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Axe and Gauger challenge Shapiro to show that their approach is wrong

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Readers may recall that in the discussion between intelligent design proponents (Dembski, Axe, Gauger) and self-organization proponent James Shapiro, Shapiro replied to Axe and Gauger, who have now replied back ( Evolution News & Views, January 20, 2012):

Background to the discussion here.

We are well aware of the many experimental studies that attempt to draw some conclusion about protein evolution, but we also know that very few of these studies take the critical approach of asking whether the presumed evolutionary mechanism really works. It’s as though most scientists are unwilling to put these fundamental ideas to a serious test.

I can make this point most clearly with a concrete example. We can go into the lab and modify bacterial cells by deleting the entire set of genes dedicated to the synthesis of tryptophan, one of the essential building blocks of proteins. When we observe what happens when these modified cells are given just enough tryptophan to grow and reproduce, we will see lots of things happening, but none that can be expected to reinvent a set of genes for making tryptophan, even in a large population over billions of years.

I know of many processes that people talk about as though they can do the job of inventing new proteins (and of many papers that have resulted from such talk), but when these ideas are pushed to the point of demonstration, they all seem to retreat into the realm of the theoretical.

But of course, as experimentalists we are very willing to see the evidence that might prove us wrong.

Over to Shapiro.

Comments
He then claims that if evolution is true, we should see the microorganism regenerate the genes in the lab, presumably within a human lifetime.
Except he did NOT say anything about "within a human lifetime".
Those genes were generated from pre-existing genes and those no longer exist in the modern organism,
Nice bald assertion as you don't have any idea how those genes arose. Your position can't even test the claim they arose via accumulations of random mutations.
which means that it would take millions of years to regenerate them de novo, under the best circumstances.
How do YOU know how long it will take? And ID is OK with beneficial mutations. And if your position had anything, anything at all, then neither Axe nor Gauger would be an IDist. So stop your whining and start presenting positive evidence for your position.Joe
January 27, 2012
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Lenski has no idea if the mutations were random in any sense of the word. And no one needs to deliberately mutate anything for a mutation to be directed by an organisms internal programming.Joe
January 27, 2012
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Just tell us what you consider "Blind Watchmaker" research to be. I take it as standard Darwinian random variation and natural selection, which Lenski is definitely doing. He's not deliberately mutating those organism's DNA or helping a lucky mutation to survive. I can't wait to see what your definition is.dmullenix
January 27, 2012
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A don't know what you mean by a "bald sequence", but you seem to be talking about the very first life. Axe is talking about taking a modern microorganism and removing one or more complete genes, leaving no trace of them at all - just some missing DNA. He then claims that if evolution is true, we should see the microorganism regenerate the genes in the lab, presumably within a human lifetime. Those genes were generated from pre-existing genes and those no longer exist in the modern organism, which means that it would take millions of years to regenerate them de novo, under the best circumstances. That's what's shocking about Axe: He's presented by the ID mavens as being their main scientist and yet his statement in the OP reveals his shocking ignorance about the basics of how evolution works. This ignorance undermines everything else he says. You can't trust this guy, he doesn't know what he's doing. Did you hear about his partner in "science", Ann Gauger? At the ID "Wistar Retrospective Symposium" in 2007, "She ... discussed 'leaky growth,' in microbial colonies at high densities, leading to horizontal transfer of genetic information, and announced that under such conditions she had actually found a novel variant that seemed to lead to enhanced colony growth. Gunther Wagner said, “So, a beneficial mutation happened right in your lab?” at which point the moderator halted questioning." Not only that, but "A few days after the meeting ended, we all received an email stating that the ID people considered the conference a private meeting, and did not want any of us to discuss it, blog it, or publish anything about it." That's damning! http://pandasthumb.org/archives/2008/02/id-intelligent.html I don't have any confidence at all in Axe, Gauger or ID.dmullenix
January 27, 2012
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dmullenix- You complain about Axe and then provide support for him. Strange. Ya see YOUR position has to account for new genes arising from just bald sequences-> think abiogenesis. Yet obvioulsy abiogenesis would take longer than the entire age of the planet. Ya see your position doesn't have any experimental support- none at all. Lenski might as well be a creationist studying baraminology.Joe
January 26, 2012
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Prove it. And if he is he is demonstrating that blind watchmaker processes don't amount to anything. Is that what you really want?Joe
January 26, 2012
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Joe, Lenski is doing "Blind Watchmaker" research, along with a host of others.dmullenix
January 26, 2012
