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Michael Behe on how the new Lenski paper demonstrates a key problem with Darwinism

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Richard Lenski’s lab is supposed to demonstrate Darwinian evolution over endless generations of bacteria:

The new paper now reports on 2,500 generations of further evolution of the citrate mutant, in nutrient media that contains either citrate alone or citrate plus glucose (as for earlier generations). As always with the Lenski lab, the research is well and thoroughly done. But the resulting E. coli is one sick puppy. Inside the paper they report that “The spectrum of mutations identified in evolved clones was dominated by structural variation, including insertions, deletions, and mobile element transpositions.” All of those are exceedingly likely to break or degrade genes. Dozens more genes were lost. The citrate mutant tossed genetic information with mindless abandon for short term advantage.

In a particularly telling result, the authors “serendipitously discovered evidence of substantial cell death in cultures of a Cit+ clone sampled from … the LTEE at 50,000 generations.” In other words, those initial random “beneficial” citrate mutations that had been seized on by natural selection tens of thousands of generations earlier had led to a death spiral. The death rate of the ancestor of the LTEE was ~10 percent; after 33,000 generations it was ~30 percent; after 50,000, ~40 percent. For the newer set of experiments, the death rate varied for different strains of cells in different media, but exceeded 50 percent for some cell lines in a citrate-only environment. Indeed, the authors identified a number of mutations — again, almost certainly degradative ones — in genes for fatty acid metabolism that, they write with admirable detachment, “suggest adaptation to scavenging on dead and dying cells.”

The degraded E. coli was eating its dead.

Lessons to Draw

Let me emphasize: the only result from the decades-long, 50,000-plus generation E. coli evolution experiment that even seemed at first blush like it had a bit of potential to yield a novel pathway in the bacterium has resulted instead in spectacular devolution.

Michael Behe, “Citrate Death Spiral” at Evolution News and Science Today

Paper. (open access)

Yes, of course that’s true. But it no longer matters. As science devolves into myth, the popular narrative prevails over the correct one. The popular narrative is easier to teach because it fits in better with prevailing opinion.

See also: Darwin Devolves Much “evolution” is about breaking or blunting complex equipment in order to arrive at a simple solution for survival.

Has anyone here heard the proverb “Silks and satins put out the kitchen fire”? Think about what it means.

