the black box becomes illuminated, speak of intelligent creation, not chance.
Is 6 years not enougth time to illuminate this?
Understanding this adaptation system could well lead to a breakthrough in disease control
Has such an understanding been reached? Is anybody that you are aware of working on reaching such an understanding from a design perspertive? Seems alot could have been done to advance your cause in the years since that was published. Has it?George L Farquhar
March 8, 2009
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What do the Creationists say about nylon eating bacteria?: Batten, D. 2003. The adaptation of bacteria to feeding on nylon waste. Journal of Creation 17(3):3–5. It concludes with:
It seems clear that plasmids are designed features of bacteria that enable adaptation to new food sources or the degradation of toxins. The details of just how they do this remains to be elucidated. The results so far clearly suggest that these adaptations did not come about by chance mutations, but by some designed mechanism. This mechanism might be analogous to the way that vertebrates rapidly generate novel effective antibodies with hypermutation in B-cell maturation, which does not lend credibility to the grand scheme of neo-Darwinian evolution.11 Further research will, I expect, show that there is a sophisticated, irreducibly complex, molecular system involved in plasmid-based adaptation—the evidence strongly suggests that such a system exists. This system will once again, as the black box becomes illuminated, speak of intelligent creation, not chance. Understanding this adaptation system could well lead to a breakthrough in disease control, because specific inhibitors of the adaptation machinery could protect antibiotics from the development of plasmid-based resistance in the target pathogenic microbes.
Joseph
March 8, 2009
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Dr. Spetner discussing transposons:
The motion of these genetic elements to produce the above mutations has been found to a complex process and we probably haven’t yet discovered all the complexity. But because no one knows why they occur, many geneticists have assumed they occur only by chance. I find it hard to believe that a process as precise and well controlled as the transposition of genetic elements happens only by chance. Some scientists tend to call a mechanism random before we learn what it really does. If the source of the variation for evolution were point mutations, we could say the variation is random. But if the source of the variation is the complex process of transposition, then there is no justification for saying that evolution is based on random events.
Joseph
March 8, 2009
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Carbon- nylon-6 contains carbon, which has been around for quite some time. And it is that carbon which the bacteria requires. IOW bacteria may not have known "nylon" but bacteria definitely knew carbon. Then all that was necessary was for the bacteria to solve the problem- how to get the carbon out of the nylon-6. And it looks like a solution was found. Why isn't that an example of a "built-in response to environmental cues" as Dr Spetner describes in his book "Not By Chance"?Joseph
March 8, 2009
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Allen, firstly the “empirical” science lesson I got from a mate: Much research has flowed from this discovery of the two species (Flavobacterium sp. K172 and Pseudomonas sp. NK87) that degrade nylon compounds in trying to elucidate the mechanism for the apparently novel ability of these bacteria. There are three enzymes involved in Flavobacterium K172: F-EI, F-EII and F-EIII, and two in Pseudomonas NK87: P-EI and P-EII. None of these have been found to have any catalytic activity towards naturally occurring amide compounds, suggesting that the enzymes are completely new, not just modified existing enzymes. Indeed no homology has been found with known enzymes. The genes for these enzymes are located on plasmids: plasmid pOAD2 in Flavobacterium and on two plasmids, pNAD2 and pNAD6, in Pseudomonas. So, is this evidence consistent with random mutation generating the new genes? Thwaites [Thwaites, W.M., New proteins without God’s help, Creation/Evolution 5(2):1–3 (issue XVI), 1985.] claimed that the new enzyme arose through a frame shift mutation. If this were the case, the production of an enzyme would indeed be a fortuitous result, attributable to ‘pure chance’. However, there are exceptionally good reasons to doubt the claim that this is an example of random mutations and natural selection generating new enzymes, quite aside from the extreme improbability of such coming about by chance. Evidence against the evolutionary explanation includes: 1. There are five transposable elements on the pOAD2 plasmid. When activated, transposase enzymes coded therein cause genetic recombination. Externally imposed stress such as high temperature, exposure to a poison, or starvation can activate transposases. The presence of the transposases in such numbers on the plasmid suggests that the plasmid is designed to adapt when the bacterium is under stress. 