Intelligent Design

Human and chimp DNA: They really are about 98% similar

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A few days ago, scientist and young-earth creationist Dr. Jay Wile wrote a post on his Proslogion blog, in which he reported that Dr. Jeff Tomkins had abandoned his claim that human and chimpanzee DNA are only about 70% similar, in favor of a revised figure of 88%. But even that figure is too low, according to the man who spotted the original flaw in Dr. Tomkins’s work.

Dr. Wile reports:

More than two years ago, Dr. Jeffrey P. Tomkins, a former director of the Clemson University Genomics Institute, performed a detailed, chromosome-by-chromosome comparison of human and chimpanzee DNA using a widely-recognized computer program known as BLAST. His analysis indicated that, on average, human and chimpanzee DNA are only about 70% similar. This is far, far, below the 95-99% numbers that are commonly cited by evolutionists, so once I read the study, I wrote a summary of it. Well, Dr. Tomkins has done a new study, and it invalidates the one he did two years ago.

The new study was done because last year, a computer programmer of financial trading algorithms (Glenn Williamson) discovered a bug in the BLAST algorithm that Tomkins used. This bug caused the program to ignore certain matches that should have been identified, which led to an artificially low similarity between the two genomes.

Here is what Glenn Williamson has to say about himself:

Yeah – 36 year old, stay-at-home father of four – including triplets, ha! 🙂

I don’t have any formal qualifications in genetics, or anything biological for that matter. I have a bachelors degree in computing science (i.e. programming) from the University of Technology in Sydney. Started my career as a programmer, but transitioned into derivatives trading, which is a lot more fun…

And for what it’s worth, I believe that my paper is more of a computing science paper than a genetics paper. It’s more my area of expertise than Jeff Tomkins’ area.

Glenn Williamson’s detailed takedown of Dr. Tomkins’s 70% similarity figure can be accessed here. Dr. Tomkins claims he submitted his paper to the creationist publication, Answers Research Journal, but it was never published. Here’s an excerpt from the paper (emphasis mine – VJT):

In this paper I carefully reproduce a subset of Dr Tomkins’ results, and show clearly and unambiguously that Dr Tomkins has fallen victim to a serious bug in the software used to obtain his results. It is this bug that causes Dr Tomkins to report the erroneous figure of 70% similarity. After correcting for both the effects of this bug and some non-trivial errors in Dr Tomkins’ methodology, I report an overall similarity of 96.90% with a standard error of ±0.21%. This figure includes indels, and the result is largely in line with the secular scientific consensus.

What happened next? Dr. Wile takes up the story:

As a result, Dr. Tomkins redid his study, using the one version of BLAST that did not contain the bug. His results are shown above… The overall similarity between the human and chimpanzee genomes was 88%.

In an update at the top of his post, Dr. Wile now admits to having cold feet, even about the revised 88% figure:

Based on comments below by Glenn (who is mentioned in the article) and Aceofspades25, there are questions regarding the analysis used in Dr. Tomkins’s study, upon which this article is based. Until Dr. Tomkins addresses these questions, it is best to be skeptical of his 88% similarity figure.

So what was wrong with Dr. Tomkins’s new study? I’ll let Glenn Williamson explain (emphasis mine – VJT):

October 16, 2015 4:22 pm

As I’ve said many times, if there is a single base pair indel in the middle of a 300bp sequence, Tomkins will say this is a 50% match.

Tomkins is most certainly aware of this, yet he chose to publish it. I think that says pretty much everything.

Another commenter named Aceofspades25 has this to add (emphases mine – VJT):

October 16, 2015 2:13 pm

The other obvious thing that Thompkins hasn’t dealt with in his BLASTN analysis, I talk about here.

There are a few cases where no match will be found because this entire sequence appears de-novo in Chimpanzees as the result of a single mutation (e.g. a novel transposable element – see here) or because humans have had a large deletion which other primates don’t. Deletions like this also likely occurred in a single mutation – see here

Thompkins (sic) would count both of these as being a 0% match (or 600 effective mutations if the sequences he was searching for were 300bp each). In reality, these probably represent just 2 mutations.

I’ll let Glenn Williamson have the final word (emphases mine – VJT):

Thanks Ace, for letting me know about this post. I reiterate here a few things about my (unpublished!) paper, and about Tomkins’ new paper.

The first thing is that he uses the “ungapped” parameter in his BLAST comparisons. As I’ve written in a few other places now, using this parameter, and calculating results in the way that Tomkins does is entirely disingenuous. If you are comparing two 300bp sequences, and one of those sequences has a single indel smack bang in the middle, Tomkins counts this as the sequences being only 50% identical.

I’ve told him at least twice that he cannot use ungapped and then calculate the result in this way. He can do one of two things:

1. Use ungapped, which ignores indels and therefore he can only report the substitution rate. (emphasis mine – VJT)If he did this, he would get a result of around 98.8%.

2. Allow gaps, and – this is what he fails to mention in his paper – get a result of around 96.9%. And this is using a very conservative method of calculation as well, since it counts a 50bp indel as having the same weight as 50 individual mutations. If you counted a 50bp indel as a single event (which it probably was), then the overall result would be pushed up towards 98%, which is the figure usually thrown around anyway.

In a comment dated 14 August 2015 (at 03:44) on an article titled, Chimp and Human DNA vs “Sophisticated Nonsense”! on a blog called Marmotism, Glenn Williamson adds:

I’ve actually written a paper on Tomkins’ 70% result, and have _ATTEMPTED_ to get it published in Answers Research Journal. Obviously they are not having a bar of it – Tomkins is the sole peer-reviewer, and he is currently refusing to provide any critique of my work – he has been silent for 8 months, while the ball is in his court ..

See the paper here:

https://www.dropbox.com/sh/dm2lgg0l93sjayv/AAATnWSJdER53EYEYZvcgiwma?dl=0

It’s the two PDFs ..

Dr. Tomkins’s latest article in Answers Research Journal (October 7, 2015) acknowledges Williamson’s work in a single sentence:

As of 2013, the issue of overall genome similarity between chimpanzee and humans seemed to be about 70% based on five different reports, three of which were based on actual data analyses. However, in 2014 , a computer programmer of financial trading algorithms discovered an apparent bug in the BLASTN algorithm and notified this author of the situation (Glenn Williamson, Tibra Capital, personal communication).

So, a submitted article only counts as a “personal communication”? Perhaps Dr. Tomkins needs to be a little more up-front about giving credit where credit is due, and acknowledging his mistakes. At any rate, the ball is definitely in his court, and his latest 88% similarity figure warrants skepticism. I have to say that Dr. Tomkins’s methodology sounds rather suspicious to me.

What do readers think?

260 Replies to “Human and chimp DNA: They really are about 98% similar

  1. 1
    Virgil Cain says:

    Perhaps the problem is we don’t know how, exactly, to compare the two genomes. Take the 1 base pair deletion mentioned above. If that is a sentence and the word “no” was deleted or inserted it would change the entire meaning of the sentence.

    The sentences could be 98% identical and mean opposite things.

  2. 2
    wd400 says:

    This has been known for … some time

    Edit: perhaps I should say this was pointed out quite some time ago, didn’t seem to change anyone’s mind.

  3. 3
    Andre says:

    So even if there is an actual 2% difference it’s still a whopping 60 000 000 Base pair difference.

    How did 60 000 000 Base pair differences become fixed in only a short 6 000 000 years of unguided evolution from out last common ancestor?

    Over to the unguided experts……

  4. 4
    awstar says:

    This has been known for … some time

    Not sure how the following supports one side of the debate or the other, but it’s very recent

    Salk scientists discover protein factories hidden in human jumping genes

    http://www.eurekalert.org/pub_.....101915.php

  5. 5
    News says:

    The whole case still doesn’t make any sense unless the genome accounts for far less than we used to think about what makes a life form. Of course there is increasing evidence that that is true.

  6. 6
    wd400 says:

    News,

    What if the genome is mostly junk?

    Andre,

    Genetic drift, mostly.

  7. 7
    bornagain says:

    Documented Anomaly in Recent Versions of the BLASTN Algorithm and a Complete Reanalysis of Chimpanzee and Human Genome-Wide DNA Similarity Using Nucmer and LASTZ
    by Jeffrey P. Tomkins on October 7, 2015
    Excerpt Summary: Thus, the actual genome similarity with human, even using the high end estimate of 88% for just the alignable regions, is realistically only about 80% or less when the cytogenetic data is taken into account.
    https://answersingenesis.org/genetics/dna-similarities/blastn-algorithm-anomaly/

  8. 8
    ppolish says:

    We share 25% of our DNA with dogs. Not sure about cats. DNA is an awesome design tool. Now will someone please scratch my belly.

  9. 9
    Sebestyen says:

    Am I the only one who thinks it’s utterly useless to try and compare genomes between species as long as we’re not even close to a complete understanding of how it all works?

    If it’s anything like software very similar sections could have vastly different effect but vastly differing sections could have a similar effect. Likewise, equal sections used in a different context could also have vastly different effects.

    Sebestyen

  10. 10
    bornagain says:

    wd400, I recall the discounting of the dissimilar regions as being merely ‘junk’, as you are currently doing, as the disingenuous method by which ENCODE skeptics, (i.e. Darwinians), denied the widespread functionality of the genome that ENCODE had found.

    DNA mostly ‘junk?’ Only 8.2 percent of human DNA is ‘functional’, study finds – July 24, 2014
    Excerpt: To reach their (8.2%) figure, the Oxford University group took advantage of the ability of evolution to discern which activities matter and which do not. They identified how much of our genome has avoided accumulating changes over 100 million years of mammalian evolution — a clear indication that this DNA matters, it has some important function that needs to be retained.
    http://www.sciencedaily.com/re.....141608.htm

    So according to these Darwinian critics of the ENCODE study, which found widespread functionality for ‘junk’ DNA by direct experimental research, actual functionality does not determine if a sequence is functional, only ‘conservation of sequence’ determines what is functional? So basically, only if Darwinian evolution is assumed as true from the outset will Darwinists be willing to accept that a given sequence of ‘junk’ DNA may be functional?
    That is called ‘assuming your conclusion into your premise’ and is an absolutely horrible way to practice science!
    Moreover, these following researchers noted that assuming most of the genome is junk, as Darwinists disingenuously insist on doing so as to protect their dogma of common descent, is a science stopper as far as bio-medical research is concerned:

    Junk or functional DNA? ENCODE and the function controversy Pierre-Luc Germain, Emanuele Ratti, Federico Boem – 21 Mar 2014
    Abstract: In its last round of publications in September 2012, the Encyclopedia Of DNA Elements (ENCODE) assigned a biochemical function to most of the human genome, which was taken up by the media as meaning the end of ‘Junk DNA’. This provoked a heated reaction from evolutionary biologists, who among other things claimed that ENCODE adopted a wrong and much too inclusive notion of function, making its dismissal of junk DNA merely rhetorical. We argue that this criticism rests on misunderstandings concerning the nature of the ENCODE project, the relevant notion of function and the claim that most of our genome is junk. We argue that evolutionary accounts of function presuppose functions as ‘causal roles’, and that selection is but a useful proxy for relevant functions, which might well be unsuitable to biomedical research. Taking a closer look at the discovery process in which ENCODE participates, we argue that ENCODE’s strategy of biochemical signatures successfully identified activities of DNA elements with an eye towards causal roles of interest to biomedical research. We argue that ENCODE’s controversial claim of functionality should be interpreted as saying that 80 % of the genome is engaging in relevant biochemical activities and is very likely to have a causal role in phenomena deemed relevant to biomedical research. Finally, we discuss ambiguities in the meaning of junk DNA and in one of the main arguments raised for its prevalence, and we evaluate the impact of ENCODE’s results on the claim that most of our genome is junk.
    http://link.springer.com/artic.....014-9441-3

    Further notes:

    Do Scientists Accept the Results of the ENCODE Project? September 12, 2013 – By Dr. Fazale Rana
    Excerpt: In a recent article, Mattick and his coauthor, Marcel Dinger, argue, like me, that the criticisms of ENCODE are unwarranted technically and are motivated by non-scientific considerations.
    One of the chief criticisms leveled at ENCODE relates to its use of a causal definition of function to determine functionality within the human genome. That is, a sequence element in the genome possesses function if it performs an observationally or experimentally identified role. ENCODE skeptics argue that this definition is faulty; instead, the project should have relied on sequence conservation (the so-called selected effect definition) as a way to measure function.
    According to the selected effect definition, sequences in genomes can be deemed functional only if they evolved under evolutionary processes to perform a particular function.,,
    Hence, functional sequences are those under the effects of selection. And based on a selected effect definition of function, only 10 percent (not 80) of the human genome could be considered functional.
    Mattick and Dinger decry the weakness of the selected effect definition.,,, (So do I)
    http://www.reasons.org/article.....de-project

    The ENCODE Embroilment, – part 3
    Excerpt: Only if we assume that strictly unguided evolutionary mechanisms produced our genome can we infer that such a small fraction of our genome is functional. Under this logic, when evolutionists cite the preponderance of junk DNA as evidence for evolution, they engage in circular reasoning.
    Junk proponents seem blind to these flaws. A co-author of the 8.2-percent paper boasted, “our approach is largely free from assumptions or hypotheses.”8 Apparently he was forgetting about assumptions and hypotheses like evolution.
    Even worse, ENCODE critic Dan Graur called it “‘idiotic’ to suggest that a part of the genome could be functional if it didn’t respond to pressure from natural selection.”9 He further charges that “what ENCODE researchers did not take into account . . . is that everything is shaped by evolution.”10 In Graur’s Darwinian world, the possibility that some important functional genetic element arose from a cause other than natural selection is simply inconceivable….
    In any case, ENCODE provides a nice empirical test of the evolutionary assumption that only conserved DNA can be functional: It finds evidence of mass functionality in “non-conserved” (i.e., unique) DNA sequences. As one lead ENCODE researcher explains: “Most elements defined by biochemical signatures lacked strong evolutionary conservation.”12 Other ENCODE defenders argue that the research shows that “absence of conservation cannot be interpreted as evidence for the lack of function.”13 –
    They conclude that ENCODE’s empirical evidence for functionality is the ultimate test: “differential expression (including extensive alternative splicing) of RNAs is a far more accurate guide to the functional content of the human genome than logically circular assessments of sequence conservation.”21 Bottom line: good evidence trumps bad theory.,,,
    A Great Divorce
    Critics like Dan Graur charge that ENCODE is guilty of “divorcing genomic analysis from its evolutionary context”22—and that’s exactly right. ENCODE’s empirically based finding that the vast majority of our genome is functional has withstood theoretical, evolution-based objections from critics. Maybe a divorce from evolutionary thinking is exactly what we need to liberate biology from bad evolutionary assumptions and explain what’s happening inside our cells.,,,
    http://www.salvomag.com/new/ar.....rt-III.php

  11. 11
    Vy says:

    Er, ~98% of what? The ~2% protein-coding regions or the ~98% non-protein-coding regions? :/

  12. 12
    wd400 says:

    Both combined.

