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Video: “How accurate are current models used in population genetics?”

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Lenski. ??? And are you purposely being misleading or are you really that far out of the loop??? Rose-Colored Glasses: Lenski, Citrate, and BioLogos - Michael Behe - November 13, 2012 Excerpt: Readers of my posts know that I'm a big fan of Professor Richard Lenski, a microbiologist at Michigan State University and member of the National Academy of Sciences. For the past few decades he has been conducting the largest laboratory evolution experiment ever attempted. Growing E. coli in flasks continuously, he has been following evolutionary changes in the bacterium for over 50,000 generations (which is equivalent to roughly a million years for large animals). Although Lenski is decidedly not an intelligent design proponent, his work enables us to see what evolution actually does when it has the resources of a large number of organisms over a substantial number of generations. Rather than speculate, Lenski and his coworkers have observed the workings of mutation and selection.,,, In my own view, in retrospect, the most surprising aspect of the oxygen-tolerant citT mutation was that it proved so difficult to achieve. If, before Lenski's work was done, someone had sketched for me a cartoon of the original duplication that produced the metabolic change, I would have assumed that would be sufficient -- that a single step could achieve it. The fact that it was considerably more difficult than that goes to show that even skeptics like myself overestimate the power of the Darwinian mechanism. http://www.evolutionnews.org/2012/11/rose-colored_gl066361.html Michael Behe's Quarterly Review of Biology Paper Critiques Richard Lenski's E. Coli Evolution Experiments - December 2010 Excerpt: After reviewing the results of Lenski's research, Behe concludes that the observed adaptive mutations all entail either loss or modification--but not gain--of Functional Coding ElemenTs (FCTs) http://www.evolutionnews.org/2010/12/michael_behes_quarterly_review041221.html Richard Lenski's Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information - September 2011 Excerpt: The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski's research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT. (Michael J. Behe, "Experimental Evolution, Loss-of-Function Mutations and 'The First Rule of Adaptive Evolution'," Quarterly Review of Biology, Vol. 85(4) (December, 2010).) http://www.evolutionnews.org/2011/09/richard_lenskis_long_term_evol051051.html 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 New Research on Epistatic Interactions Shows "Overwhelmingly Negative" Fitness Costs and Limits to Evolution - Casey Luskin June 8, 2011 Excerpt: In essence, these studies found that there is a fitness cost to becoming more fit. As mutations increase, bacteria faced barriers to the amount they could continue to evolve. If this kind of evidence doesn't run counter to claims that neo-Darwinian evolution can evolve fundamentally new types of organisms and produce the astonishing diversity we observe in life, what does? http://www.evolutionnews.org/2011/06/new_research_on_epistatic_inte047151.htmlbornagain77
December 17, 2012
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BA posted this:
So Darwinists don’t need to actually demonstrate the origination of any novel gene/protein or molecular machine by neo-Darwinian processes because???,, because???,, because??? anyone?? anyone???
Lenski.timothya
December 17, 2012
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BA posted this:
Taken together with evidence of pervasive genome transcription, these data indicate that additional protein-coding genes remain to be found.
Could you provide a cite supporting your assertion of "evidence of pervasive genome transcription"? What exactly are you referring to?timothya
December 17, 2012
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"Until cdesign proponentsists can provide evidence of how their putative designer did its work, then you are, indeed, begging the question." So Darwinists don't need to actually demonstrate the origination of any novel gene/protein or molecular machine by neo-Darwinian processes because???,, because???,, because??? anyone?? anyone???bornagain77
December 17, 2012
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And as Dr. Doug Axe recently pointed out in this video:
Dr. Doug Axe - What are the implications of the book Science & Human Origins for the Darwinian paradigm? - video (What needs an explanation is not the similarities but the differences) http://www.youtube.com/watch?v=pnFs5D-vvnI
What needs an explanation are the differences not the similarities.,,, After all is it not the differences that neo-Darwinism purports to explain? Yet the differences that can actually be explained by the mechanism of neo-Darwinism are miniscule:
Biologist Douglas Axe on evolution's ability to produce new functions http://www.youtube.com/watch?v=8ZiLsXO-dYo
Further notes:
More from Ann Gauger on why humans didn’t happen the way Darwin said - July 2012 Excerpt: Each of these new features probably required multiple mutations. Getting a feature that requires six neutral mutations is the limit of what bacteria can produce. For primates (e.g., monkeys, apes and humans) the limit is much more severe. Because of much smaller effective population sizes (an estimated ten thousand for humans instead of a billion for bacteria) and longer generation times (fifteen to twenty years per generation for humans vs. a thousand generations per year for bacteria), it would take a very long time for even a single beneficial mutation to appear and become fixed in a human population. You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect. Facing Facts But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes— sixteen anatomical features—in the time available. At most, a new binding site might affect the regulation of one or two genes. https://uncommondescent.com/intelligent-design/more-from-ann-gauger-on-why-humans-didnt-happen-the-way-darwin-said/ From Jerry Coyne, More Table-Pounding, Hand-Waving - May 2012 Excerpt: "More than 6 percent of genes found in humans simply aren't found in any form in chimpanzees. There are over fourteen hundred novel genes expressed in humans but not in chimps." Jerry Coyne - ardent and 'angry' neo-Darwinist - professor at the University of Chicago in the department of ecology and evolution for twenty years. He specializes in evolutionary genetics. http://www.evolutionnews.org/2012/05/from_jerry_coyn060271.html An integrated encyclopedia of DNA elements in the human genome - Sept. 6, 2012 Excerpt: Analysis,,, yielded 57 confidently identified unique peptide sequences in intergenic regions relative to GENCODE annotation. Taken together with evidence of pervasive genome transcription, these data indicate that additional protein-coding genes remain to be found. http://www.nature.com/nature/journal/v489/n7414/full/nature11247.html
bornagain77
December 17, 2012
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Andre posted this:
Really? And why does it not support the evidence of a common design? I beg the question
Note the phrase "evidence of common design". There isn't any evidence for common design. Your argument is based on incredulity, which is a famously bad reason to ask people to agree with you. Until cdesign proponentsists can provide evidence of how their putative designer did its work, then you are, indeed, begging the question.timothya
December 17, 2012
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Here’s the Latest Just-So Story: Recurrent Evolution - Cornelius Hunter - April 2012 Excerpt: The first step to explaining something away is to give it a name. And so evolutionists have labeled this awkward evidence as recurrent evolution.,,, If the pattern fits the evolutionary tree, then it is explained as common evolutionary history. If not, then it is explained as common evolutionary forces. Heads I win, tails you lose.,, Common descent has always been an auxiliary hypothesis for the simple reason that evolution’s theoretical core does not mandate common descent, or anything else for that matter, aside from its insistence that the species arose naturally. Beyond that, anything goes.,, Evolutionists insist the species arose naturally, their religion requires it. http://darwins-god.blogspot.com/2012/04/heres-latest-just-so-story-recurrent.html Incongruence between phylogenies derived from morphological versus molecular analyses, and between trees based on different subsets of molecular sequences has become pervasive as datasets have expanded rapidly in both characters and species. (Liliana M. Dávalos, Andrea L. Cirranello, Jonathan H. Geisler, and Nancy B. Simmons, "Understanding phylogenetic incongruence: lessons from phyllostomid bats," Biological Reviews of the Cambridge Philosophical Society, Vol. 87:991-1024 (2012).) (Shhhhsh!, maybe they won't notice) Theory Creep: The Quiet Shift in Evolutionary Thought - Douglas Axe June 25, 2012 Excerpt: But if we fast-forward two more decades, it becomes clear that the consistent picture that everyone expected -- all genes confirming the same pattern of species relationships -- is not to be. What we have instead is something of a mess, as James Degnan and Noah Rosenberg made clear in a paper published in 2009(3): "Many of the first studies to examine the conflicting signal of different genes have found considerable discordance across gene trees: studies of hominids, pines, cichlids, finches, grasshoppers and fruit flies have all detected genealogical discordance so widespread that no single tree topology predominates." And despite consistent attempts to portray this as something less than a crisis for evolutionary theory, the news found its way into the popular press. That same year, The Telegraph jumped on the story with an article titled, "Charles Darwin's tree of life is 'wrong and misleading,' claim scientists"4. http://www.evolutionnews.org/2012/06/theory_creep_th_1061301.html Phylogeny: Rewriting evolution - Tiny molecules called microRNAs are tearing apart traditional ideas about the animal family tree. - Elie Dolgin - 27 June 2012 Excerpt: “I've looked at thousands of microRNA genes, and I can't find a single example that would support the traditional tree,” he says. "...they give a totally different tree from what everyone else wants.” (Phylogeny: Rewriting evolution, Nature 486,460–462, 28 June 2012) (molecular