Comments
Seversky @ 10 states: That just indicates that Behe and ID proponents have a spectacular misconception of what evolution is about. Macro-evolution is the idea that one species becomes something genetically different over time. For 30 years, E coli. remained E coli. and there was no evidence of speciation. There was nothing genetically different. It was the equivalent of 1,000,000 years to humans with only micro-evolution to show for it. Those who point to micro as evidence of macro are the ones who don't understand what evolution is. If there had been evidence of speciation, rather than micro-evolution, the experiment would not have been stopped. No species has ever been witnessed becoming a genetically different species. Macro-evolution has never been witnessed by anyone. Macro-evolution has never had the results replicated. Without both of those happening, it remains a hypothesis. A scientific theory is based on what is witnessed and results replicated. That's how the scientific method works.BobRyan
June 19, 2020
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EDTA- The amount of misinformation contained in "On the Origins of Species..." easily canceled out any new information it provided. :cool:ET
June 18, 2020
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But that’s like saying a new book—say, Darwin’s Origin of Species when it first appeared in 1859—contains no new information, because the text has the same old letters and words that are found in other books.
Sounds like a counter-argument-by-analogy, and I thought skeptics here were opposed to arguments by analogy. And the analogy fails spectacularly too. Wholesale rearrangement of nucleotides (letters) (or other information in a cell) is not what happened. It's more like a large paragraph got duplicated, with a word or two changed--and no reader ever noticed.EDTA
June 18, 2020
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a few more notes,
The Human Gene Mutation Database The Human Gene Mutation Database (HGMD®) represents an attempt to collate known (published) gene lesions responsible for human inherited disease. Deleterious Mutation total (as of June 18. 2020) – 275,716 http://www.hgmd.cf.ac.uk/ac/ Critic ignores reality of Genetic Entropy - Dr John Sanford - 7 March 2013 Excerpt: Where are the beneficial mutations in man? It is very well documented that there are thousands of deleterious Mendelian mutations accumulating in the human gene pool, even though there is strong selection against such mutations. Yet such easily recognized deleterious mutations are just the tip of the iceberg. The vast majority of deleterious mutations will not display any clear phenotype at all. There is a very high rate of visible birth defects, all of which appear deleterious. Again, this is just the tip of the iceberg. Why are no beneficial birth anomalies being seen? This is not just a matter of identifying positive changes. If there are so many beneficial mutations happening in the human population, selection should very effectively amplify them. They should be popping up virtually everywhere. They should be much more common than genetic pathologies. Where are they? European adult lactose tolerance appears to be due to a broken lactase promoter [see Can’t drink milk? You’re ‘normal’! Ed.]. African resistance to malaria is due to a broken hemoglobin protein [see Sickle-cell disease. Also, immunity of an estimated 20% of western Europeans to HIV infection is due to a broken chemokine receptor—see CCR5-delta32: a very beneficial mutation. Ed.] Beneficials happen, but generally they are loss-of-function mutations, and even then they are very rare! http://creation.com/genetic-entropy Scientists Discover Proof That Humanity Is Getting Dumber, Smaller And Weaker By Michael Snyder, on April 29th, 2014 Excerpt: An earlier study by Cambridge University found that mankind is shrinking in size significantly. Experts say humans are past their peak and that modern-day people are 10 percent smaller and shorter than their hunter-gatherer ancestors. And if that’s not depressing enough, our brains are also smaller. The findings reverse perceived wisdom that humans have grown taller and larger, a belief which has grown from data on more recent physical development. The decline, said scientists, has happened over the past 10,000 years. http://thetruthwins.com/archives/scientists-discover-proof-that-humanity-is-getting-dumber-smaller-and-weaker If Modern Humans Are So Smart, Why Are Our Brains Shrinking? - January 20, 2011 Excerpt: John Hawks is in the middle of explaining his research on human evolution when he drops a bombshell. Running down a list of changes that have occurred in our skeleton and skull since the Stone Age, the University of Wisconsin anthropologist nonchalantly adds, “And it’s also clear the brain has been shrinking.” “Shrinking?” I ask. “I thought it was getting larger.” The whole ascent-of-man thing.,,, He rattles off some dismaying numbers: Over the past 20,000 years, the average volume of the human male brain has decreased from 1,500 cubic centimeters to 1,350 cc, losing a chunk the size of a tennis ball. The female brain has shrunk by about the same proportion. “I’d call that major downsizing in an evolutionary eyeblink,” he says. “This happened in China, Europe, Africa—everywhere we look.” http://discovermagazine.com/2010/sep/25-modern-humans-smart-why-brain-shrinking Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation George Montañez 1, Robert J. Marks II 2, Jorge Fernandez 3 and John C. Sanford 4 - May 2013 Excerpt: It is almost universally acknowledged that beneficial mutations are rare compared to deleterious mutations [1–10].,, It appears that beneficial mutations may be too rare to actually allow the accurate measurement of how rare they are [11]. 1. Kibota T, Lynch M (1996) Estimate of the genomic mutation rate deleterious to overall fitness in E. coli . Nature 381:694–696. 