  13. 13
    bornagain says:

    As somewhat hinted at in post 10, it is the regions of DNA that do not code for proteins, i.e. the regulatory regions in DNA, that most dramatically separate us from other species.

    An Interview with Stephen C. Meyer
    TT: Is the idea of an original human couple (Adam and Eve) in conflict with science? Does DNA tell us anything about the existence of Adam and Eve?
    SM: Readers have probably heard that the 98 percent similarity of human DNA to chimp DNA establishes that humans and chimps had a common ancestor. Recent studies show that number dropping significantly. More important, it turns out that previous measures of human and chimp genetic similarity were based upon an analysis of only 2 to 3 percent of the genome, the small portion that codes for proteins. This limited comparison was justified based upon the assumption that the rest of the genome was non-functional “junk.” Since the publication of the results of something called the “Encode Project,” however, it has become clear that the noncoding regions of the genome perform many important functions and that, overall, the non-coding regions of the genome function much like an operating system in a computer by regulating the timing and expression of the information stored in the “data files” or coding regions of the genome. Significantly, it has become increasingly clear that the non-coding regions, the crucial operating systems in effect, of the chimp and human genomes are species specific. That is, they are strikingly different in the two species. Yet, if alleged genetic similarity suggests common ancestry, then, by the same logic, this new evidence of significant genetic disparity suggests independent separate origins. For this reason, I see nothing from a genetic point of view that challenges the idea that humans originated independently from primates,
    http://www.ligonier.org/learn/.....-conflict/

    Evolution by Splicing – Comparing gene transcripts from different species reveals surprising splicing diversity. – Ruth Williams – December 20, 2012
    Excerpt: A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?”,,,
    A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge,,, found that gene expression is relatively conserved among species.
    On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe.,,,
    http://www.the-scientist.com/?.....plicing%2F

    MicroRNA Study: “We Liberated Ourselves” From the Evolution Requirement – And Had Great Success – Cornelius Hunter – March 2, 2015
    Excerpt: The new study found that imposing the common descent pattern, where microRNAs must be conserved across species, is hampering the search:,,,
    “In our effort to further characterize the human miRNA repertoire, we liberated ourselves from the conservation requirement: not surprisingly then, 56.7% of our newly discovered miRNAs are human-specific whereas 94.4% are primate- specific. Considering that many miRNA studies to date have focused on seeking and analyzing conserved miRNAs, it is not surprising that, of the human miRNAs in miRBase, we found a larger fraction to be conserved in rodents and invertebrates. These findings strongly suggest the possibility of a wide-ranging species-specific miRNA-ome that has yet to be characterized.”
    http://darwins-god.blogspot.co.....elves.html

    Expanding ENCODE – Aug. 2014
    Latest Encyclopedia of DNA Elements data enable researchers to compare genome regulation across species
    Excerpt: Ho and his coauthors also found key differences in the structure of heterochromatin between species.,,,
    ,,,these data show that “heterochromatin is not the same thing in different organisms, not only in terms of distribution but also in terms of composition.”
    http://www.the-scientist.com/?.....ng-ENCODE/

    Dr. Sternberg gives a very informative talk on ‘species specific’ regulatory regions in the following podcast

    Richard Sternberg PhD – podcast – On Human Origins: Is Our Genome Full of Junk DNA? Part 2. (Major differences found in higher level chromosome spatial organization, and regulatory regions, between species)
    http://www.discovery.org/multi.....-dna-pt-2/

    Moreover, mutating these significantly different, i.e. ‘species specific’, regulatory regions between species is found to be, unlike mutating an amino acid in the protein coding regions, ‘always catastrophically bad’. i.e. mutating ‘species specific’ regulatory regions of DNA is far more unforgiving than merely mutating the protein coding regions of DNA:

    A Listener’s Guide to the Meyer-Marshall Debate: Focus on the Origin of Information Question -Casey Luskin – December 4, 2013
    Excerpt: “There is always an observable consequence if a dGRN (developmental gene regulatory network) subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.” –
    Eric Davidson – developmental biologist
    http://www.evolutionnews.org/2.....79811.html

    Thus, where Darwinists most need plasticity in the genome to be viable as a theory, (i.e. developmental Gene Regulatory Networks), is the place where mutations are found to be ‘always catastrophically bad’. Yet, it is exactly in this area of the genome (i.e. regulatory networks) where substantial, ‘orders of magnitude’, differences are found between even supposedly closely related species.
    Needless to say, this is the exact opposite finding for what Darwinism would have predicted for what should have been found in the genome.
    If Darwinism were a normal science, instead of being basically the unfalsifiable ‘blind faith’ religion of atheists, this finding, by itself, should have been more than enough to falsify neo-Darwinian claims.

    Another erroneous evolutionary assumption that is overlooked is that Darwinists assume that mutations to DNA will produce fundamentally new body plans. They simply have no empirical basis whatsoever for assuming that changes to DNA will generate new body plans.

    Response to John Wise – October 2010
    Excerpt: A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism.
    http://www.evolutionnews.org/2.....38811.html

    As Dr. Stephen Meyer puts the situation, you can mutate DNA until the cows come home and it doesn’t matter because you are not going to generate new body plans:

    ‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does not insure that proteins, cell types, tissues, organs, will all be arranged in the body. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’
    Stephen Meyer – (excerpt taken from Meyer/Sternberg vs. Shermer/Prothero debate – 2009) (52:57 minute mark)
    https://youtu.be/7yqqlZ29gcU?t=3177

    “These different sources of epigenetic information in embryonic cells pose an enormous challenge to the sufficiency of the neo-Darwinian mechanism. According to neo-Darwinism, new information, form, and structure arise from natural selection acting on random mutations arising at a very low level within the biological hierarchy—within the genetic text. Yet both body-plan formation during embryological development and major morphological innovation during the history of life depend upon a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. If DNA isn’t wholly responsible for the way an embryo develops—for body-plan morphogenesis—then DNA sequences can mutate indefinitely and still not produce a new body plan, regardless of the amount of time and the number of mutational trials available to the evolutionary process. Genetic mutations are simply the wrong tool for the job at hand.”
    Stephen Meyer – Darwin’s Doubt (p. 281)

  14. 14
    Zachriel says:

    Andre: How did 60 000 000 Base pair differences become fixed in only a short 6 000 000 years of unguided evolution from out last common ancestor?

    The average human has 175 mutations or so, most of them neutral. The rate of fixation of neutral mutations is the same as the rate of introduction of neutral mutations, so 175 mutations will become fixed per generation. Six million years is about 300,000 generations, which leads to the fixation of about 50 million mutations. Give or take.


    edit maths

  15. 15
    bFast says:

    “Er, ~98% of what? The ~2% protein-coding regions or the ~98% non-protein-coding regions? :/”

    “Both combined.”

    This would be surprising, as “junk dna” should drift at a rate of about 1% per million years (if I recall correctly). Human and chimp have been separated for abt 6 million, so between the two should account for 12 million years drift. This should add to about 12% drift in “junk”.

  16. 16
    Virgil Cain says:

    The rate of fixation of neutral mutations is the same as the rate of introduction of neutral mutations,

    That is the untested claim, anyway.

  17. 17
    bornagain says:

    In supplement to post 13, to further falsify the erroneous Darwinian belief that mutations to DNA will generate new body plans, according to the following experiments, the ‘form’ of a body plan is not reducible to any conceivable mechanism of molecular reductionism, i.e. reductive materialism, as is falsely presupposed in neo-Darwinian evolution:

    HOW BIOLOGISTS LOST SIGHT OF THE MEANING OF LIFE — AND ARE NOW STARING IT IN THE FACE – Stephen L. Talbott – May 2012
    Excerpt: The question is indeed, then, “How does the organism meaningfully dispose of all its molecules, getting them to the right places and into the right interactions?”
    The same sort of question can be asked of cells, for example in the growing embryo, where literal streams of cells are flowing to their appointed places, differentiating themselves into different types as they go, and adjusting themselves to all sorts of unpredictable perturbations — even to the degree of responding appropriately when a lab technician excises a clump of them from one location in a young embryo and puts them in another, where they may proceed to adapt themselves in an entirely different and proper way to the new environment. It is hard to quibble with the immediate impression that form (which is more idea-like than thing-like) is primary, and the material particulars subsidiary.
    http://www.netfuture.org/2012/May1012_184.html#2

    What Do Organisms Mean? Stephen L. Talbott – Winter 2011
    Excerpt: Harvard biologist Richard Lewontin once described how you can excise the developing limb bud from an amphibian embryo, shake the cells loose from each other, allow them to reaggregate into a random lump, and then replace the lump in the embryo. A normal leg develops. Somehow the form of the limb as a whole is the ruling factor, redefining the parts according to the larger pattern. Lewontin went on to remark: “Unlike a machine whose totality is created by the juxtaposition of bits and pieces with different functions and properties, the bits and pieces of a developing organism seem to come into existence as a consequence of their spatial position at critical moments in the embryo’s development. Such an object is less like a machine than it is like a language whose elements… take unique meaning from their context.[3]”,,,
    http://www.thenewatlantis.com/.....nisms-mean

    “Last year I had a fair chunk of my nose removed in skin cancer surgery (Mohs). The surgeon took flesh from a nearby area to fill in the large hole he’d made. The pictures of it were scary. But in the healing process the replanted cells somehow ‘knew’ how to take a different shape appropriate for the new location so that the nose now looks remarkably natural. The doctor said he could take only half the credit because the cells somehow know how to change form for a different location (though they presumably still follow the same DNA code) . — I’m getting the feeling that we’ve been nearly as reductionist in the 20-21st century as Darwin and his peers were when they viewed cells as little blobs of jelly.”
    leodp – UD blogger
    http://www.uncommondescent.com.....ent-563451

    Epigenetics and neuroplasticity: The case of the rewired ferrets – April 3, 2014
    Excerpt: Like inventive electricians rewiring a house, scientists at the Massachusetts Institute of Technology have reconfigured newborn ferret brains so that the animals’ eyes are hooked up to brain regions where hearing normally develops.
    The surprising result is that the ferrets develop fully functioning visual pathways in the auditory portions of their brains. In other words, they see the world with brain tissue that was only thought capable of hearing sounds.
    – per UD

    If DNA really rules (morphology), why did THIS happen? – April 2014
    Excerpt: Researchers implanted human embryonic neuronal cells into a mouse embryo. Mouse and human neurons have distinct morphologies (shapes). Because the human neurons feature human DNA, they should be easy to identify.
    Which raises a question: Would the human neurons implanted in developing mouse brain have a mouse or a human morphology?
    Well, the answer is, the human neurons had a mouse morphology. They could be distinguished from the mouse ones only by their human genetic markers.
    If DNA really ruled, we would expect a human morphology.”
    – per UD

    DNA doesn’t even tell teeth what they should look like – April 3, 2014
    Excerpt: A friend writes to mention a mouse experiment where developing tooth buds were moved so that the incisors and the molars were switched. The tooth buds became the tooth appropriate to the switched location, not the original one, in direct contrast to what we would expect from a gene’centric view.
    – per UD

    I would also like to further highlight that emphasizing protein coding regions of the genome (2%), to the exclusion of almost all the rest of the ‘species specicific’ regulatory regions of the genome, as Darwinists currently do, is to miss a huge elephant in the living room. Talbott, in his unique style, puts the ‘elephant in the living room’ situation like this:

    HOW BIOLOGISTS LOST SIGHT OF THE MEANING OF LIFE — AND ARE NOW STARING IT IN THE FACE – Stephen L. Talbott – May 2012
    Excerpt: “If you think air traffic controllers have a tough job guiding planes into major airports or across a crowded continental airspace, consider the challenge facing a human cell trying to position its proteins”. A given cell, he notes, may make more than 10,000 different proteins, and typically contains more than a billion protein molecules at any one time. “Somehow a cell must get all its proteins to their correct destinations — and equally important, keep these molecules out of the wrong places”. And further: “It’s almost as if every mRNA [an intermediate between a gene and a corresponding protein] coming out of the nucleus knows where it’s going” (Travis 2011),,,
    Further, the billion protein molecules in a cell are virtually all capable of interacting with each other to one degree or another; they are subject to getting misfolded or “all balled up with one another”; they are critically modified through the attachment or detachment of molecular subunits, often in rapid order and with immediate implications for changing function; they can wind up inside large-capacity “transport vehicles” headed in any number of directions; they can be sidetracked by diverse processes of degradation and recycling… and so on without end. Yet the coherence of the whole is maintained.
    The question is indeed, then, “How does the organism meaningfully dispose of all its molecules, getting them to the right places and into the right interactions?”
    The same sort of question can be asked of cells, for example in the growing embryo, where literal streams of cells are flowing to their appointed places, differentiating themselves into different types as they go, and adjusting themselves to all sorts of unpredictable perturbations — even to the degree of responding appropriately when a lab technician excises a clump of them from one location in a young embryo and puts them in another, where they may proceed to adapt themselves in an entirely different and proper way to the new environment. It is hard to quibble with the immediate impression that form (which is more idea-like than thing-like) is primary, and the material particulars subsidiary.
    Two systems biologists, one from the Max Delbrück Center for Molecular Medicine in Germany and one from Harvard Medical School, frame one part of the problem this way:
    “The human body is formed by trillions of individual cells. These cells work together with remarkable precision, first forming an adult organism out of a single fertilized egg, and then keeping the organism alive and functional for decades. To achieve this precision, one would assume that each individual cell reacts in a reliable, reproducible way to a given input, faithfully executing the required task. However, a growing number of studies investigating cellular processes on the level of single cells revealed large heterogeneity even among genetically identical cells of the same cell type. (Loewer and Lahav 2011)”,,,
    And then we hear that all this meaningful activity is, somehow, meaningless or a product of meaninglessness. This, I believe, is the real issue troubling the majority of the American populace when they are asked about their belief in evolution. They see one thing and then are told, more or less directly, that they are really seeing its denial. Yet no one has ever explained to them how you get meaning from meaninglessness — a difficult enough task once you realize that we cannot articulate any knowledge of the world at all except in the language of meaning.,,,
    http://www.netfuture.org/2012/May1012_184.html#2

  18. 18
    Vy says:

    “Both combined.”

