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

  1. 1
    timothya says:

    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.

  2. 2
    Andre says:

    Really? And why does it not support the evidence of a common design? I beg the question Timothy….

  3. 3
    bornagain77 says:

    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.co.....rrent.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/2.....61301.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/phy.....on-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.co.....-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/ar.....-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/ar.....tml?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.’
    http://www.uncommondescent.com.....e-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/2.....l_and.html

  4. 4
    timothya says:

    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.

  5. 5
    bornagain77 says:

    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.
    http://www.uncommondescent.com.....rwin-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/2.....60271.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/j.....11247.html

  6. 6
    bornagain77 says:

    “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???

  7. 7
    timothya says:

    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?

  8. 8
    timothya says:

    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.

  9. 9
    bornagain77 says:

    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/2.....66361.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/2.....41221.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/2.....51051.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/2.....47151.html

  10. 10
    bornagain77 says:

    “Could you provide a cite supporting your assertion of “evidence of pervasive genome transcription”?”

    You mean prior to the recent ENCODE data I just cited??? Okie Dokie:

    How The Junk DNA Hypothesis Has Changed Since 1980 – Richard Sternberg – Oct. 2009 – Excellent Summary
    Excerpt: A surprising finding of ENCODE and other transcriptome projects is that almost every nucleotide of human (and mouse) chromosomes is transcribed in a regulated way.
    http://www.evolutionnews.org/2.....is_ha.html

  11. 11
    timothya says:

    Did Lenski’s experiment demonstrate that an Escherischia bacterium could develop a novel pathway to metabolise a citrate substrate? Yes he did.

    How did the the microbe develop this capability? By incorporating mutations that changed the proteins controlling the pre-existing metabolic pathways so that citrate metabolism now fits into the organism’s phenotype.

    Unless you want to claim that Lenski’s experimental microbes are not actually metabolising citrate.

    End of argument about the impossibility of novel protein evolution.

    It happened. Learn about it. Live with it.

  12. 12
    timothya says:

    BA posted this:

    You mean prior to the recent ENCODE data I just cited??? Okie Dokie:

    How The Junk DNA Hypothesis Has Changed Since 1980 – Richard Sternberg – Oct. 2009 – Excellent Summary
    Excerpt: A surprising finding of ENCODE and other transcriptome projects is that almost every nucleotide of human (and mouse) chromosomes is transcribed in a regulated way.
    http://www.evolutionnews.org/2…..is_ha.html

    Ummmm wait a second. That is not a cite from the ENCODE project. It is a claim made by the creationist universe. Why should I accept that claim as valid? Because you say so?

  13. 13
    bornagain77 says:

    So timothya, the novel protein is where in all this? The ability to digest citrate was present all along, and the ability to utilize the ability in the presense of oxygen is well within Behe’s “Edge Of Evolution”. In fact Dr. Behe stated:

    “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.”

    So you don’t have any novel protein or molecular machine, what was accomplished was trivial, moreover, if you really want to get technical, the adjustment in preexisting functionality, to environmental stress, was accomplished by processes that can be classified as ‘non-random’ processes (Shapiro), and to make matters worse, Lenski’s ‘evolved bacteria’ are less fit than the original bacteria:

    Genetic Entropy Confirmed (in Lenski’s e-coli) – June 2011
    Excerpt: No increases in adaptation or fitness were observed, and no explanation was offered for how neo-Darwinism could overcome the downward trend in fitness.
    http://crev.info/content/11060....._confirmed

    Lenski’s e-coli – Analysis of Genetic Entropy
    Excerpt: Mutants of E. coli obtained after 20,000 generations at 37°C were less “fit” than the wild-type strain when cultivated at either 20°C or 42°C. Other E. coli mutants obtained after 20,000 generations in medium where glucose was their sole catabolite tended to lose the ability to catabolize other carbohydrates. Such a reduction can be beneficially selected only as long as the organism remains in that constant environment. Ultimately, the genetic effect of these mutations is a loss of a function useful for one type of environment as a trade-off for adaptation to a different environment.
    http://www.answersingenesis.or.....n-bacteria