2. Charlesworth B, Charlesworth D (1998) Some evolutionary consequences of deleterious mutations. Genetica 103: 3–19. 3. Elena S, et al (1998) Distribution of fitness effects caused by random insertion mutations in Escherichia coli. Genetica 102/103: 349–358. 4. Gerrish P, Lenski R N (1998) The fate of competing beneficial mutations in an asexual population. Genetica 102/103:127–144. 5. Crow J (2000) The origins, patterns, and implications of human spontaneous mutation. Nature Reviews 1:40–47. 6. Bataillon T (2000) Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? Heredity 84:497–501. 7. Imhof M, Schlotterer C (2001) Fitness effects of advantageous mutations in evolving Escherichia coli populations. Proc Natl Acad Sci USA 98:1113–1117. 8. Orr H (2003) The distribution of fitness effects among beneficial mutations. Genetics 163: 1519–1526. 9. Keightley P, Lynch M (2003) Toward a realistic model of mutations affecting fitness. Evolution 57:683–685. 10. Barrett R, et al (2006) The distribution of beneficial mutation effects under strong selection. Genetics 174:2071–2079. 11. Bataillon T (2000) Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? Heredity 84:497–501. http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0006 John Sanford on (Genetic Entropy) - Down, Not Up - 2-4-2012 (at Loma Linda University) - video http://www.youtube.com/watch?feature=player_detailpage&v=PHsu94HQrL0#t=1040s Notes from John Sanford's preceding video: *3 new mutations every time a cell divides in your body * Average cell of 15 year old has up to 6000 mutations *Average cell of 60 year old has 40,000 mutations Reproductive cells are 'designed' so that, early on in development, they are 'set aside' and thus they do not accumulate mutations as the rest of the cells of our bodies do. Regardless of this protective barrier against the accumulation of slightly detrimental mutations still we find that,,, *60-175 mutations are passed on to each new generation. Dr. John Sanford Lecture at NIH (National Institute for Health): Genetic Entropy – (Human Genetic Degeneration) Can Genome Degradation be Stopped? (Short answer, NO!) https://www.youtube.com/watch?v=2Mfn2upw-O8 Can Purifying Natural Selection Preserve Biological Information? Excerpt Abstract: Most deleterious mutations have very slight effects on total fitness, and it has become clear that below a certain fitness effect threshold, such low-impact mutations fail to respond to natural selection. The existence of such a selection threshold suggests that many low-impact deleterious mutations should accumulate continuously, resulting in relentless erosion of genetic information.,,, Excerpt Conclusion: In conclusion, numerical simulation shows that realistic levels of biological noise result in a high selection threshold. This results in the ongoing accumulation of low-impact deleterious mutations, with deleterious mutation count per individual increasing linearly over time. Even in very long experiments (more than 100,000 generations), slightly deleterious alleles accumulate steadily, causing eventual extinction. These findings provide independent validation of previous analytical and simulation studies [2–13]. Previous concerns about the problem of accumula-tion of nearly neutral mutations are strongly supported by our analysis. Indeed, when numerical simulations incorporate realistic levels of biological noise, our analyses indicate that the problem is much more severe than has been acknowledged, and that the large majority of deleterious mutations become invisible to the selection process. Even apart from numerical simulation, it would seem readily obvious that the following factors should interfere with selection effectiveness and thereby increase the threshold for selection: (a) large functional genome size; (b) high mutation rate; (c) significant environmental variance; (d) randomness in the selection process; (e) extensive linkage; and (f) small or fragmented popula-tions. These factors are characteristic of all higher life forms [14] and should therefore be included in any future analyses. Our numerical simulation program incorporates all these factors, and suggests that the threshold for selection break-down should be very substantial for most eukaryotic species. As stated by Keightley and Eyre-Walker “How humans and related species evade the effects of mutation load on an evolutionary time scale is also an open question” https://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0010
bornagain77
June 18, 2020
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Lenski's e-coli are found to be in a 'death spiral' and a Darwinist's, (PavelU's), first response is,,,
"If Dr Lenski got those revealing results in just a few decades, imagine what would happen in a century or longer?"
LOL, and that quote is a shining example of the fantasy land that Darwinian advocates live in. Contrary to what PavelU so desperately wants to believe. in the face of overwhelming evidence to the contrary I might add, time is certainly not on PavelU's side. As Lee Spetner stated, "Whoever thinks macroevolution can be made by mutations that lose information is like the merchant who lost a little money on every sale but thought he could make it up on volume."