    Is that so? Who exactly are you trying to kid? I or yourself?

  19. 19
    Mapou says:

    Zachriel:

    Andre: How did 60 000 000 Base pair differences become fixed in only a short 6 000 000 years of unguided evolution from out last common ancestor?

    The average human has 175 mutations or so, most of them neutral. The rate of fixation of neutral mutations is the same as the rate of introduction of neutral mutations, so 175 mutations will become fixed per generation. Six million years is about 300,000 generations, which leads to the fixation of about 50 million mutations. Give or take.

    50 billion mutations would make no difference let alone 50 million. The search space is not 60 million but 4 ^ 60 million. Stop lying, Zachriel.

  20. 20
    wd400 says:

    This would be surprising, as “junk dna” should drift at a rate of about 1% per million years (if I recall correctly).

    You do not. Junk DNA would drift at the individual mutation rate ~ 2e-8mu/site/generation. In 15 year generations that’s’ (2e-8 mut/site) / 15 years ) * 6 million years = 0.008 mutations per site per branch

    Two branches makes 1.6% divergence which is about what we actually see. That’s a very back-of-the-envelope sort of calculation, but shows we are in about the right place.

    (you might be thinking of the so called “2% rule” for mitochondrial DNA, which has a much higher mutation rate)

  21. 21
    Larry Moran says:

    Vincent,

    Thanks for posting this. Your credibility just went way up.

    Now, please explain to your friends how the differences between chimps and humans are perfectly compatible with everything we know about evolution. They need to be educated.

  22. 22
    Mapou says:

    Moran:

    Now, please explain to your friends how the differences between chimps and humans are perfectly compatible with everything we know about evolution. They need to be educated.

    Personally I never understood why this was so important. I am an ID supporter and a Christian. I am proud to share 98% of my genes with such an awesomely and brilliantly designed animal as a chimp. I’m also proud of my 25% genetic similarity to a dog.

  23. 23
    Vy says:

    Mapou, don’t forget the 50% with a banana and 70% with a slug. 😀

  24. 24
    Mapou says:

    Vy, I love both bananas and slugs.

    PS. What really makes us special is not so much our bodies but our spirits.

  25. 25
    Virgil Cain says:

    Larry Moran:

    Now, please explain to your friends how the differences between chimps and humans are perfectly compatible with everything we know about evolution.

    Please explain how to test the claim the differences in genomes can account for all of the physiological and morphological differences between humans and chimps.

    Then tell us how to test the claim that drift and natural selection didit.

    Or you can just remain a non-credible supporter of your faith.

  26. 26
    bornagain says:

    As to genetic similarity being supposed evidence for common descent, here are a couple of references that challenge that standard Darwinian presupposition:

    Kangaroo genes close to humans
    Excerpt: Australia’s kangaroos are genetically similar to humans,,, “There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order,” ,,,”We thought they’d be completely scrambled, but they’re not. There is great chunks of the human genome which is sitting right there in the kangaroo genome,”
    http://www.reuters.com/article.....P020081118

    First Decoded Marsupial Genome Reveals “Junk DNA” Surprise – 2007
    Excerpt: In particular, the study highlights the genetic differences between marsupials such as opossums and kangaroos and placental mammals like humans, mice, and dogs. ,,,
    The researchers were surprised to find that placental and marsupial mammals have largely the same set of genes for making proteins. Instead, much of the difference lies in the controls that turn genes on and off.
    http://news.nationalgeographic.....m-dna.html

    On Human Origins: Is Our Genome Full of Junk DNA? Pt 2. – Richard Sternberg PhD. Evolutionary Biology
    Excerpt: “Here’s an example, aardvark and human chromosomes. They look very similar at the DNA level when you take small snippets of them. (Yet) When you look at how they are arranged in a linear pattern along the chromosome they turn out to be very distinct (from one another). So when you get to the folder and the super-folder and the higher order level, that’s when you find these striking differences. And here is another example. They are now sequencing the nuclear DNA of the Atlantic bottle-nose dolphin. And when they started initially sequencing the DNA, the first thing they realized is that basically the Dolphin genome is almost wholly identical to the human genome. That is, there are a few chromosome rearrangements here and there, you line the sequences up and they fit very well. Yet no one would argue, based on a statement like that, that bottle-nose dolphins are closely related to us. Our sister species if you will. No one would presume to do that. So you would have to layer in some other presumption. But here is the point. You will see these statements throughout the literature of how common things are.,,, (Parts lists are very similar, but how the parts are used is where you will find tremendous differences)
    http://www.discovery.org/multi.....-dna-pt-2/

    of related note:

    Family Ties: Completion of Zebrafish Reference Genome Yields Strong Comparisons With Human Genome – Apr. 17, 2013
    Excerpt: Researchers demonstrate today that 70 per cent of protein-coding human genes are related to genes found in the zebrafish,,,
    http://www.sciencedaily.com/re.....131725.htm

    Shark and human proteins “stunningly similar”; shark closer to human than to zebrafish – December 9, 2013
    Excerpt: “We were very surprised to find, that for many categories of proteins, sharks share more similarities with humans than zebrafish,” Stanhope said. “Although sharks and bony fishes are not closely related, they are nonetheless both fish … while mammals have very different anatomies and physiologies.
    http://www.uncommondescent.com.....zebrafish/

    Of supplemental note, there is a sharp discontinuity in both physical and intellectual evidence for a gradual transition from some chimp-like creature

    “A number of hominid crania are known from sites in eastern and southern Africa in the 400- to 200-thousand-year range, but none of them looks like a close antecedent of the anatomically distinctive Homo sapiens…Even allowing for the poor record we have of our close extinct kin, Homo sapiens appears as distinctive and unprecedented…there is certainly no evidence to support the notion that we gradually became who we inherently are over an extended period, in either the physical or the intellectual sense.”
    Dr. Ian Tattersall: – paleoanthropologist – emeritus curator of the American Museum of Natural History – (Masters of the Planet, 2012)

    Evolution of the Genus Homo – Annual Review of Earth and Planetary Sciences – Ian Tattersall, Jeffrey H. Schwartz, May 2009
    Excerpt: “Unusual though Homo sapiens may be morphologically, it is undoubtedly our remarkable cognitive qualities that most strikingly demarcate us from all other extant species. They are certainly what give us our strong subjective sense of being qualitatively different. And they are all ultimately traceable to our symbolic capacity. Human beings alone, it seems, mentally dissect the world into a multitude of discrete symbols, and combine and recombine those symbols in their minds to produce hypotheses of alternative possibilities. When exactly Homo sapiens acquired this unusual ability is the subject of debate.”
    http://www.annualreviews.org/d.....208.100202

    Leading Evolutionary Scientists Admit We Have No Evolutionary Explanation of Human Language – December 19, 2014
    Excerpt: Understanding the evolution of language requires evidence regarding origins and processes that led to change. In the last 40 years, there has been an explosion of research on this problem as well as a sense that considerable progress has been made. We argue instead that the richness of ideas is accompanied by a poverty of evidence, with essentially no explanation of how and why our linguistic computations and representations evolved.,,,
    (Marc Hauser, Charles Yang, Robert Berwick, Ian Tattersall, Michael J. Ryan, Jeffrey Watumull, Noam Chomsky and Richard C. Lewontin, “The mystery of language evolution,” Frontiers in Psychology, Vol 5:401 (May 7, 2014).)
    It’s difficult to imagine much stronger words from a more prestigious collection of experts.
    http://www.evolutionnews.org/2.....92141.html

  27. 27
    Vy says:

    One interesting observation is that the sequence divergence between chimp and human is quite large, in excess of 20% for a few regions. Some of the larger gaps are broken by regions within them that align with appropriate segments of the other species’ DNA sequence but only have distant similarity. These observations suggest that complex processes, presumably involving repeated sequences and possible conversion events, may occur that will require detailed study to understand.

    Just sayin’.

  28. 28
    Rob says:

    Mapou @ 24: Vy, I love both bananas and slugs.

    So does UC Santa Cruz 🙂

  29. 29
    bFast says:

    wd400 (20), “(you might be thinking of the so called “2% rule” for mitochondrial DNA, which has a much higher mutation rate)”
    You would be right. I picked that up studying the cytochrome c, which is mitochondrial.

  30. 30
    johnnyb says:

    The question of how to count similarities in the genetic code is, as Virgil Cain points out, the question at issue.

    This has been much debated in YEC circles, with, for instance, Todd Wood proposing that humans and chimps started with 100% DNA similarity. While I disagree with this position, I think pondering it for a bit calls us to question assumptions that were previously taken for granted (like whether or not DNA is the magic organism-builder everyone says it is).

    I tend to side more with the Tomkins side of the debate, as I have talked with him quite a bit over the years about what has been happening, and he at least seems to be attempting a fairly rigorous study, with as few assumptions (either creationary or evolutionary) as possible. I’m curious why Williamson’s criticisms of Tomkins is included above, but not Tomkins’ responses, which are in the same thread? I encourage everyone to read the thread itself.

    Now, what’s even more problematic is that the chimp data itself is built on evolutionary assumptions (rather than doing a ground-up sequence, they used a human as a template for building the genome). In fact, what is really concerning is that the people who built the chimp genome said that they actually had a construction of the chimp genome from the ground up, but only published the data of the one built on the human genome!

    Anyway, there are a lot of methodologies. Let me give you another one. Let’s say that we have two organisms whose genomes are 100% different. If large-scale deletions are allowed, then one could hypothesize a common ancestor which simply had the two genomes concatenated, and then claim that the two organisms are identical except for two deletion mutations!

    I don’t think anyone would do that, but my point is that one’s expectations certainly influence what is counted as “similar” or “different”. If we find a repetitive sequence in two different places, is that because it is a transposable element, or is it a designed, fixed element that appears twice? Genome comparisons won’t tell us.

    In any case, as Andre points out, even a 98% comparison is a huge difference, and, at the very least, means that natural selection is incapable of producing the change (but anyone with half a brain knew that already), and that unguided forces of any kind are likely not responsible.

    But I think the most interesting conception is that of Todd Wood, who rightly points out that even if the genomes were 100% identical, chimps and humans would not be identical. There is more to life than DNA. I disagree with Wood’s number, but not his point.

  31. 31
    wd400 says:

    In any case, as Andre points out, even a 98% comparison is a huge difference, and, at the very least, means that natural selection is incapable of producing the change (but anyone with half a brain knew that already), and that unguided forces of any kind are likely not responsible.

    Have you been reading? You don’t even need natural selection to explain this meany differences.

  32. 32
    Mapou says:

    wd400, have you been reading? That 2% difference amounts to a search space equal to 4 ^ 60 million. That’s an impossibly large space to search through stochastically.

    The combinatorial explosion kills Darwinian evolution dead.

  33. 33
    bornagain says:

    “You don’t even need natural selection to explain this meany differences.”
    -wd400

    Actually, natural selection is found, from mathematical considerations, to be an impediment to fixation of mutations, which is why Darwinists, such as wd400 and Moran, were forced to adopt the neutral theory of evolution whereby, apparently, the origination of humans is now, according to cutting edge ‘neutral theory’, entirely driven by pure chance since selection is persona non gratis:

    Haldane’s Dilemma
    Excerpt: Haldane was the first to recognize there was a cost to selection which limited what it realistically could be expected to do. He did not fully realize that his thinking would create major problems for evolutionary theory. He calculated that in man it would take 6 million years to fix just 1,000 mutations (assuming 20 years per generation).,,, Man and chimp differ by at least 150 million nucleotides representing at least 40 million hypothetical mutations (Britten, 2002). So if man evolved from a chimp-like creature, then during that process there were at least 20 million mutations fixed within the human lineage (40 million divided by 2), yet natural selection could only have selected for 1,000 of those. All the rest would have had to been fixed by random drift – creating millions of nearly-neutral deleterious mutations. This would not just have made us inferior to our chimp-like ancestors – it surely would have killed us. Since Haldane’s dilemma there have been a number of efforts to sweep the problem under the rug, but the problem is still exactly the same. ReMine (1993, 2005) has extensively reviewed the problem, and has analyzed it using an entirely different mathematical formulation – but has obtained identical results.
    John Sanford PhD. – “Genetic Entropy and The Mystery of the Genome” – pg. 159-160

    Kimura’s Quandary
    Excerpt: Kimura realized that Haldane was correct,,, He developed his neutral theory in response to this overwhelming evolutionary problem. Paradoxically, his theory led him to believe that most mutations are unselectable, and therefore,,, most ‘evolution’ must be independent of selection! Because he was totally committed to the primary axiom (neo-Darwinism), Kimura apparently never considered his cost arguments could most rationally be used to argue against the Axiom’s (neo-Darwinism’s) very validity.
    John Sanford PhD. – “Genetic Entropy and The Mystery of the Genome” – pg. 161 – 162

    With the adoption of the ‘neutral theory’ of evolution by many prominent neo-Darwinists, and the casting under the bus of Natural Selection as a major player in evolution, William J Murray quipped,,,

    “One wonders what would have become of evolution had Darwin originally claimed that it was simply the accumulation of random, neutral variations that generated all of the deeply complex, organized, interdependent structures we find in biology? Would we even know his name today?
    What exactly is Darwin really famous for now? Advancing a really popular, disproven idea (of Natural Selection), along the lines of Luminiferous Aether?
    Without the erroneous but powerful meme of “survival of the fittest” to act as an opiate for the Victorian intelligentsia and as a rationale for 20th century fascism, how might history have proceeded under the influence of the less vitriolic maxim, “Survival of the Happenstance”?”
    – William J Murray