    ————

    Revisiting the Central Dogma in the 21st Century – James A. Shapiro – 2009
    Excerpt (Page 12): Underlying the central dogma and conventional views of genome evolution was the idea that the genome is a stable structure that changes rarely and accidentally by chemical fluctuations (106) or replication errors. This view has had to change with the realization that maintenance of genome stability is an active cellular function and the discovery of numerous dedicated biochemical systems for restructuring DNA molecules.(107–110) Genetic change is almost always the result of cellular action on the genome. These natural processes are analogous to human genetic engineering,,, (Page 14) Genome change arises as a consequence of natural genetic engineering, not from accidents. Replication errors and DNA damage are subject to cell surveillance and correction. When DNA damage correction does produce novel genetic structures, natural genetic engineering functions, such as mutator polymerases and nonhomologous end-joining complexes, are involved. Realizing that DNA change is a biochemical process means that it is subject to regulation like other cellular activities. Thus, we expect to see genome change occurring in response to different stimuli (Table 1) and operating nonrandomly throughout the genome, guided by various types of intermolecular contacts (Table 1 of Ref. 112).
    http://shapiro.bsd.uchicago.ed.....0Dogma.pdf

  14. 14
    timothya says:

    BA posted this claim:

    The ability to digest citrate was present all along, and the ability to utilize the ability in the presense of oxygen is well within Behe’s “Edge Of Evolution”.

    What piece of research supports this? (A cite would be useful).

  15. 15
    bornagain77 says:

    Ummmm wait a second. That is not a cite from the ENCODE project. It is a claim made by the creationist universe. Why should I accept that claim as valid?

    So you unquestionably the (ahem) dogma free spin of Darwinists and think that Dr. Sternberg is purposely being misleading??? 🙂 Well in that case,,,

    ENCODE pilot project – 2007
    Excerpt: The human genome is pervasively transcribed, such that the majority of its bases are associated with at least one primary transcript and many transcipts link distal regions to established protein coding loci.,,,,
    Concluding statement of the ENCODE study:
    “we have also encountered a remarkable excess of experimentally identified functional elements lacking evolutionary constraint, and these cannot be dismissed for technical reasons. This is perhaps the biggest surprise of the pilot phase of the ENCODE Project, and suggests that we take a more ‘neutral’ view of many of the functions conferred by the genome.”
    http://www.genome.gov/Pages/Re.....e05874.pdf

  16. 16
    bornagain77 says:

    excuse me,, “unquestionably accept the”

  17. 17
    bornagain77 says:

    You were given the cite

  18. 18
    bornagain77 says:

    check,,, Moderator there seems to be a programming glitch in the page.,, stuck on bold type

  19. 19
    timothya says:

    BA claims that the results of the ENCODE project support the idea that the majority (>=80%) of the human genome is “transcribed”. I will stop here and ask any competent biologist reading this blog: do you support or deny this claim?

  20. 20
    timothya says:

    BA, I will repeat my request. You claimed this:

    The ability to digest citrate was present all along, and the ability to utilize the ability in the presense of oxygen is well within Behe’s “Edge Of Evolution”.

    Can you please provide a cite that supports this claim?

  21. 21
    bornagain77 says:

    “I will stop here and ask any competent biologist”

    Such as Dr. Moran?