2. All five transposable elements are identical, with 764 base pairs (bp) each. This comprises over eight percent of the plasmid. How could random mutations produce three new catalytic/degradative genes (coding for EI, EII and EIII) without at least some changes being made to the transposable elements? Negoro speculated that the transposable elements must have been a ‘late addition’ to the plasmids to not have changed. But there is no evidence for this, other than the circular reasoning that supposedly random mutations generated the three enzymes and so they would have changed the transposase genes if they had been in the plasmid all along. Furthermore, the adaptation to nylon digestion does not take very long (see point 5 below), so the addition of the transposable elements afterwards cannot be seriously entertained. 3. All three types of nylon degrading genes appear on plasmids and only on plasmids. None appear on the main bacterial chromosomes of either Flavobacterium or Pseudomonas. This does not look like some random origin of these genes—the chance of this happening is exceptionally low. If the genome of Flavobacterium is about two million bp, and the pOAD2 plasmid comprises 45,519 bp, and if there were say 5 pOAD2 plasmids per cell (~10% of the total chromosomal DNA), then the chance of getting all three of the genes on the pOAD2 plasmid would be about 0.0015. If we add the probability of the nylon degrading genes of Pseudomonas also only being on plasmids, the probability falls to 2.3 x 10-6. If the enzymes developed in the independent laboratory-controlled adaptation experiments (see point 5, below) also resulted in enzyme activity on plasmids (almost certainly, but not yet determined), then attributing the development of the adaptive enzymes purely to chance mutations becomes even more implausible. 4. The antisense DNA strand of the four nylon genes investigated in Flavobacterium and Pseudomonas lacks any stop codons. This is most remarkable in a total of 1,535 bases. The probability of this happening by chance in all four antisense sequences is about 1 in 1012. Furthermore, the EIII gene in Pseudomonas is clearly not phylogenetically related to the EII genes of Flavobacterium, so the lack of stop codons in the antisense strands of all genes cannot be due to any commonality in the genes themselves (or in their ancestry). Also, the wild-type pOAD2 plasmid is not necessary for the normal growth of Flavobacterium, so functionality in the wild-type parent DNA sequences would appear not to be a factor in keeping the reading frames open in the genes themselves, let alone the antisense strands. Some statements by Yomo et al., [Yomo T, Urabe I, Okada H (May 1992) “No stop codons in the antisense strands of the genes for nylon oligomer degradation”. Proc Natl Acad Sci USA. 89 (9): 3780–4.] express their utter consternation at the findings: “These results imply that there may be some unknown mechanism behind the evolution of these genes for nylon oligomer-degrading enzymes. “The presence of a long NSF (non-stop frame) in the antisense strand seems to be a rare case, but it may be due to the unusual characteristics of the genes or plasmids for nylon oligomer degradation. “Accordingly, the actual existence of these NSFs leads us to speculate that some special mechanism exists in the regions of these genes.” It looks like recombination of codons (base pair triplets), not single base pairs, has occurred between the start and stop codons for each sequence. This would be about the simplest way that the antisense strand could be protected from stop codon generation. The mechanism for such a recombination is unknown, but it is highly likely that the transposase genes are involved. Interestingly, Yomo et al. also show that it is highly unlikely that any of these genes arose through a frame shift mutation, because such mutations (forward or reverse) would have generated lots of stop codons. This nullifies the claim of Thwaites that a functional gene arose from a purely random process (an accident). 5. The Japanese researchers demonstrated that nylon degrading ability can be obtained de novo in laboratory cultures of Pseudomonas aeruginosa [strain] POA, which initially had no enzymes capable of degrading nylon oligomers. This was achieved in a mere nine days! The rapidity of this adaptation suggests a special mechanism for such adaptation, not something as haphazard as random mutations and selection. 6. The researchers have not been able to ascertain any putative ancestral gene to the nylon-degrading genes. They represent a new gene family. This seems to rule out gene duplications as a source of the raw material for the new genes. P. aeruginosa is renowned for its ability to adapt to unusual food sources—such as toluene, naphthalene, camphor, salicylates and alkanes. These abilities reside on plasmids known as TOL, NAH, CAM, SAL and OCT respectively. Significantly, they do not reside on the chromosome (many examples of antibiotic resistance also reside on plasmids). The chromosome of P. aeruginosa has 6.3 million base pairs, which makes it one of the largest bacterial genomes sequenced. Being a large genome means that only a relatively low mutation rate can be tolerated within the actual chromosome, otherwise error catastrophe would result. There is no way that normal mutations in the chromosome could generate a new enzyme in nine days and hypermutation of the chromosome itself would result in non-viable bacteria. Plasmids seem to be adaptive elements designed to make bacteria capable of adaptation to new situations while maintaining the integrity of the main chromosome. Now, to look at stasis in bacteria: P. aeruginosa was first named by Schroeter in 