    Berlinski was a bit more scathing than Murray was in his quip against neutral theory

    Majestic Ascent: Berlinski on Darwin on Trial – David Berlinski – November 2011
    Excerpt: The publication in 1983 of Motoo Kimura’s The Neutral Theory of Molecular Evolution consolidated ideas that Kimura had introduced in the late 1960s. On the molecular level, evolution is entirely stochastic, and if it proceeds at all, it proceeds by drift along a leaves-and-current model. Kimura’s theories left the emergence of complex biological structures an enigma, but they played an important role in the local economy of belief. They allowed biologists to affirm that they welcomed responsible criticism. “A critique of neo-Darwinism,” the Dutch biologist Gert Korthof boasted, “can be incorporated into neo-Darwinism if there is evidence and a good theory, which contributes to the progress of science.”
    By this standard, if the Archangel Gabriel were to accept personal responsibility for the Cambrian explosion, his views would be widely described as neo-Darwinian.
    per ENV

    Of related note, the math simply, no matter how much wd400 protests to the contrary, does not work out for Darwinists:

    Neo-Darwinism’s Catch-22: Before Evolving New Features, Organisms Would Be Swamped by Genetic Junk – Casey Luskin – April 10, 2015
    Excerpt: A new peer-reviewed paper in the journal Complexity presents a computational model of evolution which shows that evolving new biological structures may be deterred by an unavoidable catch-22 problem.,,,
    This is a bit complex — let’s go over it again. Darwinian evolution either (1) produces nothing new, or (2) it’s destined to produce boatloads of deadly junk. In the case of (2), the reward for trying new things is high compared to the cost of building new structures. But in order for the ratio to be high enough for complexity to increase, the cost of building new things must be negligible. Novelties proliferate, but the fraction,, that’s vestigial grows, and the organism is eventually swamped and overwhelmed by harmful vestigial features. However, if you try to avoid the problem of (2) by making the reward-to-cost ratio lower, as in (1), then nothing new ever evolves.
    The authors think real biological organisms are closer to position (1). Indeed, study in the field of systems biology increasingly finds that biological systems contain very little junk.,,,
    http://www.evolutionnews.org/2.....95121.html

    Biological Information – Purifying Selection (Mendel’s Accountant) 12-20-2014 by Paul Giem
    https://www.youtube.com/watch?v=SGJZDsQG4kQ

    Using Numerical Simulation to Test the Validity of Neo-Darwinian Theory – 2008
    Abstract: Evolutionary genetic theory has a series of apparent “fatal flaws” which are well known to population geneticists, but which have not been effectively communicated to other scientists or the public. These fatal flaws have been recognized by leaders in the field for many decades—based upon logic and mathematical formulations. However population geneticists have generally been very reluctant to openly acknowledge these theoretical problems, and a cloud of confusion has come to surround each issue.
    Numerical simulation provides a definitive tool for empirically testing the reality of these fatal flaws and can resolve the confusion. The program Mendel’s Accountant (Mendel) was developed for this purpose, and it is the first biologically-realistic forward-time population genetics numerical simulation program. This new program is a powerful research and teaching tool. When any reasonable set of biological parameters are used, Mendel provides overwhelming empirical evidence that all of the “fatal flaws” inherent in evolutionary genetic theory are real. This leaves evolutionary genetic theory effectively falsified—with a degree of certainty which should satisfy any reasonable and open-minded person.
    http://www.icr.org/i/pdf/techn.....Theory.pdf

    Of directly related interest is this recent paper by Dr. John Sanford (inventor of the biolistic ‘gene gun’ and pioneer in transgenetic crops):

    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/pm.....MC4573302/

  34. 34
    Mapou says:

    By comparison, the number of particles in the universe is estimated to be 10 ^ 87. Read it and weep.

    !!!!!

  35. 35
    wd400 says:

    What does “search space” have to do with anything when we’re ignoring selection. There is nothing special about any state in that space under that assumption…

  36. 36
    Mapou says:

    wd400 is pulling a Zachriel. Irrelevant and deceptive comment that makes no sense.

    Look, man. We’re talking about going from chimp to humans via RM+NS. It never happened. Why? Because the combinatorial explosion killed it before it was born.

    Wisdom starts with gonads. Grow a pair.

  37. 37
    bornagain says:

    Of supplemental note as to how biased Darwinists can be in their handling of the genetic evidence, this following article shows that over 1000 completely unique ‘ORFan’ genes, that are completely unique to humans and not found in any other species, were stripped from the gene count of humans simply because the evolutionary scientists could not find corresponding genes in primates. In other words evolution, of humans from primates, was assumed to be true in the first place and then the genetic evidence was directly molded to fit in accord with their unproven assumption. It would be hard to find a more biased and unfair example of practicing science!

    Human Gene Count Tumbles Again – 2008
    Excerpt: Scientists on the hunt for typical genes — that is, the ones that encode proteins — have traditionally set their sights on so-called open reading frames, which are long stretches of 300 or more nucleotides, or “letters” of DNA, bookended by genetic start and stop signals.,,,, The researchers considered genes to be valid if and only if similar sequences could be found in other mammals – namely, mouse and dog. Applying this technique to nearly 22,000 genes in the Ensembl gene catalog, the analysis revealed 1,177 “orphan” DNA sequences. These orphans looked like proteins because of their open reading frames, but were not found in either the mouse or dog genomes.,,, the researchers compared the orphan sequences to the DNA of two primate cousins, chimpanzees and macaques. After careful genomic comparisons, the orphan genes were found to be true to their name — they were absent from both primate genomes.
    http://www.sciencedaily.com/re.....161406.htm

    This “ORFan problem” has only gotten worse for Darwinists since that extremely biased 2008 paper came out.
    Even the militant atheist Jerry Coyne stated:

    “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 – militant atheist – retired professor at the University of Chicago in the department of ecology and evolution for twenty years. He specializes in evolutionary genetics. – 2012

    more notes on the “ORFan problem”

    Mechanisms and dynamics of orphan gene emergence in insect genomes – January 2013
    Excerpt: Orphans are an enigmatic portion of the genome since their origin and function are mostly unknown and they typically make up 10 to 30% of all genes in a genome.
    http://gbe.oxfordjournals.org/.....l.pdf+html

    “However, with the advent of sequencing of full genomes, it became clear that approximately 20–40% of the identified genes could not be associated with a gene family that was known before. Such genes were originally called ‘orphan’ genes”
    http://ccsb.dfci.harvard.edu/w.....S_2013.pdf

    A Surprise Source of Life’s Code – August 18, 2015
    Excerpt: Just last month, research presented at the Society for Molecular Biology and Evolution in Vienna identified 600 potentially new human genes. “The existence of de novo genes was supposed to be a rare thing,” said Mar Albà, an evolutionary biologist
    https://www.quantamagazine.org/20150818-a-surprise-source-of-lifes-code/

    Proteins and Genes, Singletons and Species – Branko Kozuli? PhD. Biochemistry
    Excerpt: Horizontal gene transfer is common in prokaryotes but rare in eukaryotes [89-94], so HGT cannot account for (ORFan) singletons in eukaryotic genomes, including the human genome and the genomes of other mammals.,,,
    The trend towards higher numbers of (ORFan) singletons per genome seems to coincide with a higher proportion of the eukaryotic genomes sequenced. In other words, eukaryotes generally contain a larger number of singletons than eubacteria and archaea.,,,
    That hypothesis – that evolution strives to preserve a protein domain once it stumbles upon it contradicts the power law distribution of domains. The distribution graphs clearly show that unique domains are the most abundant of all domain groups [21, 66, 67, 70, 72, 79, 82, 86, 94, 95], contrary to their expected rarity.,,,
    Evolutionary biologists of earlier generations have not anticipated [164, 165] the challenge that (ORFan) singletons pose to contemporary biologists. By discovering millions of unique genes biologists have run into brick walls similar to those hit by physicists with the discovery of quantum phenomena. The predominant viewpoint in biology has become untenable: we are witnessing a scientific revolution of unprecedented proportions.
    http://vixra.org/pdf/1105.0025v1.pdf

    Darwin’s (Failed Predictions) – Similar species share similar genes – Cornelius Hunter PhD.
    Excerpt: As much as a third of the genes in a given species may be unique, and even different variants within the same species have large numbers of genes unique to each variant. Different variants of the Escherichia coli bacteria, for instance, each have hundreds of unique genes. (Daubin and Ochman)
     
    Significant genetic differences were also found between different fruit fly species. Thousands of genes showed up missing in many of the species, and some genes showed up in only a single species. (Levine et. al.) As one science writer put it, “an astonishing 12 per cent of recently evolved genes in fruit flies appear to have evolved from scratch.” (Le Page) These novel genes must have evolved over a few million years, a time period previously considered to allow only for minor genetic changes. (Begun et. al.; Chen et. al., 2007)
     
    Initially some evolutionists thought these surprising results would be resolved when more genomes were analyzed. They predicted that similar copies of these genes would be found in other species. But instead each new genome has revealed yet more novel genes. (Curtis et. al.; Marsden et. al.; Pilcher)
     
    Next evolutionists thought that these rapidly-evolving unique genes must not code for functional or important proteins. But again, many of the unique proteins were in fact found to play essential roles. (Chen, Zhang and Long 1010; Daubin and Ochman; Pilcher) As one researcher explained, “This goes against the textbooks, which say the genes encoding essential functions were created in ancient times.” (Pilcher)
    https://sites.google.com/site/darwinspredictions/similar-species-share-similar-genes

    Finding a fairly large percentage of unique ORFan genes in humans, or in any other species for that matter, is certainly not a minor problem for Darwinists:

    Could Chance Arrange the Code for (Just) One Gene?
    “our minds cannot grasp such an extremely small probability as that involved in the accidental arranging of even one gene (10^-236).”
    http://www.creationsafaris.com/epoi_c10.htm

    “Is it really credible that random processes could have constructed a reality, the smallest element of which—a functional protein or gene— is complex beyond our own creative capacities, a reality which is the very antithesis of chance, which excels in every sense anything produced by the intelligence of man?”
    ~ Michael Denton

    The Extreme Complexity Of Genes – Dr. Raymond G. Bohlin – video (28 second mark)
    https://www.youtube.com/watch?v=vo3OKSGeFRQ&index=2&list=PL9C519B84FE6C1202

    Design In DNA – Alternative Splicing, Duons, and Dual coding genes – video (5:05 minute mark)
    http://www.youtube.com/watch?v=Bm67oXKtH3s#t=305

  38. 38
    Robert Byers says:

    This YEC welcomes 99% ldna with apes. its not evidence of anything but the obvious. We look the same and so have the same origins of looks. DNA.
    We also have the same, lesser, with animals of all types.
    its a common blueprint and only could be that way.
    IF we looked like apes as we do and were only 10 or 40 % dna alike then it would be strange.
    It works in creationism better that we alone of creatures are alike with a other creature.
    This because we don’t jave our own body. The only ones.
    We have another creatures body in order to be in the spectrum of biology but keep our special identity as created in Gods image.
    its been a careless error to thinbk we should not look like apes.
    its not evidence of ape common ancestry but thats only a line of reasoning form comparative anatomy etc.
    Not evidence at all. Just filling in dots.

  39. 39
    wd400 says:

    Mapou,

    Not sure you’re following so here’s a recap.

    Several people think that fixing this many mutations in 6 million years is beyond the power of selection.

    In fact, you don’t even need selection to fix this many differences — mutation and random sampling are quite enough.

    You then talked about the “search space” implied by the ~2% of sites that differ between humans and chimps. But this can hardly be relevant to a discussion about a purely neutral process, where all states within that space are equal.

    Hope that helps.

  40. 40
    Andre says:

    And again WD400 spews out nonsense. The 60 000 000 neutral changes still had to happen apparantly while the multiple DNA integrity check systems, repair mechanisms and the multiple Apoptosis systems stood in the way. Did you forget that these systems are evolutionary conserved to start with and if they fail necrosis kicks in and thus self destructs the organism.

    Did people also forget that the fold determine the function and if the fold is not 100% correct there is no function.

  41. 41
    wd400 says:

    Mutations happen, Andre. Those calculations above are based on the observed mutation rate after all those “integrity” checks.

  42. 42
    Mapou says:

    wd400 @39

    You are too stupid to insult my intelligence. You’re pathetic, man. You and Zachriel should shack up together. Two of a kind.

    PS. Did I ever tell you you were a jackass?

  43. 43
    Andre says:

    WD400

    And mutations are always at a fitness cost. Try again with actual evidence please.

  44. 44
    wd400 says:

    Do you really believe that? When we are each born with ~70 mutations? Do you really think DNA changes that don’t alter proteins in protein coding genes are universally bad?

  45. 45
    Box says:

    WD400,

    Are you saying that the difference between human and chimp DNA is mostly a difference in junk-DNA?
    If so, how do we explain the obvious differences between humans and chimps from DNA?

  46. 46
    Virgil Cain says:

    This goes for wd400 also:

    Please explain how to test the claim the differences in genomes can account for all of the physiological and morphological differences between humans and chimps.

    Then tell us how to test the claim that drift and natural selection didit.

    Or you can just remain a non-credible supporter of your faith.

  47. 47
    Virgil Cain says:

    Yes mutations happen and they can accumulate. The BIG questions are – Can accumulations of mutations account for the physiological and morphological change required? How can we test that claim?

  48. 48
    bornagain says:

    There is something interesting about having multiple levels of “integrity checks” that directly challenges the ‘bottom up’ thinking of the modern synthesis of Darwinian evolution.