    What an Evolution Advocate’s Response to the ENCODE Project Tells Us about the Evolution Debate – Casey Luskin September 10, 2012
    Excerpt: Larry Moran and other vocal Internet evolution-activists are welcome to disagree and protest these conclusions, but it’s clear that the consensus of molecular biologists — people who actually study how the genome works — now believe that the idea of “junk DNA” is essentially wrong.,,,
    http://www.evolutionnews.org/2.....64101.html

    Here is a response to Darwinist Larry Moran by a ENCODE researcher:
    “That said, I can’t help but notice a trend: over time, “junk DNA” is disappearing. Good riddance: this is just a term for DNA that we don’t have any guesses about its function. The more we learn about the genome, the more functions we uncover, thus fewer unknowns and a more seemingly “useful” genome. Where will it end? I have no idea,,,”
    http://www.reddit.com/r/asksci.....of/c667vqi

    Why the Case for Junk DNA 2.0 Still Fails – September 27, 2012
    Excerpt: Confronted with the ENCODE results that attribute “function” to at least 80% of the genome, some Darwinist bloggers and critics of intelligent design have established a defensive perimeter around the precious idea of Junk DNA. It truly is that critically important to them. Their favored critique of ENCODE — call it the case for Junk DNA 2.0 — is that ENCODE’s definition of functionality is wrong. “Well, maybe it’s technically functional,” they say, “but it really isn’t.”,,,
    As Jonathan Wells documented in Chapter 7 of The Myth of Junk DNA, we already know of several non-biochemical functions of non-protein-coding DNA,,,
    if anything, ENCODE uses too narrow a definition of function — by limiting it to “biochemical” function. For this reason, the (80%) functionality reported by ENCODE surely underestimates the total.,,,
    The Darwinist bloggers are defending a ragged flag on a rapidly shrinking ice floe, insisting that the vast ocean around them is nothing to worry about. But if trends continue, as ENCODE gives us excellent reason to expect they will, then before long those defenders of junk DNA will be planting their flag in open water.
    http://www.evolutionnews.org/2.....64771.html

    Junk No More: ENCODE Project Nature Paper Finds “Biochemical Functions for 80% of the Genome” – Casey Luskin September 5, 2012
    Excerpt: The Discover Magazine article further explains that the rest of the 20% of the genome is likely to have function as well:
    “And what’s in the remaining 20 percent? Possibly not junk either, according to Ewan Birney, the project’s Lead Analysis Coordinator and self-described “cat-herder-in-chief”. He explains that ENCODE only (!) looked at 147 types of cells, and the human body has a few thousand. A given part of the genome might control a gene in one cell type, but not others. If every cell is included, functions may emerge for the phantom proportion. “It’s likely that 80 percent will go to 100 percent,” says Birney. “We don’t really have any large chunks of redundant DNA. This metaphor of junk isn’t that useful.””
    We will have more to say about this blockbuster paper from ENCODE researchers in coming days, but for now, let’s simply observe that it provides a stunning vindication of the prediction of intelligent design that the genome will turn out to have mass functionality for so-called “junk” DNA. ENCODE researchers use words like “surprising” or “unprecedented.” They talk about of how “human DNA is a lot more active than we expected.” But under an intelligent design paradigm, none of this is surprising. In fact, it is exactly what ID predicted.
    http://www.evolutionnews.org/2.....64001.html

    In fact Timothya, The complexity being revealed is ‘jaw dropping’ elegant

    Bits of Mystery DNA, Far From ‘Junk,’ Play Crucial Role – September 2012
    Excerpt: The system, though, is stunningly complex, with many redundancies. Just the idea of so many switches was almost incomprehensible, Dr. Bernstein said.
    There also is a sort of DNA wiring system that is almost inconceivably intricate.
    “It is like opening a wiring closet and seeing a hairball of wires,” said Mark Gerstein, an Encode researcher from Yale. “We tried to unravel this hairball and make it interpretable.”
    There is another sort of hairball as well: the complex three-dimensional structure of DNA. Human DNA is such a long strand — about 10 feet of DNA stuffed into a microscopic nucleus of a cell — that it fits only because it is tightly wound and coiled around itself. When they looked at the three-dimensional structure — the hairball — Encode researchers discovered that small segments of dark-matter DNA are often quite close to genes they control. In the past, when they analyzed only the uncoiled length of DNA, those controlling regions appeared to be far from the genes they affect.
    http://www.nytimes.com/2012/09.....wanted=all