1872. It still has the same features that identify it as such. So, in spite of being so ubiquitous, so prolific and so rapidly adaptable, this bacterium has not evolved into a different type of bacterium. Note that the number of bacterial generations possible in over 130 years is huge—equivalent to tens of millions of years of human generations, encompassing the origin of the putative common ancestor of ape and man, according to the evolutionary story, indeed perhaps even all primates. And yet the bacterium shows no evidence of directional change—stasis rules, not progressive evolution. This alone should cast doubt on the evolutionary paradigm. Flavobacterium was first named in 1889 and it likewise still has the same characteristics as originally described. It seems clear that plasmids are designed features of bacteria that enable adaptation to new food sources or the degradation of toxins. The details of just how they do this remains to be elucidated. The results so far clearly suggest that these adaptations did not come about by chance mutations, but by some designed mechanism. This mechanism might be analogous to the way that vertebrates rapidly generate novel effective antibodies with hypermutation in B-cell maturation, which does not lend credibility to the grand scheme of neo-Darwinian evolution. Further research will show that there is a sophisticated, irreducibly complex, molecular system involved in plasmid-based adaptation—the evidence strongly suggests that such a system exists. This system will once again, as the black box becomes illuminated, speak of intelligent design, not chance. I LOVE empirical evidence! But when scientists try to use empirical evidence to show the short-comings of Neo-Darwinian methods they aren’t published in a “peer-reviewed scientific journal”. You should have rewritten it as “Darwinian-orthodoxy-reviewed journal”. That is more appropriate, but that wouldn’t be such a good line now, would it!. Apologists for materialism, such as you, latched onto these findings as an example of evolution of new information by random mutations and natural selection. You obviously don’t critically evaluate anything you read as your ongoing mantra shows. To rework your own words, “… then all you have done is express your uncritical (and, in this case, mistaken) opinion.” Your example is irrelevant to goo-to-you evolution. If this is your best work, and I never know anyone to provide their B and C games to convince someone of a point, then I can confidently go back to my original point: "Natural selection, though, adds no information." Bring on your 'A' game, Allen, your 'A' game.AussieID
March 8, 2009
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Allen #70 "This discovery led geneticist Susumu Ohno to propose that the gene for one of the enzymes, 6-aminohexanoic acid hydrolase, had come about from the combination of a gene duplication event with a frame shift mutation" Gene duplication + "frame shift" = no new information. Back to the drawing board, Allen.mad doc
March 7, 2009
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Allen, Do you want to hold up these references as the cutting edge of evolutionary biology change? Is this it? I fully expect you can dig for more but the nature of these examples is telling. Now I admit I am not a biologist so what I have to go on is what is claimed by these studies and others that you have introduced. And because I am not an expert in this, it will take me some time. Are these covered in any textbook or any review article on macro evolution. After all the references you gave me are 11-20 years old and the article by Brosius which is a review article did not list a lot of examples. I want to be able to put them in layman's language so that I and others can judge them accordingly. Remember that ID does not dispute that your 50+ (to replace the 47+) engines of variation exist and can cause many changes to a genome and occasionally some are selected for. But new selected for characteristics is not necessarily something that will lead organisms on the path from microbes to man. The issue has always been the origin of complex new capabilities or the creations of systems within the organism that did not exist before as the result of changes to the genome by your engines of variation. Do you want to offer these up as examples of such? Otherwise it is just another diversion and does not reflect well on any synthesis that people adhere to in evolutionary biology if a published exposition of major changes leading to new functionality of organisms does not exist. All the microbe examples while interesting do not represent such changes. I am sure that new research will provide more examples and I always maintain that until there are substantial mappings of genomes and an understanding on just how all the genomic elements affect the operation of the organism and development we will still be in a guessing game. Until that time it looks like the 50+ engines as the driver of macro evolution will be just speculation. Thank you for all the stuff you provide us. We learn each time you help us.jerry
March 7, 2009
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There's lots more here: http://www.evol.nw.ru/labs/lab38/spirov/hox_pro/evol_tes.htmlAllen_MacNeill
March 7, 2009
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In #68 jerry wrote:
"...now is the time for the evolutionary synthesis people to walk the walk."