    The following studies are good for highlighting that ‘something interesting’:

    The World’s Toughest Bacterium – 2002
    Excerpt: “When subjected to high levels of radiation, the Deinococcus genome is reduced to fragments,” (…) “RecA proteins may play role in finding overlapping fragments and splicing them together.”
    http://www.genomenewsnetwork.o.....ccus.shtml

    Extreme Genome Repair – 2009
    Excerpt: If its naming had followed, rather than preceded, molecular analyses of its DNA, the extremophile bacterium Deinococcus radiodurans might have been called Lazarus. After shattering of its 3.2 Mb genome into 20–30 kb pieces by desiccation or a high dose of ionizing radiation, D. radiodurans miraculously reassembles its genome such that only 3 hr later fully reconstituted nonrearranged chromosomes are present, and the cells carry on, alive as normal.,,,
    http://www.ncbi.nlm.nih.gov/pm.....MC3319128/

    In the lab, scientists coax E. coli to resist radiation damage – March 17, 2014
    Excerpt: ,,, John R. Battista, a professor of biological sciences at Louisiana State University, showed that E. coli could evolve to resist ionizing radiation by exposing cultures of the bacterium to the highly radioactive isotope cobalt-60. “We blasted the cultures until 99 percent of the bacteria were dead. Then we’d grow up the survivors and blast them again. We did that twenty times,” explains Cox.
    The result were E. coli capable of enduring as much as four orders of magnitude more ionizing radiation, making them similar to Deinococcus radiodurans, a desert-dwelling bacterium found in the 1950s to be remarkably resistant to radiation. That bacterium is capable of surviving more than one thousand times the radiation dose that would kill a human.
    http://www.news.wisc.edu/22641

    Pond scum smashes genome into over 225k parts, then rebuilds it – Sept. 9, 2014
    Excerpt: The pond-dwelling, single-celled organism Oxytricha trifallax has the remarkable ability to break its own DNA into nearly a quarter-million pieces and rapidly reassemble those pieces when it’s time to mate,
    http://www.uncommondescent.com.....builds-it/

    Since mutations to DNA are suppose to be the main driver for Darwinian evolution, exactly how does the rest of the cell know how to put its DNA back together in the correct order? Exactly where does the ‘integrity check’ information reside in the cell?

    As with many other lines of evidence, this is not a minor problem for Darwinian thinking.

    As Shapiro, Noble, and others have pointed out, DNA is an organ of the cell, not its dictator, as was, and is, falsely presupposed in the modern synthesis of neo-Darwinism:

    “The genome is an ‘organ of the cell’, not its dictator”
    – Denis Noble – President of the International Union of Physiological Sciences

    How life changes itself: the Read-Write (RW) genome. – 2013
    Excerpt: Research dating back to the 1930s has shown that genetic change is the result of cell-mediated processes, not simply accidents or damage to the DNA. This cell-active view of genome change applies to all scales of DNA sequence variation, from point mutations to large-scale genome rearrangements and whole genome duplications (WGDs). This conceptual change to active cell inscriptions controlling RW genome functions has profound implications for all areas of the life sciences.
    http://www.ncbi.nlm.nih.gov/pubmed/23876611

    "It is difficult (if not impossible) to find a genome change operator that is truly random in its action within the DNA of the cell where it works'
    James Shapiro – Evolution: A View From The 21st Century – (Page 82)

    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

    Physiology is rocking the foundations of evolutionary biology – Denis Noble – 17 MAY 2013
    Excerpt: The ‘Modern Synthesis’ (Neo-Darwinism) is a mid-20th century gene-centric view of evolution, based on random mutations accumulating to produce gradual change through natural selection.,,, We now know that genetic change is far from random and often not gradual.,,,
    http://onlinelibrary.wiley.com.....4/abstract

    Dr. Wells weighs in here as to the 'surprise' of finding DNA to be an "organ of the cell, not its dictator":

    Ask an Embryologist: Genomic Mosaicism – Jonathan Wells – February 23, 2015
    Excerpt: humans have a "few thousand" different cell types. Here is my simple question: Does the DNA sequence in one cell type differ from the sequence in another cell type in the same person?,,,
    The simple answer is: We now know that there is considerable variation in DNA sequences among tissues, and even among cells in the same tissue. It's called genomic mosaicism.
    In the early days of developmental genetics, some people thought that parts of the embryo became different from each other because they acquired different pieces of the DNA from the fertilized egg. That theory was abandoned,,,
    ,,,(then) "genomic equivalence" — the idea that all the cells of an organism (with a few exceptions, such as cells of the immune system) contain the same DNA — became the accepted view.
    I taught genomic equivalence for many years. A few years ago, however, everything changed. With the development of more sophisticated techniques and the sampling of more tissues and cells, it became clear that genetic mosaicism is common.
    I now know as an embryologist,,,Tissues and cells, as they differentiate, modify their DNA to suit their needs. It's the organism controlling the DNA, not the DNA controlling the organism.
    http://www.evolutionnews.org/2.....93851.html

  49. 49
    EugeneS says:

    The size of the alphabet = 4. Therefore on average two random strings of the same length will be 25% similar. Any gibberish and a biologically meaningful string will be on average 25% similar. So if for a pair of genomes the homology is estimated to 25% or less, I would say that either the method of measuring is not right or the two species are unrelated completely (they do not have a common ancestor at all maybe).

    I agree with the comment pointing out that until we have a precise genotype-phenotype mapping for a pair of species under investigation, comparing two variants of “we-do-not-know-what” does not make much sense.

    And, of course, the 98% similarity refers to 2% of the genomes in question.

    We simply do not know in relative phenotypical terms what is 2% really, a lot or almost nothing. And probably the same percentage would translate to different amounts of phenotypical similarity for different pairs of genomes.

    It’s too complicated to wave flags just yet. Crude comparisons are not telling us much.

  50. 50
    Andre says:

    WD400

    If by mutation you mean my eyes are blue instead of green like my father then you really have nothing it’s not like my mutations are growing wings on my back that would confirm your speculation.

  51. 51
    bFast says:

    Further to Virgil Cain (46), “Then tell us how to test the claim that drift and natural selection didit.”

    Lets start with a serious look at the challenge of the HAR1F. I contend that a minimum of 6 mutations were required to cause the gene to choose the human looping pattern. We know from the fact that it is ultra-conserved between mice and chickens that every single point mutation is deleterious. Any analysis of the 3d configuration of the gene would cause us to conclude that mutation 2, 3, 4 and 5 are deleterious also. This transformation is far above the edge of evolution.

  52. 52
    Vy says:

    “And, of course, the 98% similarity refers to 2% of the genomes in question.”

    Right.

    So in essence, it’s basically 1.6% – 1.8% of the entire genome, evodelusionary distinction between DNA and the mythical “junk” DNA notwithstanding.

  53. 53
    Zachriel says:

    bFast: Lets start with a serious look at the challenge of the HAR1F. I contend that a minimum of 6 mutations were required to cause the gene to choose the human looping pattern.

    There are actually 18 substitutions since the posited common ancestors with chimpanzees.

    bFast: We know from the fact that it is ultra-conserved between mice and chickens that every single point mutation is deleterious.

    HAR1 is conserved, with only two point mutations since the common ancestor of chickens and non-human primates. That doesn’t mean every substitution will be deleterious if other aspects of the human lineage have changed. A simple example would be a bigger skull being deleterious, unless accompanied by wider hips for childbearing in the female (which is actually still deleterious in humans, leading to a higher risk for the mother and baby, but compensated for by the advantage of a larger brain).

    A similar burst of evolution is seen in Lenski’s E. coli Long-term Evolution Experiment. There were potentiating mutations, then a tandem repeat, in a sub-population of bacteria under study. Once this occurred, it was followed by a burst of evolution, as multiple optimizing mutations became fixed in the citrate strain.

  54. 54
    Virgil Cain says:

    It is very telling that all our opponents can do is equivocate, erect strawman after strawman and misrepresent.

  55. 55
    Vy says:

    “A similar burst of evolution is seen in Lenski’s E. coli Long-term Evolution Experiment. There were potentiating mutations, then a tandem repeat, in a sub-population of bacteria under study. Once this occurred, it was followed by a burst of evolution, as multiple optimizing mutations became fixed in the citrate strain.”

    The way you evos equivocate adaptation and evolution is truly amazing. Do you guys listen to yourselves or do you enjoy the mental gymnastics it takes to accomplish it?

    The only evolution that occurred in Lenski’s experiment is the one that exists only, and only, in the minds of Darwinists (theistic or otherwise) where adaptation (a fully valid pre-Darwinian mechanism) = evolution (an invalid representation of reality that elevates probablymaybecouldness, time, the laws of nature etc. to “god”level).

  56. 56
    Zachriel says:

    Vy: The only evolution that occurred in Lenski’s experiment is the one that exists only, and only, in the minds of Darwinists (theistic or otherwise) where adaptation (a fully valid pre-Darwinian mechanism) = evolution (an invalid representation of reality that elevates probablymaybecouldness, time, the laws of nature to “god”level).

    The mechanism of adaptation in Lenski’s Experiment was clearly due to evolutionary processes; in particular, the burst of optimizing evolution. Many of the details of that historical transition are now known. See Blount, Genomic analysis of a key innovation in an experimental Escherichia coli population, Nature 2012.

  57. 57
    Vy says:

    “The mechanism of adaptation in Lenski’s Experiment was clearly due to evolutionary processes; in particular, the burst of optimizing evolution.”

    Burst of optimizing evolution eh?

    So bacteria adapting to use citrate for carbon growth which it could already metabolize and transport is somehow a “burst of optimizing evolution”?

    That’s like saying the fact that a child born on Antarctica could survive a day in the Sahara desert is a “burst of optimizing evolution”. Total and utter crap!

    What I do see clearly is that you’ve answered my question, you do enjoy the mental gymnastics, that’s why this

    After an enormous amount of work, having sequenced the genomes of many clones along the lineages that led to the ability to use citrate, as well as lineages that never did, and testing the phenotypes of identified mutations, Blount et al. have now reported that Behe was largely right. The key innovation was a shift in regulation of the citrate operon, caused by a rearrangement that brought it close to a new promoter.

    It certainly is an example of reusing existing information in a new context, thus producing a new niche for E coli in lab cultures. But if the definition of innovation is something genuinely new, such as a new transport molecule or a new enzyme, then no, this adaptation falls short as an innovation. And no one should be surprised.

    … translates to “clearly a burst of optimizing evolution” in your mind (or brain, considering that generally doesn’t exist for you guys).

    And seriously, “optimizing” evolution??? Blindly “optimized” randomness???

  58. 58
    JoeCoder says:

    @VJTorley:

    They really are about 98% similar

    That number doesn’t include sequences that are in one species but not the other. Is this comment 100% similar to your original post above because I quote you?

    I think it’s more meaningful to cite numbers like these:

    their genomes are not 98% or 99% identical … One consequence of the numerous duplications, insertions, and deletions, is that the total DNA sequence similarity between humans and chimpanzees is not 98% to 99%, but instead closer to 95% to 96%, although the rearrangements are so extensive as to render one-dimensional comparisons overly simplistic — Todd Preuss, PNAS, 2012

    one finds that the human and chimpanzee genomes are indeed about 95% identical, genome wide — Dennis Venema, of BioLogos

  59. 59
    wd400 says:

    Vy,

    That’s like saying the fact that a child born on Antarctica could survive a day in the Sahara desert is a “burst of optimizing evolution”.

    No. It’s really really not at all like that. What are you going on about?

    The “optimizing evolution” Zachriel is talking about is the pretty rapid accumulation of evolutionary changes that followed the establishment of the cit+ phenotype. In other words, there is a fairly long waiting time for the combination of mutations that create the new phenotype, but once that phenotype is established substitutions which increase its effectiveness are fixed rapidly.

  60. 60
    Virgil Cain says:

    The mechanism of adaptation in Lenski’s Experiment was clearly due to evolutionary processes;

    Zachriel’s continued equivocation is duly noted.

  61. 61
    EugeneS says:

    “Accumulate rapidly”

    And that surely explains the differences between the chimp and the human?

  62. 62
    Virgil Cain says:

    wd400:

    The “optimizing evolution” Zachriel is talking about is the pretty rapid accumulation of evolutionary changes that followed the establishment of the cit+ phenotype. In other words, there is a fairly long waiting time for the combination of mutations that create the new phenotype, but once that phenotype is established substitutions which increase its effectiveness are fixed rapidly.

    And the equivocation continues.

    It is very telling that all our opponents can do is equivocate, erect strawman after strawman and misrepresent.

    Pathetic, actually

  63. 63
    Vy says:

    “No. It’s really really not at all like that. What are you going on about?”

    Could ask you the same.

    We’ve gone from “burst of evolution” to adaptation due to “evolutionary processes” to accumulation of “evolutionary changes”. Pretty interesting use of terms.

    When someone gets around to ending the bait-and-switch, do inform me.

  64. 64
    wd400 says:

    If you guys want to explain what on earth you are going on about let me know. Like, what is contradictory about those terms Vy?

    A burst of evolution is obviously an evolutionary process and includes the accumulation of evolutionary changes? What’s the bait? What’s the switch?

  65. 65
    Zachriel says:

    Vy: So bacteria adapting to use citrate for carbon growth which it could already metabolize and transport is somehow a “burst of optimizing evolution”?

    Did you bother to read the paper?
    http://www.nature.com/nature/j.....4-f1.2.jpg

    Vy: Blount et al. have now reported that Behe was largely right. The key innovation was a shift in regulation of the citrate operon, caused by a rearrangement that brought it close to a new promoter.

    What Behe actually wrote was “If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.” In this case, we have potentiating mutations AND gene-duplication with sequence divergence AND the gain of a new regulatory relationship AND a burst of optimizing mutations.

  66. 66
    Virgil Cain says:

    A burst of evolution is expected if organisms are designed to evolve. The equivocation comes from using all examples of evolution as support for blind watchmaker evolution.

  67. 67
    bFast says:

    Zachriel (53): “There are actually 18 substitutions since the posited common ancestors with chimpanzees.”

    That is correct. However, there is a change in the loop structure of one of the nodes. To invoke this loop structure change takes 6 mutations. (I give nature the HUGE benefit of the doubt that when the loop structure changed, the result was somehow at least as good as the non-human HAR1F.) Every possible single point mutation within this loop has been tried a gazillion times, and been removed a gazillion (minus 1) by natural selection. Why? BECAUSE EVERY SINGLE POINT MUTATION IS DELETERIOUS! That’s what the theory says — honest.

    If each individual mutation that forms the loop is deleterious, and if it takes 6 to re-form the loop, then a minimum of 5 deleterious mutations must have combined together waiting for lucky #6 to produce the loop transformation.