    DNA – Replication, Wrapping & Mitosis – video
    https://vimeo.com/33882804

    Perhaps the following may help you get past your Darwinian blinders:

    Information Storage in DNA by Wyss Institute – video
    https://vimeo.com/47615970

    Quote from preceding video:
    “The theoretical (information) density of DNA is you could store the total world information, which is 1.8 zetabytes, at least in 2011, in about 4 grams of DNA.”
    Sriram Kosuri PhD. – Wyss Institute

    Harvard Scientists Write the Book on Intelligent Design—in DNA – Dr. Fazale Rana – September 10, 2012
    Excerpt: One gram of DNA can hold up to 455 exabytes (one exabyte equals 10^18 bytes). In comparison, a CD-ROM holds about 700 million (7 x 10^8) bytes of data. (One gram of DNA holds the equivalent amount of data as 600 billion CD-ROMs. Assuming a typical book requires 1 megabyte of data-storage capacity, then one gram of DNA could harbor 455 trillion books.)
    http://www.reasons.org/article.....ign-in-dna

  22. 22
    bornagain77 says:

    Per Dr. Behe: In a recent publication in Nature (Blount et al. 2012) they report the multiple mutations that confer and increase the ability to transport citrate in an atmosphere containing oxygen. They divide the mutations conceptually into three categories: 1) potentiation; 2) actualization; and 3) refinement. “Actualization” is the name they give to the mutation that first confers a weak ability to transport citrate into the laboratory E. coli. (It turns out that the bacterium is lacking only a protein to transport citrate into the cell in the presence of oxygen; all other enzymes needed to further metabolize citrate are already present.) The gene for the citrate transporter, citT, that works in the absence of oxygen is directly upstream from the genes for two other proteins that have promoters that are active in the presence of oxygen. A duplication of a segment of this region serendipitously placed the citT gene next to one of these promoters, so the citT gene could then be expressed in the presence of oxygen. Gene duplication is a type of mutation that is known to be fairly common, so this result, although requiring a great deal of careful research to pin down, is unsurprising.

    Over time the mutant got better at utilizing citrate, which the authors called “refinement.” Further work showed this was due to multiple duplications of the mutant gene region, up to 3-9 copies. Again, gene duplication is a fairly common process, so again it is unsurprising. In another experiment Lenski and co-workers showed that increasing the concentration of the citrate transporter gene was sufficient in itself to account for the greater ability of E. coli to grow on citrate. No other mutations were needed.

    A more mysterious part of the whole process is what the group called “potentiation.” It turns out that the original E. coli they began with decades ago could not benefit from the gene duplication that brought together a citT gene with an oxygen-tolerant promoter. Before it could benefit, a preliminary mutation had to occur in the bacterium somewhere other than the region containing the citrate-metabolism genes. Exactly what that mutation was, Lenski and coworkers were not able to determine. However, they examined the bacterium for mutations that may contribute to potentiation, and speculated that “A mutation in arcB, which encodes a histidine kinase, is noteworthy because disabling that gene upregulates the tricarboxylic acid cycle.” (They tried, but were unable to test this hypothesis.) In other words, the “potentiation” may involve degradation of an unrelated gene.

    Lenski’s lab did an immense amount of careful work and deserves much praise. Yet the entirely separate, $64,000 question is, what do the results show about the power of the Darwinian mechanism? The answer is, they do not show it to be capable of anything more than what was already known. For example, in my review of lab evolution experiments I discussed the work of Zinser et al. (2003) where a sequence rearrangement brought a promoter close to a gene that had lacked one. I also discussed experiments such as Licis and van Duin (2006) where multiple sequential mutations increased the ability of a FCT. Despite Lenski’s visually startling result — where a usually clear flask became cloudy with the overgrowth of bacteria on citrate — at the molecular level nothing novel occurred.