"The neo-Darwinians would like us to believe that large evolutionary changes can result from a series of small events if there are enough of them. But if these events all lose information they can’t be the steps in the kind of evolution the neo-Darwin theory is supposed to explain, no matter how many mutations there are. Whoever thinks macroevolution can be made by mutations that lose information is like the merchant who lost a little money on every sale but thought he could make it up on volume." Lee Spetner (Ph.D. Physics - MIT - Not By Chance) Time: The Unlikely Villain Excerpt: When confronted with the problem of equilibrium, most scientific materialists will appeal to the magic ingredient of time. In chapter one we saw this appeal by Nobel Laureate, George Wald: “Time is in fact the hero of the plot. Given so much time the impossible becomes possible, the possible probable, and the probable virtually certain. One has only to wait: Time itself performs the miracles.” 49 However, Dr. (Harold F.) Blum, who is a materialist, points out that Wald’s faith in the miraculous ingredient of time is mere wishful thinking. Prolonged time periods, he asserts, actually worsen the dilemma: “I think if I were rewriting this chapter [on the origin of life] completely, I should want to change the emphasis somewhat. I should want to play down still more the importance of the great amount of time available for highly improbable events to occur. One may take the view that the greater the time elapsed the greater should be the approach to equilibrium, the most probable state, and it seems that this ought to take precedence in our thinking over the idea that time provides the possibility for the occurrence of the highly improbable.” 50 http://www.bibliotecapleyades.net/ciencia/esp_ciencia_life13.htm Douglas Axe: Can Evolution Work (even) if you have Billions of Years? https://www.youtube.com/watch?list=PLR8eQzfCOiS3-MQT4SEaLNloU5v2poZKf&v=npJyQLhz7Ic When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied. http://biologicinstitute.org/2011/04/16/when-theory-and-experiment-collide/ The waiting time problem in a model hominin population – 2015 Sep 17 John Sanford, Wesley Brewer, Franzine Smith, and John Baumgardner Excerpt: The program Mendel’s Accountant realistically simulates the mutation/selection process,,, Given optimal settings, what is the longest nucleotide string that can arise within a reasonable waiting time within a hominin population of 10,000? Arguably, the waiting time for the fixation of a “string-of-one” is by itself problematic (Table 2). Waiting a minimum of 1.5 million years (realistically, much longer), for a single point mutation is not timely adaptation in the face of any type of pressing evolutionary challenge. This is especially problematic when we consider that it is estimated that it only took six million years for the chimp and human genomes to diverge by over 5 % [1]. This represents at least 75 million nucleotide changes in the human lineage, many of which must encode new information. While fixing one point mutation is problematic, our simulations show that the fixation of two co-dependent mutations is extremely problematic – requiring at least 84 million years (Table 2). This is ten-fold longer than the estimated time required for ape-to-man evolution. In this light, we suggest that a string of two specific mutations is a reasonable upper limit, in terms of the longest string length that is likely to evolve within a hominin population (at least in a way that is either timely or meaningful). Certainly the creation and fixation of a string of three (requiring at least 380 million years) would be extremely untimely (and trivial in effect), in terms of the evolution of modern man. It is widely thought that a larger population size can eliminate the waiting time problem. If that were true, then the waiting time problem would only be meaningful within small populations. While our simulations show that larger populations do help reduce waiting time, we see that the benefit of larger population size produces rapidly diminishing returns (Table 4 and Fig. 4). When we increase the hominin population from 10,000 to 1 million (our current upper limit for these types of experiments), the waiting time for creating a string of five is only reduced from two billion to 482 million years. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573302/ Whale Evolution vs. (The Waiting Time Problem of) Population Genetics – Richard Sternberg and Paul Nelson – (excerpted from ‘Living Waters’ video) (2015) https://youtu.be/0csd3M4bc0Q etc.. etc.. etc...
bornagain77
June 18, 2020
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And the lie- no one was going to teach ID in Dover schools. Only pathetic losers try to make that case.ET
June 18, 2020
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The only misconceptions belong to seversky and the evos. E coli already has the ability to utilize citrate. All that happened was the CiT+ transport gene was duplicated. If you have two copies of the same book you don't have any new information from the 2nd copy. So the ONLY gene that could possibly help the E coli in this scenario was duplicated and put under the control of a promoter that was NOT turned off by the presence of O2. This sounds exactly like what Dr. Spetner discussed in "Not By Chance"- a built-in response to an environmental cueET
June 18, 2020
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Let me emphasize: the only result from the decades-long, 50,000-plus generation E. coli evolution experiment that even seemed at first blush like it had a bit of potential to yield a novel pathway in the bacterium has resulted instead in spectacular devolution. Michael Behe, “Citrate Death Spiral” at Evolution News and Science Today
That just indicates that Behe and ID proponents have a spectacular misconception of what evolution is about. As Blount and Lenski write here:
“No new genetic information” The authors assert repeatedly (last sentence of their Importance statement, and first and last paragraphs of their Discussion) that “no new genetic information evolved.” However, that statement flatly contradicts the fact that in their experiments, and ours, E. coli gained the new ability to grow on citrate in the presence of oxygen. We would further add (which we have not emphasized before) that these Cit+ strains can grow on citrate as a sole carbon source—when E. coli grows anaerobically on citrate, it requires a second substrate for growth in order to use the citrate (a phenomenon called “co-metabolism”). The claim that “no new genetic information evolved” is based on the fact that the bacteria gained this new ability by rearranging existing structural and regulatory genetic elements. But that’s like saying a new book—say, Darwin’s Origin of Species when it first appeared in 1859—contains no new information, because the text has the same old letters and words that are found in other books. In an evolutionary context, a genome encodes not just proteins and patterns of expression, but information about the environments where an organism’s ancestors have lived and how to survive and reproduce in those environments by having useful proteins, expressing them under appropriate conditions (but not others), and so on. So when natural selection—that is, differential survival and reproduction—favors bacteria whose genomes have mutations that enable them to grow on citrate, those mutations most certainly provide new and useful information to the bacteria. That’s how evolution works—it’s not as though new genes and functions somehow appear out of thin air. As the bacterial geneticist and Nobel laureate François Jacob wrote (Science, 1977): “[N]atural selection does not work as an engineer works. It works like a tinkerer—a tinkerer who does not know exactly what he is going to produce but uses whatever he finds around him, whether it be pieces of string, fragments of wood, or old cardboards; in short, it works like a tinkerer who uses everything at his disposal to produce some kind of workable object.” To say there’s no new genetic information when a new function has evolved (or even when an existing function has improved) is a red herring that is promulgated by the opponents of evolutionary science. In this regard, it seems relevant to point out that the corresponding author, Scott Minnich, is a fellow of the Discovery Institute and was an expert witness for the losing side that wanted to allow the teaching of “intelligent design” as an alternative to evolution in public schools in the landmark Kitzmiller v. Dover case.
Seversky
June 18, 2020
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Except for the fact that there isn't anything in Lenski's experiment that says prokaryotes can evolve into something other than prokaryotes. And that is given billions of years.ET
June 18, 2020
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Dr Behe might be wrong because Dr Lenski's experiment has lasted only a few decades, but evolution had billions of years at its disposition. If Dr Lenski got those revealing results in just a few decades, imagine what would happen in a century or longer?PavelU
June 18, 2020
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BobRyan, Good points. I agree.jawa
June 18, 2020
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The closing statement in Dr Behe’s article in EN is excellent: “Thanks in very large part to the fine work done over decades at Michigan State we can now be certain that, like the citrate-eating E. coli, as an explanation for the great features of life Darwin’s theory itself is in a death spiral.”jawa
June 18, 2020
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as to
"Let me emphasize: the only result from the decades-long, 50,000-plus generation E. coli evolution experiment that even seemed at first blush like it had a bit of potential to yield a novel pathway in the bacterium has resulted instead in spectacular devolution." - Michael Behe, “Citrate Death Spiral”
Hmmm, interesting. I remember that, not too long ago, Darwinists here on UD would often claim that Lenski's Citrate adaptation was (finally) real time experimental proof for speciation, i.e. macro-evolution,, for instance, this claim
"But I don’t see why we need that, when the evolutionary process has been demonstrated and observed directly in controlled laboratory conditions (i.e. Lenski's citrate adaptation)": https://uncommondescent.com/intelligent-design/larry-morans-revisionist-history-debunked/#comment-587342
In fact, Lenski himself had once claimed that the Citrate adaptation was experimental proof for speciation,
"More strikingly, however, he (Lenski) found that one of the 12 bacterial lines he has maintained has developed into what he believes is a new species, able to use a compound in the solution called citrate — a derivative of citric acid, like that found in some fruit — for food." https://news.harvard.edu/gazette/story/2014/02/evolution-in-real-time/
That claim from Lenski that the Citrate adaptation was (finally) proof for speciation was shot down by Scott Minnich and company in 2016. i.e. "We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved. "
Rapid Evolution of Citrate Utilization by Escherichia coli by Direct Selection Requires citT and dctA. - Minnich - Feb. 2016 The isolation of aerobic citrate-utilizing Escherichia coli (Cit(+)) in long-term evolution experiments (LTEE) has been termed a rare, innovative, presumptive speciation event. We hypothesized that direct selection would rapidly yield the same class of E. coli Cit(+) mutants and follow the same genetic trajectory: potentiation, actualization, and refinement. This hypothesis was tested,,, Potentiation/actualization mutations occurred within as few as 12 generations, and refinement mutations occurred within 100 generations.,,, E. coli cannot use citrate aerobically. Long-term evolution experiments (LTEE) performed by Blount et al. (Z. D. Blount, J. E. Barrick, C. J. Davidson, and R. E. Lenski, Nature 489:513-518, 2012, http://dx.doi.org/10.1038/nature11514 ) found a single aerobic, citrate-utilizing E. coli strain after 33,000 generations (15 years). This was interpreted as a speciation event. Here we show why it probably was not a speciation event. Using similar media, 46 independent citrate-utilizing mutants were isolated in as few as 12 to 100 generations. Genomic DNA sequencing revealed an amplification of the citT and dctA loci and DNA rearrangements to capture a promoter to express CitT, aerobically. These are members of the same class of mutations identified by the LTEE. We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved. http://www.ncbi.nlm.nih.gov/pubmed/26833416 Re-interpreting Long-Term Evolution Experiments: A Conversation with Dr. Scott Minnich – March 2017 - video https://www.youtube.com/watch?v=6rpNPzQAMck