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Ok, Joe, let me explain why I was so shocked by Axe (especially the part you highlighted) and why further thought has shown the situation to be quite a bit worse than I first thought. First of all, in your quoted text, Axe proposes “deleting the entire set of genes dedicated to the synthesis of tryptophan”. He doesn’t say how large those genes (plural) are, but let’s be conservative and say they total out to 1000 base pairs. This is surely a very conservative figure. He then goes on to say, “When we observe what happens when these modified cells are given just enough tryptophan to grow and reproduce, we will see lots of things happening, but none that can be expected to reinvent a set of genes for making tryptophan, even in a large population over billions of years.” How long did he look? The Biologic institute wasn’t incorporated until late 2005. If Axe started his experiment the next day (he didn’t) and watched it until October of last year, (he didn’t) then he watched for six years at the most. Lenski’s experiment took from 1988 to 2008, which is 20 years and about 30,000 generations, to start utilizing citrate as a source of energy. This seems to have taken at least two and maybe three to five separate mutations. If it was five, then that averages one mutation every four years. So at a bare minimum and assuming a tiny 1000 BP gene, it would have taken Axe about 4 x 1000 base pairs or 4,000 years to have given evolution a chance to work, not six. And the real genes (plural) were certainly a lot longer than 1000 BP. Worse yet, the tryptophan genes are a specific target. Lenski’s experiment didn’t set out to create anything in particular. The ability to utilize citrate was just the first dramatic improvement that happened. It’s a lot harder and would take much longer to achieve the specific goal of synthesizing the tryptophan gene. How much longer? I think it would be somewhat proportional to how big the tryptophan genes are compared to the whole genome. Hundreds of times longer? Thousands? Maybe millions. Whatever the answer, it’s going to take a long, long time. But even 4000 years would have been way too short. The tryptophan gene didn’t suddenly appear out of nowhere. It was formed by mutating an earlier gene. And that earlier gene isn’t there any more – there’s just a big gap where the current gene used to be. Most or all of the precursors are gone, which means the entire modern gene has to be synthesized de novo. Multiply the time needed by another thousand or million or probably even more. Finally, and most damning, so far as I can tell, Axe did nothing like “deleting the entire set of genes dedicated to the synthesis of tryptophan”. Instead, he seems to have “knocked out” or disabled the genes. This is done by bombarding the genes with point mutations until one of them disables the gene, typically by mutating some codon into a STOP codon. This leaves all the rest of the gene in place. “All” you have to do to “un-knock out” the genes is to mutate the mutated STOP codon back to whatever it was originally. But, again, this is a targeted search. You’re trying to mutate that one specific base pair that converts that one STOP codon back to whatever it was originally. E coli is a typical bacterium. It has about 4.6 billion base pairs in its genome and you’re trying to mutate one particular base pair. But Axe is fairly young. If he starts that experiment right now and takes good care of himself, I think he might live to see results. Concluding, Axe: A: Doesn’t seem to realize that if he actually removed the entire set of genes, as he claimed he did, he would also be removing some or all of the predecessors to those genes, making the re-evolving of the genes enormously harder. (I didn’t spot this at first.) B: Re-evolving the genes would be an example of a targeted search, which would take much much longer than Lenski’s open ended “search” and that seems to have taken at least four years per base pair or 4,000 years for even a tiny 1000 BP set of genes. C: He presented us with a bogus experiment. He said “delete the entire set of genes”, which I don’t think anybody has ever done. At the most he probably just disabled one or more of the genes, which is much easier to undo. D: He didn’t look anywhere near long enough to declare even the experiment he actually did a failure. BA77: A: When Lenski’s mean benefits leveled off after 20,000 generations, the bacteria were growing 70% faster than originally. Then, around generation 33,000, the cells learned to utilize citrate and growth rates increased again, dramatically. That’s Evolution in Action! B: Ralph Seelke will be glad to know that it took at least two and maybe as many as five mutations before the bacteria learned to use citrate. C: I repeat from above – first the bacteria increased their growth rate by 70% and then they learned to use citrate and growth increased dramatically again. D: When combinations of beneficial mutations antagonize each other, the new organism dies while its ancestors carry on until a beneficial mutation that does not antagonize the others appears. E: Yes, most mutations are non-adaptive. The organisms that carry them die, the bad mutations die with them, and their ancestors carry on with their original non-mutated DNA. On the rarer occasions when an adaptive mutation occurs, the lucky organisms that get them live and the adaptive mutations are saved in their genomes and passed on to their ancestors.. F: Maybe someone can inform Dr. Behe that if a coded element is “broken” and the new organism survives where their siblings die, then that “broken” coded element is beneficial. Staying alive instead of dropping dead is very beneficial. G: Perhaps someone can also inform Dr. Behe that it’s a lot easier to “break” or “degrade” an existing gene so it performs a new function than it is to evolve a new gene, so we see a lot more of the former than of the latter. But if they keep the organism alive when it would otherwise die, then both are beneficial. Staying alive is better than dropping dead. H: Yes, if conditions revert to the way they were before the coded element was “broken”, then, under those new conditions, the mutation is no longer beneficial and when a mutation “breaks” the gene back to its original form, the lucky organism that gets that new mutation will live while its siblings die. Again, staying alive instead of dropping dead is very beneficial.dmullenix
January 26, 2012
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dmullenix, The problem is your position doesn't have any way to test its claim experimentally. Also it appears that you have reading comprehension issues:
I can make this point most clearly with a concrete example. We can go into the lab and modify bacterial cells by deleting the entire set of genes dedicated to the synthesis of tryptophan, one of the essential building blocks of proteins. When we observe what happens when these modified cells are given just enough tryptophan to grow and reproduce, we will see lots of things happening, but none that can be expected to reinvent a set of genes for making tryptophan, even in a large population over billions of years.
Not even in billions of years. BTW ID research is being conducted by all scientists as there isn't any scientists doing blind watchmaker research.Joe
January 25, 2012
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Well, that's as fine a pair of non-answers as I've ever seen. Axe and Gauger make a statement that is absolutely, excruciatingly, ignorant, one so bad that normally only a totally uninformed commenters would make it, and yet here they are, telling us to kill off not just a single gene, but a whole series of genes, and then if the organisms don't re-evolve the whole shooting match in a few weeks or months, evolution is disproved! And these two are your star scientists. As far as I know, they are the only people doing actual ID research. They're the ones whose work you hold up to us and tell us, "See? Proteins can't evolve! Evolution is impossible and Doug Axe and Ann Gauger have proven it in the lab!" What's scarey is that you don't seem to be embarassed by this, you don't try to hide it or shuffle it out of sight, you actually hold this silliness up and show it off as if it proved something other than the total vapidity of ID. I'll ask again: are the pulling our legs? Is ID pulling the world's leg?dmullenix
January 25, 2012
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Is dmullenix (and wikipedia) trying to pull our legs?
Lenski ran his experiment for 22 years (50,000 generations) and he estimates “that only 10 to 20 beneficial mutations achieved fixation in each population,
Yet when we look closer we find?
' Mutations : when benefits level off - June 2011 - (Lenski's e-coli after 50,000 generations) Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually. http://www2.cnrs.fr/en/1867.htm?theme1=7
Further notes:
Response from Ralph Seelke to David Hillis Regarding Testimony on Bacterial Evolution Before Texas State Board of Education, January 21, 2009 Excerpt: He has done excellent work showing the capabilities of evolution when it can take one step at a time. I have used a different approach to show the difficulties that evolution encounters when it must take two steps at a time. So while similar, our work has important differences, and Dr. Bull’s research has not contradicted or refuted my own. http://www.discovery.org/a/9951 Epistasis between Beneficial Mutations - July 2011 Excerpt: We found that epistatic interactions between beneficial mutations were all antagonistic—the effects of the double mutations were less than the sums of the effects of their component single mutations. We found a number of cases of decompensatory interactions, an extreme form of antagonistic epistasis in which the second mutation is actually deleterious in the presence of the first. In the vast majority of cases, recombination uniting two beneficial mutations into the same genome would not be favored by selection, as the recombinant could not outcompete its constituent single mutations. https://uncommondescent.com/epigenetics/darwins-beneficial-mutations-do-not-benefit-each-other/
Not that you will care dmullenix, but there is actually a very good reason for why combinations of supposed 'beneficial mutations' lead to antagonistic epistasis;
Poly-Functional Complexity equals Poly-Constrained Complexity http://docs.google.com/Doc?docid=0AYmaSrBPNEmGZGM4ejY3d3pfMjdoZmd2emZncQ DNA - Evolution Vs. Polyfuctionality - video http://www.metacafe.com/watch/4614519
Further notes:
“The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain - Michael Behe - December 2010 Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain.(that is a net 'fitness gain' within a 'stressed' environment i.e. remove the stress from the environment and the parent strain is always more 'fit') http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/
Michael Behe talks about the preceding paper on this podcast:
Michael Behe: Challenging Darwin, One Peer-Reviewed Paper at a Time - December 2010 http://intelligentdesign.podomatic.com/player/web/2010-12-23T11_53_46-08_00 Where's the substantiating evidence for neo-Darwinism? https://docs.google.com/document/d/1q-PBeQELzT4pkgxB2ZOxGxwv6ynOixfzqzsFlCJ9jrw/edit
Verse and Video:
John 3:10 Jesus answered him, “Are you the teacher of Israel and yet you do not understand these things? What we need is a living encounter with God! http://www.youtube.com/watch?v=BnlTIODfbhY
bornagain77
January 24, 2012
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Yeah unfortunately for Lenski his experiment provides support for baraminology. And Lenski did not demonstrate any new genes arising.Joe
January 24, 2012
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Is Axe trying to pull our legs? Did Axe actually try that experiment? How long did he watch it? Days? Weeks? A few months? Lenski ran his experiment for 22 years (50,000 generations) and he estimates "that only 10 to 20 beneficial mutations achieved fixation in each population, with less than 100 total point mutations (including neutral mutations) reaching fixation in each population." http://en.wikipedia.org/wiki/E._coli_long-term_evolution_experiment How many base pairs are in the entire set of genes dedicated to the synthesis of tryptophan? Divide that number by 20, multiply the result by 22 years, run your experiment for that long and get back to us. By the way, I have an iron-clad proof that the Great Wall of China was built by Space Aliens. Get a whole pile of bricks and a few dozen Chinese laborers and watch them for a year or two. If they don't get the Great Wall built in that time, then it's obvious that the Chinese couldn't have built the wall and that means that only Space Aliens or The Designer could have done the work. Q.E.D.dmullenix
January 24, 2012
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