    Another person who follows Lenski’s results closely is Dennis Venema, chair of the Biology Department at Trinity Western University and contributor to the BioLogos website. Founded by Francis Collins, BioLogos defends the compatibility of Darwinian science and Christian theology. I agree that the Darwinian mechanism (rightly understood) is theoretically compatible with Christian theology. However, I also think Darwinism is grossly inadequate on scientific grounds. A number of BioLogos writers think it is adequate, and attempt to defend it against skeptics of Darwinism, most especially against proponents of intelligent design such as myself.

    In several posts at BioLogos, Professor Venema compared the results of Lenski’s current citrate work to arguments I had made in my QRB review and in my 2007 book, The Edge of Evolution. Whereas I had argued that there was a limit to the number of unselected (either detrimental or neutral) mutations we could reasonably expect an undirected, Darwinian process to have at its disposal in building a complex system, Venema thought Lenski’s recent work showed that limit to be exceeded. Furthermore, while I had pointed out that none of the mutations seen in Lenski’s work up to the date of the review was a gain-of-FCT, Venema wrote the newly published citrate mutations constituted such a feature.

    I disagree on both counts. The gene duplication which brought an oxygen-tolerant promoter near to the citT gene did not make any new functional element. Rather, it simply duplicated existing features. The two FCTs comprising the oxygen tolerant citrate transporter locus — the promoter and the gene — were functional before the duplication and functional after. I had written in my review that one type of mutation that could be categorized as a gain-of-FCT was gene duplication with subsequent sequence modification, to allow the gene to specialize in some task. Venema thinks the mutation observed by Lenski is such an event. He has overlooked the fact that there was no subsequent sequence modification; a segment of DNA simply tandemly duplicated, bringing together two pre-existing FCTs. (It is true that the sequence of the protein coded by the duplicated gene includes a fragment from one of the nearby genes, but there is no evidence nor reason to think that the fused fragment is necessary for the activity of the protein.) In my review I classify that as a modification-of-function event. An example of a true gain-of-FCT by duplication cited in my review was the work of Olsthoorn and van Duin (1996) where a 14-nucleotide duplication led to the formation of new functional coded elements (it did not simply repeat pre-existing elements), so it is not just a modification-of-function mutation. The citrate mutation did nothing like that.

    Venema counts the number of mutations needed to get a fully functioning citrate-importing function in Lenski’s work, and arrives at roughly a half-dozen. Unfortunately, several of those are tandem duplications of the weak citT transporter, which clearly are selectable, beneficial mutations. In arriving at the limits to Darwinism, I emphasized that that mechanism would certainly work if gradually-increasing, serial, beneficial mutations could do the job. Thus such mutations do not count in estimating the limit. Only required deleterious and neutral mutations count against the limit to Darwinian evolution. Venema argues that perhaps all of complex functional biology could be reached by gradual, beneficial mutations. Well, bless his optimistic heart, but the data give us no reason to think that, because gradually increasing one protein’s total cellular activity by sequential gene duplication is successively beneficial, all routes to complex systems involving multiple distinct elements will be. Quite the opposite, as I have often argued.

    Professor Venema also counts several “potentiating” mutations as contributing to the system. Unfortunately, whatever those mutations are, they are not part of the citrate metabolic system itself. Rather, they are at most part of the genetic background. If Lenski and co-workers’ speculations are correct (Blount et al. 2012), at least one of the potentiating mutations degrades an unrelated gene, and thus itself counts as a loss-of-FCT mutation. When counting the mutations contributing to the edge of evolution for building a feature, only the ones directly involved in the feature are counted, not ones that indirectly contribute to a receptive genetic background (which are legion). Thus, unlike Venema, I count perhaps three to four mutations — the original duplication placing the oxygen-tolerant promoter near the citT gene, plus several rounds of duplication of that region. All of the mutations are modification-of function ones in the classification system I described. I should add that there is no reason to think that Darwinian processes cannot produce gain-of-FCT mutations, and I reviewed several such events. But they are greatly outnumbered by loss-of-FCT and modification-of-function beneficial mutations.