What was Lenski's response? Well, in typical Darwinian fashion, he, instead of humbly admitting that he was wrong in his claim for experimental proof of speciation, responded with an ad hominem attack against Dr. Minnich, i.e. "In a disgraceful move, Lenski impugned Scott Minnich's character. Since he's a "fellow of the Discovery Institute" sympathetic with intelligent design,,,"
Richard Lenski and Citrate Hype -- Now Deflated - Michael Behe - May 12, 2016 Excerpt: ,,, for more than 25 years Lenski's lab has continuously grown a dozen lines of the bacterium E. coli in small culture flasks, letting them replicate for six or seven generations per day and then transferring a portion to fresh flasks for another round of growth. The carefully monitored cells have now gone through more than 60,000 generations, which is equivalent to over a million years for a large animal such as humans.,,, In 2008 Lenski's group reported that after more than 15 years and 30,000 generations of growth one of the E. coli cell lines suddenly developed the ability to consume citrate,,, the authors argued it might be pretty important.,,, They also remarked that,,, perhaps the mutation marked the beginning of the evolution of a brand new species.,, One scientist who thought the results were seriously overblown was Scott Minnich, professor of microbiology at the University of Idaho ,,, So Minnich's lab re-did the work under conditions he thought would be more effective. The bottom line is that they were able to repeatedly isolate the same mutants Lenski's lab did as easily as falling off a log -- within weeks, not decades.,,, Richard Lenski was not pleased.,,, In a disgraceful move, Lenski impugned Scott Minnich's character. Since he's a "fellow of the Discovery Institute" sympathetic with intelligent design,,, (Regardless of the ad hominem) With regard to citrate evolution, the Minnich lab's results have revealed E. coli to be a one-trick pony.,,, The take-home lesson is that,,, (Lenski's overinflated) hype surrounding the (implications of the citrate adaptation) has seriously misled the public and the scientific community. It's far past time that a pin was stuck in its (Lenski's citrate) balloon. http://www.evolutionnews.org/2016/05/richard_lenski102839.html
Thus in conclusion, not only was Lenski's Citrate adaptation never proof for speciation, macro-evolution, in the first place, but, as Dr Behe points out in his current article, the Citrate adaptation turns out to be proof that evolutionary processes, in the long run, actually send species on a 'death spiral', i.e. into "spectacular devolution." Which is exactly the opposite kind of real-time empirical evidence that Darwinists need in order to. (finally), substantiate their theory. Of related note:
Darwin Devolves: The New Science About DNA That Challenges Evolution – released February 26, 2019 - by Michael J. Behe - per Amazon GENETIC ENTROPY - It's Down NOT Up... - John Sanford https://www.geneticentropy.org/ NIH (National Institute of Health) Presentation - John Sanford – Mutation Accumulation: Is it a Serious Health Risk? - https://www.youtube.com/watch?v=eqIjnol9uh8
bornagain77
June 18, 2020
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Jawa: I get the feeling that the $10,000,000 will remain unclaimed for a great many years to come. I wondered if anyone ever asked Hawking where gravity came from? Laws do not write themselves into existence.BobRyan
June 18, 2020
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BobRyan, You asked: “how did the universe come into existence” According to Stephen Hawking, it did thanks to the law of gravity. Go figure. “how did life begin?” Dr Cronin and Dr Szostak will explain it soon. Then they’ll get the Evo2.0 OOL $10M prize to invest it in SETI. :)jawa
June 18, 2020
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Remove ID and you are left with believing magic, since science must be suspended completely. The universe must have created itself from nothing, but science dictates that something cannot come from nothing. The universe somehow created the laws of physics, but the Big Bang was purely a chaotic event. Chaos cannot create order, yet that is what the laws of physics are. Mathematics was created by the same magic that created the laws of physics, since math shows order. The origin of life is a return to something being created from nothing, which is a scientific impossibility. Logic dictates that questions must be asked. Energy cannot be created or destroyed. It can only be transferred. Energy that exists today has been around for billions of years. If energy cannot be created, where did the energy come from? If something cannot come from nothing, how did the universe come into existence and how did life begin? If chaos cannot create order, it only creates more chaos, where did the laws of physics and mathematical formulas come from? Only ID answers those questions. Einstein made his point clear. The more he studied the universe, the more he believed in God.BobRyan
June 17, 2020
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The good news is that Darwin really ISN'T the popular narrative. Polls consistently show about 40% of people go with creation, 30% with natural selection, 30% with some kind of 'guided creation' or ID.polistra
June 17, 2020
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