For many documented examples of how transposons and retrotransposition have played important roles in evolution, start here: http://www.evol.nw.ru/labs/lab38/spirov/hox_pro/mge-intro.html and then follow up the embedded links. And while you're doing that, please post some citations to published empirical research that indicates that "attainment of more than a few functional proteins is beyond the scope of the processes described." Thanks!Allen_MacNeill
March 7, 2009
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In #69 aussieD wrote:
"There is not a known case otherwise where a mutation does not destroy information or render it neutral."
Here's just one example (out of thousands): In 1975 a team of Japanese scientists discovered a strain of Flavobacterium living in ponds containing waste water from a factory producing nylon that was capable of digesting certain byproducts of nylon 6 manufacture, such as the linear dimer of 6-aminohexanoate, even though those substances are not known to have existed before the invention of nylon in 1935. Further study revealed that the three enzymes the bacteria were using to digest the byproducts were significantly different from any other enzymes produced by other Flavobacterium strains (or any other bacteria for that matter), and not effective on any material other than the manmade nylon byproducts. This discovery led geneticist Susumu Ohno to propose that the gene for one of the enzymes, 6-aminohexanoic acid hydrolase, had come about from the combination of a gene duplication event with a frame shift mutation. A series of recent studies by a team led by Seiji Negoro of the University of Hyogo, Japan, suggest that a different mutation was involved in the evolution of the 6-aminohexanoic acid hydrolase. Scientists have also been able to induce another species of bacteria, Pseudomonas aeruginosa, to evolve the capability to break down the same nylon byproducts in a laboratory by forcing them to live in an environment with no other source of nutrients. The Pseudomonas aeruginosa strain did not seem to use the same enzymes that had been utilized by the original Flavobacterium strain. Other scientists were able to get the ability to generate the enzymes to transfer from the Flavobacterium strain to a strain of E. coli bacteria via a plasmid transfer. To sum up: There is a scientific consensus that the capacity to synthesize nylonase most probably developed as a single-step mutation that survived because it improved the fitness of the bacteria possessing the mutation. Sources: Kinoshita, S.; Kageyama, S., Iba, K., Yamada, Y. and Okada, H. (1975) "Utilization of a cyclic dimer and linear oligomers of e-aminocaproic acid by Achromobacter guttatus" Agricultural & Biological Chemistry 39 (6): 1219?23. Kinoshita S, Kageyama S, Iba K, Yamada Y, Okada H (1981) "Utilization of a cyclic dimer and linear oligomers of ?-aminocapronoic acid by Achromobacter guttatus K172". Agric. Biol. Chem. 116: 547-551. Negoro S, Taniguchi T, Kanaoka M, Kimura H, Okada H (July 1983) "Plasmid-determined enzymatic degradation of nylon oligomers". J. Bacteriol. 155 (1): 22–31. Ohno S. (April 1984) "Birth of a unique enzyme from an alternative reading frame of the preexisted, internally repetitious coding sequence" Proc Natl Acad Sci USA. 81 (8): 2421–5. Yomo T, Urabe I, Okada H (May 1992) "No stop codons in the antisense strands of the genes for nylon oligomer degradation". Proc Natl Acad Sci USA. 89 (9): 3780–4. Prijambada ID, Negoro S, Yomo T, Urabe I (May 1995) "Emergence of nylon oligomer degradation enzymes in Pseudomonas aeruginosa PAO through experimental evolution". Appl. Environ. Microbiol. 61 (5): 2020–2. Okamura K, Feuk L, Marquès-Bonet T, Navarro A, Scherer SW (December 2006) "Frequent appearance of novel protein-coding sequences by frameshift translation" Genomics 88 (6): 690–7. Negoro S, Ohki T, Shibata N, et al (June 2007) "Nylon-oligomer degrading enzyme/substrate complex: catalytic mechanism of 6-aminohexanoate-dimer hydrolase" J. Mol. Biol. 370 (1): 142–56. So, your assertion that there is no known case where a mutation does not destroy information or render it neutral is completely and demonstrably false. You can make all the unsupported assertions you want, but doing so doesn't make them true. Indeed, unless you present empirical evidence and cite who obtained the evidence, where and when it was published in a peer-reviewed scientific journal, and how we can all read it for ourselves, then all you have done is express your uninformed (and, in this case, mistaken) opinion.Allen_MacNeill