    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.

    References:

    Barrick,J.E., Yu,D.S., Yoon,S.H., Jeong,H., Oh,T.K., Schneider,D., Lenski,R.E., and Kim,J.F. 2009. Genome evolution and adaptation in a long-term experiment with Escherichia coli. Nature 461:1243-1247.

    Behe,M.J. 2010. Experimental Evolution, Loss-of-function Mutations, and “The First Rule of Adaptive Evolution.” Q. Rev. Biol. 85:1-27.

    Behe,M.J. 2007. The Edge of Evolution: the Search for the Limits of Darwinism. Free Press: New York.

    Blount,Z.D., Borland,C.Z., and Lenski,R.E. 2008. Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli. Proc. Natl. Acad. Sci. U. S. A 105:7899-7906.

    Blount,Z.D., Barrick,J.E., Davidson,C.J., and Lenski,R.E. 2012. Genomic analysis of a key innovation in an experimental Escherichia coli population. Nature 489:513-518.

    Licis,N. and van,D.J. 2006. Structural constraints and mutational bias in the evolutionary restoration of a severe deletion in RNA phage MS2. J. Mol. Evol. 63:314-329.

    Olsthoorn,R.C. and van Duin,D.J. 1996. Evolutionary reconstruction of a hairpin deleted from the genome of an RNA virus. Proc. Natl. Acad. Sci. U. S. A 93:12256-12261.

    Venema,D. 2012. Behe, Lenski and the “Edge” of Evolution, Part 1: Just the FCTs, Please. The Biologos Forum. http://biologos.org/blog/behe-.....ion-part-1.

    Zinser,E.R., Schneider,D., Blot,M., and Kolter,R. 2003. Bacterial evolution through the selective loss of beneficial Genes. Trade-offs in expression involving two loci. Genetics 164:1271-1277.
    http://www.evolutionnews.org/2.....66361.html

  23. 23
    timothya says:

    BA, please pay attention. You claimed that >=80% of the human genome is transcribed. Do you have any scientific evidence that this claim is true?

    Is there any biologist in the world who supports this claim?

  24. 24
    Joe says:

    timothya- ENCODE said 80% of the human genome is transcribed- as for Lenski, well that is true also. Geez, don’t you stay current?

  25. 25
    timothya says:

    Joe

    No, the ENCODE program did not claim that =>80% of the human genome is transcribed.

    Perhaps you wish it had claimed that, but it didn’t. Currency involves knowing what actually happens in the world of science, not what you, personally, hope happens.

    Oh well. Better luck next time.

  26. 26
    Joe says:

    timothya-

    The ENCODE paper says that 80% of the genome is functional and they define that as the % that gets transcribed.

    If you think otherwise then make your case

  27. 27
    bornagain77 says:

    Landscape of transcription in human cells – Sept. 6, 2012
    Excerpt: Here we report evidence that three-quarters of the human genome is capable of being transcribed, as well as observations about the range and levels of expression, localization, processing fates, regulatory regions and modifications of almost all currently annotated and thousands of previously unannotated RNAs. These observations, taken together, prompt a redefinition of the concept of a gene.
    http://www.nature.com/nature/j.....11233.html

    footnotes:

    The Extreme Complexity Of Genes – Dr. Raymond G. Bohlin – video
    http://www.metacafe.com/watch/8593991/

    Time to Redefine the Concept of a Gene? – Sept. 10, 2012
    Excerpt: As detailed in my second post on alternative splicing, there is one human gene that codes for 576 different proteins, and there is one fruit fly gene that codes for 38,016 different proteins!
    While the fact that a single gene can code for so many proteins is truly astounding, we didn’t really know how prevalent alternative splicing is. Are there only a few genes that participate in it, or do most genes engage in it? The ENCODE data presented in reference 2 indicates that at least 75% of all genes participate in alternative splicing. They also indicate that the number of different proteins each gene makes varies significantly, with most genes producing somewhere between 2 and 25.
    Based on these results, it seems clear that the RNA transcripts are the real carriers of genetic information. This is why some members of the ENCODE team are arguing that an RNA transcript, not a gene, should be considered the fundamental unit of inheritance.
    http://networkedblogs.com/BYdo8