    “HAR1 is conserved, with only two point mutations since the common ancestor of chickens and non-human primates.” Actually, on the tail of this 118 nucleotide RNA gene there are three points that wander like the wind. (One just happens to be the same with chickens and humans, but with other animals there is a third wanderer.) Except for these three wanderers, this thing is rock stable for all mammals and birds (but it doesn’t exist at all in reptiles, go figure.)

    “A simple example would be a bigger skull being deleterious” That’s a stupid statement Zachriel. First, still takes at least 6 approximately simultaneous mutations. Second — there is huge variability within mammals and birds. Bet bones that whales have bigger skulls than humans.

    “A similar burst of evolution is seen in Lenski’s E. coli Long-term Evolution Experiment.” Let me see, before there was a gene duplication (which was not deleterious) a point mutation wouldn’t work. Once the duplication was there, the point mutation became effective. This is well inside the “edge of evolution”. This is hardly a parallel to the HAR1F.

  68. 68
    Vy says:

    “In this case, we have potentiating
    mutations AND gene-duplication with sequence
    divergence AND the gain of a new regulatory
    relationship AND a burst of optimizing mutations.”

    * the E. Coli already had the ability to comfortably use citrate albeit under anaerobic conditions.

    * the organism controls the DNA not vice versa, so under the “eat_citrate_or_starve_to_death” lab conditions, the E. Coli chose to eat by tweaking already existing information to work under the lab environments.

    * no new information was dropped from space, ergo, no evolution, whether burst, process or change. Simply adaptation due to tweaking of already existing functionality to work under new conditions which conversely lead to a loss of function:

    Each of these mutant strains has an antagonistic pleiotropy characteristic. An existing system is traded for an altered phenotype that is better suited to survive the specific stressful environment. Regulation is reduced to enable overexpression. DNA repair and DNA polymerase fidelity are reduced to enable increased mutation rates (increasing the probability of a “beneficial” mutation). A gene is inactivated by a process that concurrently activates a silent gene.Such trade-offs provide a temporary benefit to the bacterium, increasing its chances of surviving specific starvation conditions. However, these mutations do not account for the origin of the silenced genes, as their prior existence is essential for the mutation to be beneficial. (Anderson and Purdom)

    We have adaptation and loss of function, clear enough?

  69. 69
    Zachriel says:

    bFast: Second — there is huge variability within mammals and birds.

    As is clear from the context, we were referring to humans.

    You ignored the point. You are claiming that the mutations must have been deleterious. What might be deleterious in one context might not be deleterious in another. Other changes in the human genome may have resulted in potentiating changes.

    Vy: * the organism controls the DNA not vice versa, so under the “eat_citrate_or_starve_to_death” lab conditions, the E. Coli chose to eat by tweaking already existing information to work under the lab environments.

    That’s clearly not supported by the evidence. It took 30 thousand generations for Cit+ to evolve, and then, only in some lineages. The results are consistent with random mutation.

    Vy: * no new information was dropped from space, ergo, no evolution, whether burst, process or change.

    The burst of evolution occurred after Cit+ evolved, as a mutator strain arose leading to rapid optimization of the trait.

  70. 70
    bFast says:

    Zachriel, “What might be deleterious in one context might not be deleterious in another.”

    Let me see, you are trying to tell me that in all of the contexts that all of the mammals and all of the birds experience the chimp way is the best, come human, poof now having mutations that destroy the 3d shape of this thing cease to be important.

    Why don’t you get honest and say that you haven’t a clue how the HAR1F pulled off this change — but you are certain that it was naturalistic because the other option is anathema.

  71. 71
    Zachriel says:

    This is your claim.

    bFast: BECAUSE EVERY SINGLE POINT MUTATION IS DELETERIOUS!

    Can you support this statement?

  72. 72
    Vy says:

    “That’s clearly not supported by the evidence.”

    Actually, it is. Except of course you want to lie and claim the e. coli didn’t already have the ability to use citrate under anaerobic conditions prior to forcing it use it under aerobic conditions which would be totally understandable BTW, it’s not like you guys are known for your honesty.

    “It took 30 thousand generations for Cit+ to evolve, and then, only in some lineages.”

    It took 30 thousand generations for e. coli to tweak it’s DNA well enough to use citrate under aerobic conditions.

    “The results are consistent with random mutation.”

    Right, they just randomly got stuck in a citrate-high petri dish, randomly already knew how to use citrate under anaerobic conditions, and many other “randoms”.

    “The burst of evolution occurred after Cit+ evolved, as a
    mutator strain arose leading to rapid optimization of the
    trait.”

    And here we go again.

  73. 73
    bFast says:

    Zachriel (71)
    No, I can’t. The reason I can’t is that there seems to be DNA that is highly conserved even when it has no apparent purpose. As such, there is clearly some other preservative for DNA beside Natural Selection (and those pesky DNA repair systems ostensibly developed via RM+NS.)

    However, if we assume that natural selection (and its progeny which are presumably leaky) is the only preservative, then the fact that this 180 some odd nucleotide sequence is conserved through so many different species should be proof enough.

    So there are two options:
    1 – All point mutation within the 180 are deleterious
    or
    2 – There is something other than natural selection and known repair mechanisms conserving it.

    That said, simple logic, the 3d shape of the thing, strongly supports the “deleterious” hypothesis.

    Your theory still is best supported by the anathema principle.

  74. 74
    Zachriel says:

    Vy: Actually, it is. Except of course you want to lie and claim the e. coli didn’t already have the ability to use citrate under anaerobic conditions prior to forcing it use it under aerobic conditions which would be totally understandable BTW, it’s not like you guys are known for your honesty.

    But that’s not the claim you made, which was that the bacteria “chose to eat by tweaking already existing information to work under the lab environments.” It’s clear the bacteria didn’t choose, or all the bacteria would have chosen to eat citrate in the aerobic conditions they found themselves in. Instead, only after having tried billions of mutations was the pathway to Cit+ found, and only in a sub-population.

    bFast: BECAUSE EVERY SINGLE POINT MUTATION IS DELETERIOUS!

    Zachriel: Can you support this statement?

    bFast: No, I can’t.

    There are you are then.

    bFast: That said, simple logic, the 3d shape of the thing, strongly supports the “deleterious” hypothesis.

    Do you have support for that claim?

    bFast: So there are two options: 1 – All point mutation within the 180 are deleterious or 2 – There is something other than natural selection and known repair mechanisms conserving it.

    Or there were potentiating changes leading to accelerated evolution of the region.

  75. 75
    Virgil Cain says:

    It took 30 thousand generations for Cit+ to evolve, and then, only in some lineages.

    That’s because it wasn’t a required change- it wasn’t required for survival.

    How many generations did it take before humans discovered alternating current?

  76. 76
    Vy says:

    “But that’s not the claim you made”

    Sure? Here it is, again:

    * the organism controls the DNA not vice versa, so under the “eat_citrate_or_starve_to_death” lab conditions, the E. Coli chose to eat by tweaking already existing information to work under the lab environments.

    Wanna try again?

    It’s clear the bacteria didn’t choose, or all the bacteria would have chosen to eat citrate in the aerobic conditions they found themselves in.”

    Say what? All because of?

    “Instead, only after having tried billions of mutations was the pathway to Cit+ found, and only in a sub-population.

    So did Cit+ pop out of nowhere or is it a tweaked version of something that already existed? Was there or was there no reason for the e. coli to tweak this already existing functionality?

  77. 77
    Zachriel says:

    Vy: you want to lie and claim the e. coli didn’t already have the ability to use citrate under anaerobic conditions prior to forcing it use it under aerobic conditions which would be totally understandable

    This is false. We have never claimed that E. coli didn’t have the ability to utilize citrate under anaerobic conditions.

    Vy: the E. Coli chose to eat by tweaking already existing information to work under the lab environments.

    This is the statement we objected to, and the one that is unsupported.

    Vy: All because of?

    Because if its a choice, all the bacteria would choose to have more resources.

    Vy: So did Cit+ pop out of nowhere or is it a tweaked version of something that already existed?

    All evolution is a tweaked version of something that already existed. In this case, it requires potentiating mutations, a tandem duplication, then additional optimizing mutations. The time it took to evolve is consistent with random mutation.

  78. 78
    Vy says:

    “This is false. We have never claimed that E. coli didn’t have the ability to utilize citrate under anaerobic conditions.”

    Don’t quote me out of context. Read it:

    Except of course you want to lie and claim the e. coli didn’t already …

    “This is the statement we objected to, and the one that is unsupported.”

    Actually, you quoted a large text with two “claims” and objected to it so there is no this is the one.

    “Because if its a choice, all the bacteria would choose to have more resources.

    Again, because of? Why bother with something you might never encounter?

    “All evolution is a tweaked version of something that already existed.

    Finally, the honesty. With that, I say adaptation, not evolution. Please don’t give me that story about adaptation being a mechanism of evolution or whatnot.

    “In this case, it requires potentiating mutations, a tandem duplication, then additional optimizing mutations.”

    First, it required a reason, eat citrate aerobically or die. Everything else that happened was because of that.

    “The time it took to evolve is consistent with random mutation.”

    There you go again with the equivocation. Sheesh! As for “random” mutations, that’s not an exact representation of reality.

  79. 79
    Zachriel says:

    Vy: Except of course you want to lie and claim the e. coli didn’t already have the ability to use citrate under anaerobic conditions prior to forcing it use it under aerobic conditions which would be totally understandable BTW, it’s not like you guys are known for your honesty.

    As we never made that claim, or implied that claim, or held that view, your statement is false.

    Vy: * the organism controls the DNA not vice versa, so under the “eat_citrate_or_starve_to_death” lab conditions, the E. Coli chose to eat by tweaking already existing information to work under the lab environments.

    This is the statement to which we objected. E. Coli didn’t choose. Rather, the results support random mutation.

    Zachriel: All evolution is a tweaked version of something that already existed.

    Vy: Finally, the honesty. With that, I say adaptation, not evolution.

    Evolution by natural selection is adaptation through modification of existing forms. See Darwin, Origin of Species, 1859.

    Vy: eat citrate aerobically or die.

    That’s not the case. Citrate utilization evolved in the same medium that had been used for 30 thousand generations. Genomic studies show that the trait evolved through potentiating mutations in a single lineage, then a tandem duplication, followed by optimizing mutations. Most lineages never developed the trait, and the number of generations is consistent with random mutation.

    Vy: As for “random” mutations, that’s not an exact representation of reality.

    Mutations are not purely random. They have a number of causes and biases. However, they are random (uncorrelated) with respect to fitness. That’s why Cit+ took so long for the potentiating mutations to occur.

  80. 80
    Virgil Cain says:

    This is the statement to which we objected. E. Coli didn’t choose. Rather, the results support random mutation.

    LoL! It took the only gene the organism had to transport citrate and put it under the control of a promoter that allowed the gene to be expressed in the presence of O2.

    Why did it take so long? It wasn’t a required change for survival and it isn’t the only solution to the survival question.

  81. 81
    vjtorley says:

    Hi everyone,

    Thank you all for your comments. Several readers have made the valid point that even a 2% difference between human and chimp DNA is still a very large difference, and in any case, we are not the product of our DNA: a bottom-up account of life just won’t work. I entirely agree.

    Other readers queried the possibility of tens of millions of base pair changes becoming fixed in the human population over a period of just 5 or 6 million years. Darwinian natural selection would not be able to account for this, but as it turns out, the majority of base pair changes are neutral or near-neutral, and could become fixed through a process of genetic drift. At one point, I sued to be very skeptical of the possibility of fixation occurring so rapidly. See my posts here: http://www.uncommondescent.com.....lles-heel/ and http://www.uncommondescent.com.....-fixation/ . As I sifted through the arguments, I was forced to change my mind, and I finally concluded that it could have happened, as I acknowledged here: http://www.uncommondescent.com.....-im-wrong/ .

    Of course, that does not address the vital question as to whether the key differences between humans and chimps could have arisen via an unguided process, and on this point, my answer would be in the negative. The changes in the human brain alone, over the past few million years, have been quite extraordinary.

    That’s all for now, but I’ll have more to say in a day or so.

  82. 82
  83. 83
    butifnot says:

    VJ – Soo much more has been brought up in this thread. I would like to see these other more significant points addressed. Will compile a summary if someone else doesn’t.

  84. 84
    tjguy says:

    VJ said:

    Other readers queried the possibility of tens of millions of base pair changes becoming fixed in the human population over a period of just 5 or 6 million years. Darwinian natural selection would not be able to account for this, but as it turns out, the majority of base pair changes are neutral or near-neutral, and could become fixed through a process of genetic drift. At one point, I sued to be very skeptical of the possibility of fixation occurring so rapidly.

    OK, can someone help me understand this sentence: “the majority of base pair changes are neutral or near-neutral, and could become fixed through a process of genetic drift.”

    I understand what a neutral or near neutral mutation is. It is one that has little to no effect on the functioning of the organism. I understand how these mutations could become fixed in the population, but not sure why it has to be through genetic drift.

    But what I don’t understand is this: How does this qualify as Darwinian evolution? I thought evolution posits that each change was a small step of progress which gives the organism enough of a benefit that it is selected for and becomes fixed in the population. But now it seems we are saying that the changes were meaningless – didn’t help not did it hurt. Is that correct?

    And then the claim is what? That all these meaningless mutations got fixed thru whatever means and that they just happened to be the right mutations to enable a new function, gene, etc. to emerge? So, evolution goes in leaps and bounds as once in a great while all the neutral mutations that have gotten fixed in the population somehow just happen to be the right code for a new gene, etc?

    I’m probably wrong on that, but could someone explain to me how a bunch of neutral changes are thought to have contributed to the upwards evolution of the organism?

    Is this the theory of neutral evolution? Is this the Materialist answer to irreducible complexity? They think the parts somehow built up on their own and then self-assembled to form whatever was needed to adapt to a changing environment?

    So, have we left Neo-Darwinian evolution in the dust?

    When will this be announced by scientists – that neo-Darwinian evolution is wrong?

    So, IDers and creationists were right in challenging the new-darwinian paradigm after all?

    I’m sure we will never see any admission of this in the popular press.