March 7, 2009
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Allen, You are missing not only the big picture, but the very brushstrokes that cause it. (More on this later) 'Variety' - the end product of your machines of variation - involves no addition of complex new genetic information. Most of the variation in populations arises from reshuffling of previously existing genes and from mutations. Variety, Allen, does not provide new genetic information. For example, what has occured in bacteria, in many cases, is that bacteria already had the genes for resistance to the antibiotics. Some bacteria, retrieved by thawing sources which had been frozen before antibiotics were developed, has shown to be antibiotic-resistant. Now apply antibiotics to a population of bacteria: those that are lacking resistance are killed off. Any genetic information they carry is destoyed. The survivors are carrying less information but they are all still resistant. We find that the same principle can apply to insects supposedly ‘evolving’ resistance to pesticides. The resistance was already there. Animals without this resistance are eliminated. This also applies to rat colonies. On the other hand, some antibiotic resistance is the result of a mutation. There is not a known case otherwise where a mutation does not destroy information or render it neutral. Resistance to the antibiotic penicillin is a case in point. The appearance of a new trait doesn't have to add new information via the DNA coding. It is so unlikely that it could ever be the basis for the increased information needed for evolution as you tout it. Information content is measured by the specified complexity of a base sequence or the protein amino acid sequence. A mutation could never do anything but scramble the information, thus reducing the information. Of the many studies of antibiotic, insecticide herbicide and resistance mechanisms studied at the biochemical level, none have added specified complexity in the DNA. New traits, due to mutations, that have arisen all involve LOSS of information. Variety is everywhere. But not because of the build up of new information but the imparting and reshuffling of existing information. I'll try an analogy: consider the colour wheel. We'll go for the red/blue/yellow primaries. By examining the inter-relationships between the colours the variety of colours that can be created from these three is immense. With shades and tints of black and white the colours able to be produced is, almost, immeasurably extended. Now, with all these abilities to combine tertiary, secondary, intermediate, ect. with black and white, then the variety that can be witnessed is massive. Now make the colour silver. Or bronze. What about copper? You may say they are variations of grey, brown or yellow. Correct, but there is new information required that isn't present in the original to create these metallic shades. I know that the colour wheel can not show all colours, but this is not my premise. You need new information to create new colours. Variety can be immense, but not a useful tool in this case. You write, that variety "produce(s) genuinely new information." Nope. You are wrong.AussieID
March 7, 2009
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"So, jerry, you are correct when you assert that “this is the theory”, but you need to do some more homework, because the evidence you say we should be looking for has already been accumulating for almost two decades." Well, then someone present it. I did not see it in Brosius's article. Only assertions. After all this time, we come down to finally summing up the theory, now is the time for the evolutionary synthesis people to walk the walk. The ID position is that the attainment of more than a few functional proteins is beyond the scope of the process described.jerry
March 7, 2009
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