palaeobiologist - Kevin Peterson) Mark Springer, (a molecular phylogeneticist working in DNA states),,, “There have to be other explanations,” he says. Peterson and his team are now going back to mammalian genomes to investigate why DNA and microRNAs give such different evolutionary trajectories. “What we know at this stage is that we do have a very serious incongruence,” says Davide Pisani, a phylogeneticist,,, http://www.nature.com/news/phylogeny-rewriting-evolution-1.10885 This Paper Discusses Problems With the Evolutionary Tree That You Didn’t Learn in Biology Class - Cornelius Hunter - May 2012 Excerpt: In fact, it is impossible to construct a realistic evolutionary tree using all the (genetic) data. Evolutionists routinely construct evolutionary trees using a select, more cooperative, subset of the data. And even then the resulting trees are unrealistic. That is, they require evolutionary change for which there is no known mechanism. This is true even according to evolutionists who are quite liberal in allowing for speculation.,,, So neighboring species on the evolutionary tree may have a great many similarities, but in many cases they have some big differences, which evolutionary theory cannot explain beyond vague speculation. http://darwins-god.blogspot.com/2012/05/this-paper-discusses-problems-with.html Why Darwin was wrong about the (genetic) tree of life: - 21 January 2009 Excerpt: "Roughly 50 per cent of its genes have one evolutionary history and 50 per cent another," Syvanen says. ."We've just annihilated the tree of life. It's not a tree any more, it's a different topology entirely," says Syvanen. "What would Darwin have made of that?" http://www.newscientist.com/article/mg20126921.600-why-darwin-was-wrong-about-the-tree-of-life.html The tree of life, one of the iconic concepts of evolution, has turned out to be a figment of our imagination, says Graham Lawton http://www.thedivineconspiracy.org/Z5221S.pdf Accidental origins: Where species come from – March 2010 Excerpt: If speciation results from natural selection via many small changes, you would expect the branch lengths to fit a bell-shaped curve.,,, Instead, Pagel’s team found that in 78 per cent of the trees, the best fit for the branch length distribution was another familiar curve, known as the exponential distribution. Like the bell curve, the exponential has a straightforward explanation – but it is a disquieting one for evolutionary biologists. The exponential is the pattern you get when you are waiting for some single, infrequent event to happen.,,,To Pagel, the implications for speciation are clear: “It isn’t the accumulation of events that causes a speciation, it’s single, rare events falling out of the sky, so to speak.” http://www.newscientist.com/article/mg20527511.400-accidental-origins-where-species-come-from.html?page=2 Guy who DOESN’T support ID: Genomics has “overturned” Darwin’s iconic Tree of Life Excerpt: The genomics revolution, Koonin argues, … 'effectively overturned the central metaphor of evolutionary biology (and, arguably, of all biology), the Tree of Life (TOL), by showing that evolutionary trajectories of individual genes are irreconcilably different. Whether the TOL can or should be salvaged — and, if so, in what form — remains a matter of intense debate that is one of the important themes of this book. Uprooting the TOL is part of what I consider to be a ‘metarevolution,’ a major change in the entire conceptual framework of biology.' https://uncommondescent.com/darwinism/guy-who-doesn%E2%80%99t-support-id-genomics-has-%E2%80%9Coverturned%E2%80%9D-darwins-iconic-tree-of-life/ Testing the Orchard Model and the NCSE’s Claims of “Nested Patterns” Supporting a “Tree of Life” Excerpt: Perhaps the reason why different genes are telling “different evolutionary stories” and “one group suggests one biogeographic pattern, and another group suggests another” is because the genes and organisms have wholly different stories to tell, namely stories that indicate that not all living organisms are ancestrally related, thereby fulfilling a testable prediction of the orchard model. http://www.evolutionnews.org/2010/03/testing_the_orchard_model_and.htmlbornagain77
December 17, 2012
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Really? And why does it not support the evidence of a common design? I beg the question Timothy....Andre
December 17, 2012
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What a load of nonsense. The null hypothesis for common ancestry is that no ancestry tree exists. So, we run analyses across the available DNA data and what do we find? Every phylogenetic analysis yields a relatedness tree that contradicts the null hypothesis. Every. Single. One. And what do we then find? Despite the inconsistencies of one analysis to another (reflecting the choice of the specific DNA markers to be included in the particular analysis) . . . B'golly, b'gosh: all of the derived trees (all of them) converge on a single, common-ancestry tree. Perhaps one branch should be placed here instead of there, but every single piece of evidence supports the hypothesis that modern species inherited their genetic structures from common ancestors. Every. Single. One.timothya
December 17, 2012
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