  85. 85
    Mapou says:

    the majority of base pair changes are neutral

    I have to strongly disagree with this. The truth is that the majority of mutations are deleterious. We would all die if the genome were not continually busy repairing mutated sequences. The so-called neutral or near-neutral mutations are those that the system allows to happen. By design, of course.

  86. 86
    Mapou says:

    It almost seems as if VJ Torley is turning Darwinist on us.

    Someone please correct me if I’m wrong.

  87. 87
    wd400 says:

    TJGuy

    THis is indeed the neutral theory of evolution — which is not a competitor with Darwinian evolution. The majority of fixed differences between human and chimps have not phenotypic consequence. That doesn’t mean other mutations where not fixed as a result of selection. There’s certainly no theory of evolution that ” posits that each change was a small step of progress which gives the organism enough of a benefit that it is selected for and becomes fixed in the population”.

  88. 88
    bFast says:

    Mapou, “It almost seems as if VJ Torley is turning Darwinist on us.”

    Actually, I think that VJ is following the evidence where it leads. Drift does explain some stuff. However, neither it nor natural selection explains stuff like: the HAR1F gene (discusses above by me) and functional orphan genes. As VJ said, “The changes in the human brain alone, over the past few million years, have been quite extraordinary.” If VJ ceases to find this to be incompatible with a naturalistic model, then I will be very intrigued to study his case. After all, I too am trying to follow the evidence where it leads.

  89. 89
    Andre says:

    Dr Torley

    I am only sceptical about the genetic drift claim because I cannot see how this happened with all the evolutionary conserved mechanisms in play preventing it from happening in the first place. These systems are highly regulated to boot.

    Again;

    Multiple integrity checks.
    Multiple repair mechanisms
    Multiple Apoptosis mechanisms
    Necrosis

    You know three guys just won the Nobel prize for science highlighting these exquisite systems. Without them being there from the start life would never even start. So until it can be shown how drift, NS & RM can somehow sneak past this to benefit or improve organisms I do not buy into the possibility. Checks and balances counter, protect and keep things in order. They don’t improve a system they keep a system as is. When the checks and balances and the repairs fail the system fails it never improves or recovers ever.

  90. 90
    vjtorley says:

    Hi Vy at #82,

    I had a quick look at the paper you referenced (“The waiting time problem in a model hominin population” by J. Sanford et al. in Theoretical Biology and Medical Modelling 2015, 12:18 doi:10.1186/s12976-015-0016-z) at http://www.tbiomed.com/content/12/1/18 . I notice that the paper makes use of a program called Mendel’s Accountant.

    Zachriel (who comments on UD from time to time) critiqued
    Mendel’s Accountant back in 2009 at http://www.antievolution.org/c.....ntry147439 .

    In a recent comment on the Skeptical Zone at http://theskepticalzone.com/wp.....ment-85371 , Zachriel recapitulated his problems with Mendel’s Accountant:

    We analyzed Mendel’s Accountant in 2009.

    The calculation of “working fitness” was broke. From Mendel’s Accountant (Fortran):

    do i=1,total_offspring
    work_fitness(i) = work_fitness(i)/(randomnum(1) + 1.d-15)
    end do

    We can test this by taking a series of fitnesses from 1.001 to 2 (Basic),

    For k = 1 To 1000
    Cells(k, “a”) = 1+ k / 1000
    Cells(k, “b”) = Cells(k, “a”) / Rnd
    Next k

    This is a typical result.

    9 Average
    31 St.Dev.
    362% Relative St.Dev.
    1.04 Min
    533 Max

    Note the min and max.

    ETA: both random functions return 0-1. Dividing by 0-1 is the same as multiplying by 1 to infinity.

    In a subsequent comment at http://theskepticalzone.com/wp.....ment-85497 , Zachriel added:

    Here’s the website. We had emailed the author in 2009, but never received a response. The current version still has the bug.
    http://mendelsaccount.sourceforge.net/

    Simple tests show that the program doesn’t comport with biological observations. The question we had was why it didn’t work.

    Working fitness is the result of random effects on adaptive fitness. However, the divide by zero-to-one function largely erases any signal from adaptive fitness. Nor is it a tunable parameter. This single line means that adaptive fitness is of negligible effect, which renders the entire program non-functional and meaningless. The claimed genetic meltdown is an artifact of bad programming.

    In order to replicate Mendel’s Accountant’s exciting achievement of overthrowing a century of evolutionary science, we created an alternative program, Gregor’s Bookkeeper (unpublished), which uses a tunable noise parameter to represent random effects, gamma distribution of beneficial to deleterious mutations, roulette wheel mating, dominant and recessive alleles, as well as drift in fecundity, population size, and mutation rate.

    In a subsequent comment at http://theskepticalzone.com/wp.....ment-85508 , he added:

    The recent Sanford et al. paper links to http://sourceforge.net/projects/mendelsaccount/, which indicates that the program is written in Fortran, Perl, and JavaScript. The download still includes the Fortran source code, with the bug. Perhaps it’s no longer being used. If so, do you have the actual working source code?

    If the bug was removed at some point, that should have been documented somewhere, and the original results thrown out. Even someone with a rudimentary knowledge of arithmetic can see why the division severely dilutes the signal from natural selection, meaning the program doesn’t even properly model simple cases that are easily observed in nature.

    I have no idea whether Zachriel’s complaints about Mendel’s Accountant are legitimate, as I lack the relevant background in biology. However, at the very least, I would say that arguments which are based on such a program are questionable.

  91. 91
    vjtorley says:

    Hi Andre.

    You wrote:

    You know three guys just won the Nobel prize for science highlighting these exquisite systems. Without them being there from the start life would never even start. So until it can be shown how drift, NS & RM can somehow sneak past this to benefit or improve organisms I do not buy into the possibility.

    I agree with you. I share your skepticism about the ability of any of these unguided mechanisms to generate complex structures in organisms.

  92. 92
    Vy says:

    As we never made that claim, or implied that claim, or held that view, your statement is false.

    As I never claimed that you held that view, your claim that I made such a claim is false. It seems you’re selectively blind as that’s the only explanation for why you’ve missed Except several times.

    This is the statement to which we objected. E. Coli didn’t choose. Rather, the results support random mutation.

    Again:

    Actually, you quoted a large text with two “claims” and objected to it so there is no “this is the one “.

    Evolution by natural selection is adaptation through modification of existing forms. See Darwin, Origin of
    Species, 1859.

    Ah, here we go with the bait-and-switch dancing with the terms.

    Microevolution is macroevolution on a small scale. No, it’s adaptation. No, adaptation is microevolution. No, it’s evolution. If you accept adaptation, you have to accept microevolution and evolution as a whole.

    That and a whole bunch of other nonsense word-plays that I’ve seen before. Evolution is basically unguided and blindly selected randomness with no purpose, adaptation isn’t.

    The fact that evolution is modelled around a bunch of valid phenomena (like adaptation and speciation) doesn’t make it any less absurd.

    That’s not the case.

    That is the case. That is why wild bacteria which have little use for citrate under aerobic conditions do not spontaneously mutate into citrate gobbling microbes.

    Citrate utilization evolved in the same medium that had been used for 30 thousand generations.

    Correction, e. coli gained the ability to use citrate under aerobic conditions after 31,500 generations.

    Genomic studies show that the trait evolved through potentiating mutations in a single lineage, then a tandem duplication, followed by optimizing mutations.

    And besides proving that others are better at finding the solution than others, what else?

    Trying to get 64 from Math.random() with two variables might look like it’s random but it isn’t. It might go over 1 – 63 and 65 – x over and over but it’ll eventually get to 64. The fact that it doesn’t get to it the first time or that the way it eventually arrives at 64 doesn’t prove anything was random or that that was the only way.

    Most lineages never developed the trait

    So???

    and the number of generations is consistent with random mutation.

    It’s consistent with goal-oriented trial and error.

    Mutations are not purely random. They have a number of causes and biases. However, they are random (uncorrelated) with respect to fitness.

    Right. That’s why e. coli forced to take citrate eventually did or others forced to be resistant to antibiotic X eventually became so.

    That’s why Cit+ took so long for the potentiating mutations to occur.

    An assumption based on the assumption that simply because other lineage failed to develop the trait, it must have been because of the blind selectiveness, randomness, and unguidedness of assumed evolutionary processes.

  93. 93
    Vy says:

    I have not failed. I’ve just found 10,000 ways that won’t work. – Thomas Edison

    There’s a way to do it better – find it. – Thomas Edison

  94. 94
    Vy says:

    Zachriel, why do your comments have legion-speak i.e. My name is Legion for we are many???

    You keep saying we are, we didn’t, we but last time I checked, you are one guy, not we guys.

    I could say you have DID but that’s an assumption.

  95. 95
    bornagain says:

    vjtorley, I usually think of you as being fair and unbiased, but in this instance I certainly do not think that you are being fair and unbiased.

    The list of references at the end of Sanford’s paper is fairly extensive and show that his results are indeed completely consistent with many other previous results. Yet you do not mention this fact but only list some technical critique, (from less than reputable atheistic websites no less), that you yourself said you were not qualified to judge, so as to support your apriori bias for common descent. With no mention of the extensive previous work.

    This is certainly NOT the same unbiased Dr. Torley that I have come to know through the years! But then again, come to think of it, I’ve noticed that when its common descent you do have a tendency to ‘turn a blind eye’ to any evidence that might falsify your semi-religious belief in it.

    For instance of your sin of ‘turning a blind eye’

    Britten RJ: Divergence between samples of chimpanzee and human DNA sequence is 5 % counting indels.
    Proc Natl Acad Sci U S A. 2002

    Haldane JBS: The cost of natural selection.
    J Genetics. 1957, 55:511-524.

    Kimura M: Evolutionary rate at the molecular level.
    Nature. 1968, 217:624-626.

    Bataillon T: Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations?
    Heredity. 2000, 84:497-501.

    Bataillon T, Bailey SF. Effects of new mutations on fitness: insights from models and data. doi:10.1111/nyas.12460 Ann N Y Acad Sci. 2014;1320:76–92.

    Elena SF, Ekunwe L, Hajela N, Oden SA, Lenski RE: Distribution of fitness effects caused by random insertion mutations in Escherichia coli.
    Genetica 1998, 102/103:349-358.

    Gerrish PJ, Lenski RE: The fate of competing beneficial mutations in an asexual population.
    Genetica 1998, 102/103:127-144.

    Montañez G, Marks R, Fernandez J, Sanford J: Multiple overlapping genetic codes profoundly reduce the probability of beneficial mutation. http://www.worldscientific.com.....08728_0006

    Sanford. Genetic Entropy. 4th ed. FMS Publications; 2014.

    Lynch M: Rate, molecular spectrum, and consequences of human mutation.
    Proc Natl Acad Sci U S A 2010, 107(3):961-968.

    Roach JC, Glusman G, Smit AFA, Huff CD, Hubley R, Shannon PT, et al.: 2010. Analysis of genetic inheritance in a family quartet by whole-genome sequencing.
    Science 2010, 328:636-9.

    Campbell CD, Eichler EE: Properties and rates of germline mutations in humans.
    Trends Genet. 2013, 29:575-584.

    Behe MJ, Snoke DW: Simulating evolution by gene duplication of protein features that require multiple amino acid residues.
    Protein Sci. 2004, 13:2651-2654.

    Behe MJ: The mathematical limits of Darwinism. In The Edge of Evolution. Edited by Behe MJ. Free Press, New York NY, USA; 2007:44-63.

    Lynch M: Simple evolutionary pathways to complex proteins.
    Protein Sci. 2005, 14:2217-2225.

    Durrett R, Schmidt D: Waiting for regulatory sequences to appear.
    The Annals of Applied Probability 2007, 17(1):1-32.

    Durrett R, Schmidt D: Waiting for two mutations: with applications to regulatory sequence evolution and the limits of Darwinian evolution.
    Genetics 2008, 180(3):1501-1509.

    Behe MJ: Waiting longer for two mutations.
    Genetics. 2009, 181:819-820. PubMed

    Durrett R, Schmidt D: Reply to Michael Behe.
    Genetics. 2009, 181:821-822.

    Axe DD: The case against a Darwinian origin of protein folds.
    BIO-Complexity. 2010, 1:1-12.

    Axe DD: The limits of complex adaptation: an analysis based on a simple model of structured bacterial populations.
    BIO-Complexity. 2010, 4:1-10

    Gauger A, Ebnet S, Fahey PF, Seelke R: Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness.
    BIO-Complexity. 2010, 2:1-9.

    Gauger A, Axe D: The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway.
    BIO-Complexity 2011, 1:1-17.

    Axe D, Gauger AK: Explaining metabolic innovation: neo-Darwinian versus design. In Biological Information – New Perspectives. Edited by Marks RJ II, Behe MJ, Dembski WA, Gordon BL, Sanford JC. World Scientific, London; 2013:489-507.

    Lynch M, Abegg A: The rate of establishment of complex adaptations.
    Mol Biol Evol 2010, 27(6):1404-1414.

    Reeves MA, Gauger AK, Axe DD: Enzyme families-shared evolutionary history or shared design? A study of the GABA-aminotransferase family.
    BIO-Complexity. 2014, 4:1-16.

    Sanford J, Baumgardner J, Brewer W, Gibson P, ReMine W. Mendel’s Accountant: a biologically realistic forward-time population genetics program. Scalable Computing: Practice and Experience. 2007;8(2):147–65..

    Sanford JC, Baumgardner J, Brewer W, Gibson P, ReMine W. Using computer simulation to understand mutation accumulation dynamics and genetic load. In: Shi Y, editor. ICCS 2007, Part II, LNCS 4488. Berlin, Heidelberg: Springer-Verlag; 2007. p. 386–92. http://bioinformatics.cau.edu......aproof.pdf.

    Sanford J, Nelson C. (2012). The Next Step in Understanding Population Dynamics: Comprehensive Numerical Simulation, Studies in Population Genetics, in: M. Carmen Fusté (Ed.), ISBN: 978-953-51-0588-6, OpenURL

    Sanford J, Baumgardner J, Brewer W: Selection Threshold Severely Constrains Capture of Beneficial Mutations.
    In Biological Information – New Perspectives Edited by Marks RJ II, Behe MJ, Dembski WA, Gordon BL, Sanford JC. World Scientific, London; 2013, 264-297.