    Further Thoughts on the ENCODE/Junk DNA Debates – James Shapiro – Sept. 18, 2012
    Excerpt: The ENCODE scientists have learned that it is wise to avoid interpreting the data from a fixed view of genome organization. That is why they speak of “DNA Elements” rather than genes or any other artificial categories. They tend to restrict themselves wisely to operationally defined features, such as transcription start sites (TSSs) and splice sites at exon-intron boundaries.
    Diogenes and like-minded people argue that we knew enough in the 1970s to understand the basic principles of genome organization. They do not accept that the flood of new information from genome sequencing and the kind of methodologies exemplified by the ENCODE project will fundamentally alter our genetic concepts. While they are certainly entitled to these opinions, I think we have to recognize that they are nothing more than that — simply opinions that fly in the face of scientific history.
    http://www.huffingtonpost.com/.....93984.html

  28. 28
    bornagain77 says:

    Also of interest to the linear sequence of letters in the genome, it is interesting to point out that the linear sequence of letters is the bottom level of information in the ‘dimensional’ information hierarchy of the cell:

    Multidimensional Genome – Dr. Robert Carter – video (Notes in video description)
    http://www.metacafe.com/w/8905048

    footnote to ‘3-Dimensional’ information in the cell:

    Shoddy Engineering or Intelligent Design? Case of the Mouse’s Eye – April 2009
    Excerpt: — The (entire) nuclear genome is thus transformed into an optical device that is designed to assist in the capturing of photons. This chromatin-based convex (focusing) lens is so well constructed that it still works when lattices of rod cells are made to be disordered. Normal cell nuclei actually scatter light. — So the next time someone tells you that it “strains credulity” to think that more than a few pieces of “junk DNA” could be functional in the cell – remind them of the rod cell nuclei of the humble mouse.
    http://www.evolutionnews.org/2.....ellig.html

    Here are a couple of ‘jaw dropping’ videos showing that ‘higher dimensional’ information in action:

    An Electric Face: A Rendering Worth a Thousand Falsifications – September 2011
    Excerpt: The video suggests that bioelectric signals presage the morphological development of the face. It also, in an instant, gives a peak at the phenomenal processes at work in biology. As the lead researcher said, “It’s a jaw dropper.”
    http://darwins-god.blogspot.co.....usand.html

    The (Electric) Face of a Frog – video
    http://www.youtube.com/watch?v=ndFe5CaDTlI

    Let there be sight: Retinal waves wire visual system – video
    http://player.vimeo.com/video/51010591
    Video description: A wave of ‘spontaneous’ activity sweeps across axons of retinal ganglion cells in the mid-brain of a 6-day old mouse. Such activity primes (presages) the developing neuronal circuits, enabling mice to process visual information after they open their eyes, usually between 10 days and two weeks.,,,
    The development of animals from a fertilized egg into trillions of intricately connected and specialized cells is the result of a precisely timed expression of genes. However, the Nature paper introduces another necessary factor—a mysterious wave of activity arising in the retina itself that propagates through several regions of the brain. Crair terms this wave an ’emergent property’, or a trait possessed by a complex system that cannot be directly traced to its individual parts. This experiment in living, neonatal mice shows that this (preceeding) wave is crucial to the proper wiring not only of the visual system but other brain areas as well.
    Entire article here:
    Burst of fetal neural activity necessary for vision – October 11, 2012
    http://medicalxpress.com/news/.....n.html#jCp

  29. 29
    Axel says:

    Pity so much leading-edge research appears to be lost on Tim. No acknowledgements. Just further questions.

  30. 30
    Andre says:

    So there is all the evidence will you take some time to actually study it Timothya?

  31. 31
    Mung says:

    I watched this video when it was posted over at ENV. imo, Ann wasn’t at her best. She went off-topic too often and there’s not enough meat to the short content. Ah well.

  32. 32
    Mung says:

    timothya:

    What a load of nonsense. The null hypothesis for common ancestry is that no ancestry tree exists.

    Do you mean that the null hypothesis is that every species was specially created. How is that science?

  33. 33
    bornagain77 says:

    OT: New Form of Cell Division Found: Natural Back-Up Mechanism During Faulty Cell Division – Dec. 17, 2012
    Excerpt: Burkard and his team were making cells with too many chromosomes–to mimic cancer. The scientists blocked cytokinesis with a chemical and waited to see what happened.
    “We expected to recover a number of cells with abnormal sets of chromosomes,” Burkard explains.
    The researchers found that, rather than appearing abnormal, daughter cells ended up looking normal most of the time. Contrary to Boveri’s hypothesis, abnormal cell division rarely had long-term negative effects in human cells.
    So the group decided to see how the human cells recovered normal sets of chromosomes by watching with a microscope that had the ability to take video images.
    “We started with two nuclei in one cell,” Burkard says. “To our great surprise, we saw the cell pop apart into two cells without going through mitosis.”
    Each of the two new cells inherited an intact nucleus enveloping a complete set of chromosomes. The splitting occurred, unpredictably, during a delayed growth phase rather than at the end of mitosis.
    The scientists did a number of additional experiments to carefully make sure that the division they observed was different than cytokinesis.
    “We had a hard time convincing ourselves because this type of division does not appear in any textbook,” Burkard says.
    http://www.sciencedaily.com/re.....140328.htm

    related note:

    DNA – Replication, Wrapping & Mitosis – video
    https://vimeo.com/33882804

  34. 34
    Mung says:

    We had a hard time convincing ourselves because this type of division does not appear in any textbook

    They weren’t looking in a math book.

  35. 35
    wd400 says:

    I would be very dissapointed if a 2nd year student made this many mistakes in so short a time. Population genetics and phylogenetics are distinct (although their applications over lap to some extend), and trees are a consequence of simple population genetic models (not an assumption). Homoplasy is well understood in phylogenetics, and, indeed it’s only thanks to phylogenetic methods (as opposed to this “similarity” business Gauger is own about) that we know some characters are homoplasies (how else could we know how many times the eye was invented, say?)

    If this is posted in support of the ID movement, then that movement really is in poor shape.

  36. 36
    Mung says:

    wd400:

    Population genetics and phylogenetics are distinct (although their applications over lap to some extend), and trees are a consequence of simple population genetic models (not an assumption).

    Making her point. They are inter-related.

    And you have no idea how many times the eye was invented, given all the gaps in the fossil record.

    If this is posted in support of the ID movement, then that movement really is in poor shape.

    If you all can’t address the actual argument and evidence instead of these peripheral red herring issues your position is in sad shape.

    ENV response the the “critics.”

    Fast, Furious and Irrelevant: Darwinists Reply to Ann Gauger on Human Origins

  37. 37
    wd400 says:

    Gaguer would have to make an actual argument for someone to address it. I didn’t realise the thing about the green screen before you provided that link – hilarious.

  38. 38
    bornagain77 says:

    as to: “(Dr.) Gauger would have to make an actual argument for someone to address it.”

    Seems that I don’t recall neo-Darwinists ever honestly addressing this following ‘actual argument’ from Dr. Gauger:

    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.
    http://www.uncommondescent.com.....rwin-said/

    Perhaps wd400, you would care to address this argument with actual empirical evidence instead of pseudo-scientific rhetoric?

  39. 39
    Joe says:

    LoL! @ wd400- perhaps evos should make an actual argument so that someone can address it.

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