    Brewer W, Baumgardner J, Sanford J: Biological Information – New Perspectives
    In Using Numerical Simulation to Test the “Mutation-Count” Hypothesis Edited by Marks RJ II, Behe MJ, Dembski WA, Gordon BL, Sanford JC. London, World Scientific; 2013, 298-311.
    http://www.worldscientific.com.....08728_0012

    Brewer W, Smith F, Sanford J: Information loss: potential for accelerating natural genetic attenuation of RNA viruses.
    In Biological Information – New Perspectives Edited by Marks RJ II, Behe MJ, Dembski WA, Gordon BL, Sanford JC. World Scientific, London; 2013, 369-384.

    Baumgardner J, Brewer W, Sanford J: Can Synergistic Epistasis Halt Mutation Accumulation? Results from Numerical Simulation
    In Biological Information – New Perspectives Edited by Marks RJ II, Behe MJ, Dembski WA, Gordon BL, Sanford JC. World Scientific, London; 2013, 312-337.

    Gibson P, Baumgardner J, Brewer W, Sanford J: Can Biological Information Be Sustained By Purifying Natural Selection?
    In Biological Information – New Perspectives Edited by Marks RJ II, Behe MJ, Dembski WA, Gordon BL, Sanford JC. World Scientific, London; 2013, 232-263.

    Eyre-Walker A, Keightley P: High genomic deleterious mutation rates in Hominids.
    Nature. 1999, 397:344-347. PubMed Abstract | Publisher Full Text OpenURL

    Behrens S, Vingron M Studying the evolution of promoter sequences: a waiting time problem. Journal of Computational Biology. 2010;17:1591-1606.

    Hughes AL. Evolution of adaptive phenotypic traits without positive Darwinian selection. Heredity. 2012;108:347–53.

    Marks II RJ, Behe MJ, Dembski WA, Gordon BL, Sanford JC, editors. Biological Information – New Perspectives. London: World Scientific; 2013. p. 1–563.

    Moreover, I note that you neglected many of the other substantial lines of evidence against your position that I listed above, (For instance body plans are NOT reducible to mutations to DNA, Meyer, Talbott, see posts 13 and 17 of this thread), as apparently both you, and neo-Darwinists, presuppose in your reasoning.

    I’m disappointed that you would display such an overt bias in your reasoning towards the neo-Darwinian position Dr. Torley and hope that you would return to the more balanced view that you usually employ, at least more balanced in matters not relating to this issue of common descent.

    Of supplemental note:

    Also see ‘Darwin’s Doubt’ for more thorough critique of the ‘central dogma’

  96. 96
    EugeneS says:

    Zachriel et al,

    Start from explaining the gene duplication mechanism via Darwinian evolution. Provide the details.

  97. 97
    bornagain says:

    in addition to posts 13 and 17, also see post 48 of this thread in regards to Body Plans not being reducible to DNA

  98. 98
    Dr JDD says:

    Unfortunately this is why I personally shied away from even considering the 70% claim as fact as this question raised by wd400 and others around the indels causing false low homology was not sufficiently answered before when we were discussing this. I searched vastly for an answer to the “gap” criteria in the blast programme and never found a straightforward explanation thus personally expected this to happen sooner or later.

    This highlights what we really must be careful of – not to allow what we want to be true to cloud our sound judgement of methodology. Ie something we can actually test rather than merely infer.

    Many years ago I personally deferred to the idea that chimp and human were actually much closer to 100% homology when first designed but deteriorated over time. I still would defer to that being plausible and what materialists never accept (which many pro-ID people have stated for a long time before and after Tompkins claim) is that homology is not evidence for common descent. Not evidence in the sense of persuasion. Why? Because it offers nothing over competing theories. Namely, everything we know about common design infers the reuse of design plans. Therefore if there was a common designer theeexpectation of such a theory is similar design plans.

    Secondly, what has been continually raised from time to time are the existing problems even with the % of homology as stated by evolutionists independent of people like Tompkins. Some of these have been raised here already. For example:

    – homology is only by comparison of aligned sequences (eg. The genome sizes are different, there are many genes are stretches that do not align at all that are not taken into consideration in homology assessments, etc)
    – junk apparently must adhere to the same rate of divergence yet the Y chromosome can happily be < 70% similar (as apparently it is not under selective pressure so it can diverge more but this is inconsistent with the previous argument)
    – the genomes were constructed assuming homology and gaps filled in based on common ancestry
    – the rate of germ line mutation is assumed from a small sample set and a single point in time (differs quite dramatically to model organisms used to study evolution)
    – the predicted "divergence time" from CA with chimps is based on aligned region divergence, not all the new information as well (novel genes, orfans, etc)
    – the homology is very high given the dramatic difference in phenotype between chimps and humans and this is not aligned with the differences observed between other non-human primates – suggesting DNA is not the main driver is phenotypic difference
    – recent discoveries in overlapping codes in DNA (multiple open reading frames within one gene even and overlapping) as well as differences in triplet codes for the same aa (redundant mutations) demonstrate that apparent redundancy may in fact be pseudo – redundancy and allow for greater genetic diversity. Thus an apparent neutral mutation has a net effect on the organism (alternative genes, difference in translation or transcription timings affecting gene or protein turn over thus the control, etc)
    – the fact that only ~50% of the human peptidome can be assigned to known and aligned ORFs / genes

    etc.
    These are all challenges for unguided UCD and I rarely see for any of these some rational, evidence led explanations for these. They are typically brushed aside as not a problem and insignificant but to anyone who is not biased to the paradigm that requires these issues to be minor, these are real unanswered challenges. And that with the assumption that homology between chimps and humans is ~96% (which id and even YECs are more than comfortable with).

  99. 99
    EugeneS says:

    Vy

    “Ah, here we go with the bait-and-switch dancing with the terms.”

    Although I haven’t followed your argument with Zachriel in this thread, that is exactly my personal experience having discussions with Zachriel. I strongly suspect that Zachriel is really a group of people posting comments of significantly varying level of error in them. E.g. sometimes their comments even demonstrate lack of common secondary school knowledge. That is my personal experience. I sympathise with you.

    Frankly, I think that spending time on Zachriel’s comments is not worth it. If I engage in a discussion with Zachriel, I mostly answer not to pursuade Zachriel, because I think this is impossible, but so that people capable of unbiased judgement without a hidden agenda can see my responses.

  100. 100
    bornagain says:

    Thanks at 98 Dr JDD, although I disagree with your ‘much closer to 100% homology’ hypothesis, I very much enjoyed your critique of the extremely biased way in which sequences are constructed with the assumption common descent being true.

    i.e. I’ve heard it called the ‘fit, DAMN YOU, FIT!!!’ method of science! 🙂

    For an instance of the extreme bias that goes into trying to artificially make the genomes seem much more similar than they actually are, Dr. Fazale Rana comments:

    DNA Comparisons between Humans and Chimps – Fazale Rana – 2010
    Excerpt: When performing the comparison, the researchers examined only about 2.4 billion base pairs, which represent around 75 to 80 percent of the genomes. As the authors note:
    “Best reciprocal nucleotide-level alignments of the chimpanzee and human genomes cover ~2.4 gigabases (Gb) of high-quality sequence, including 89 Mb from chromosome X and 7.5 Mb from chromosome Y.9”
    The reason for this limited comparison stems from the fact that they struggled to get a significant fraction of the genomes to align, in part, because of differences.
    A few months later, a team from the Max Planck Institute achieved a similar result when they compared over 10,000 regions (encompassing nearly 3,000,000 nucleotide base pairs). Only two-thirds of the sequences from the chimp genome aligned with the sequences in the human genome. As expected in those that did align, a 98.76 percent genetic similarity was measured—yet one-third found no matches.12
    It is interesting that when evolutionary biologists discuss genetic comparisons between human and chimpanzee genomes, the fact that, again, as much as 25 percent of the two genomes won’t align receives no mention. Instead, the focus is only on the portions of the genome that display a high-degree of similarity. This distorted emphasis makes the case for the evolutionary connection between humans and chimps seem more compelling than it may actually be.
    In many respects this discussion is moot, unless there is a clear understanding as to how the genetic differences between humans and chimpanzee translate into the biological (i.e. body plans) and (the) profound behavioral differences between these two species.
    http://www.reasons.org/dna-com.....del-part-2

  101. 101
    Virgil Cain says:

    wd400 @ 87:

    There’s certainly no theory of evolution…

    You got that right. 😉

  102. 102
    Dr JDD says:

    BA77 @100:

    I do not hold to that dogmatically nor do I believe it to be true. I believe it is a possibility that our DNA was once more similar than it is now but I would not subscribe to it being ever identical.

    I believe that everyone is essentially playing guessing games – on both sides of the discussion. The problem for materialists is greater though as they have had to limit their divergence with their estimated time-frames which works nicely when you consider the bits that align and you get a ball-park figure which you can shoe-horn the fossil record into with some bias, however as your link states and I and others have stated, the divergence is much greater than those ~60m bp differences. Perhaps at ~70 mutations per generation you can account for that but what you cannot also account for is the large bits that do not align, and are functional and not deleterious.

    And, everyone who is honest with themselves knows that the overwhelming majority of mutations are deleterious or have negative impact.

  103. 103
    Zachriel says:

    tjguy: I understand how these mutations could become fixed in the population, but not sure why it has to be through genetic drift.

    It’s a consequence of arithmetic. If a neutral mutation represents 0.01% of the population, there’s a 0.01% chance of fixation by chance alone. Also, the rate of fixation of new neutral mutation is equal to the rate of introduction of such mutations. Humans have an average of about 100-200 mutations per individual, most of which are neutral.

    tjguy: How does this qualify as Darwinian evolution?

    It’s usually considered non-Darwinian in the sense of not being to due evolution by natural selection. However, it is consistent with Darwin’s theory, and Darwin was aware of contingency in evolution.

    tjguy: And then the claim is what? That all these meaningless mutations got fixed thru whatever means and that they just happened to be the right mutations to enable a new function, gene, etc. to emerge?

    No. Adaptation still requires natural selection, but drift provides a vast repertoire of variations available for natural selection.

    bFast: However, neither it nor natural selection explains stuff like: the HAR1F gene (discusses above by me)

    Zachriel: Can you support this statement?

    bFast: No, I can’t.

    Zachriel: There are you are then.

    Andre: I am only sceptical about the genetic drift claim because I cannot see how this happened with all the evolutionary conserved mechanisms in play preventing it from happening in the first place.

    The average human has 100-200 mutations in their germ cells, far more in their somatic cells.

    vjtorley: I have no idea whether Zachriel’s complaints about Mendel’s Accountant are legitimate, as I lack the relevant background in biology.

    It’s more of a mathematical problem. The signal for natural selection is obscured by the division by a near zero factor.

    Vy: Microevolution is macroevolution on a small scale. No, it’s adaptation. No, adaptation is microevolution.

    That is incorrect. Adaptation is evolution resulting in phenotypic advantageous changes. This can occur on a microevolutionary scale or a macroevolutionary scale. Nor is all evolution adaptive.

    Vy: Evolution is basically unguided and blindly selected randomness with no purpose, adaptation isn’t.

    And yet we can show that mutations are random with respect to fitness, and that they can lead to adaptation.

    Vy: e. coli gained the ability to use citrate under aerobic conditions after 31,500 generations.

    Which contradicts your statement “eat citrate aerobically or die.” They couldn’t eat citrate for 30 thousand generations, but didn’t die. That’s because the Davis minimal broth had another resource, glucose. Citrate is only added as an chelating agent.
    http://myxo.css.msu.edu/ecoli/dm25liquid.html

    Vy: Math.random()

    Math.random is (pseudo) random.

    Vy: It’s consistent with goal-oriented trial and error.

    We can show mutations are random with respect to fitness. We can show that the bacteria simply try mutations randomly. If one works, great. You can say it’s goal-oriented, but there’s no evidence of that.

    Vy: That’s why e. coli forced to take citrate eventually did

    They weren’t forced to take citrate. The Cit+ strain lived in the same Davis minimal broth as its last 30 thousand ancestors had.

    Vy: An assumption based on the assumption that simply because other lineage failed to develop the trait, it must have been because of the blind selectiveness, randomness, and unguidedness of assumed evolutionary processes.

    No, the results are consistent with random mutation. It’s like claiming you were meant to roll a natural in Craps, when the house makes money every day on the odds.

    EugeneS: Start from explaining the gene duplication mechanism via Darwinian evolution.

    Mechanisms of gene duplication
    https://en.wikipedia.org/wiki/Gene_duplication#Mechanisms_of_duplication

  104. 104
    Vy says:

    I strongly suspect that Zachriel is really a group of people posting comments of significantly varying level of error in them.

    Exactly what I’ve been thinking.

    There’s an interesting prevalence of what I call legion-speakwe said … instead of I said …

  105. 105
    bornagain says:

    Of semi-related note to this issue of the hypothetical common descent of humans from some chimp-like ancestor, I would like to point out that this same overt bias that is found with Darwinists trying to force fit the genetic evidence into their preconceived bias of common descent, is also found in the fossil evidence.
    That is to say, although the discontinuity of the overall fossil record is fairly well accepted, (even among many leading evolutionists), when it comes to hypothetical human evolution, a severe bias in the handling of evidence becomes evident.

    Phillip Johnson comments on that overt bias by Darwinists here:

    “What I saw about the fossil record again,, was that Gould and Eldridge were experts in the area where the animal fossil record is most complete. That is marine invertebrates.,, And the reason for this is that when,, a bird, or a human, or an ape, or a wolf, or whatever, dies,, normally it does not get fossilized. It decays in the open, or is eaten by scavengers. Things get fossilized when they get covered over quickly with sediments so that they are protected from this natural destructive process. So if you want to be a fossil, the way to go about it is to live in the shallow seas, where you get covered over by sediments when you die,,. Most of the animal fossils are of that kind and it is in that area where the fossil record is most complete. That there is a consistent pattern.,, I mean there is evolution in the sense of variation, just like the peppered moth example. Things do vary, but they vary within the type. The new types appear suddenly, fully formed, without an evolutionary history and then they stay fundamentally stable with (cyclical) variation after their sudden appearance, and stasis (according) to the empirical observations made by Gould and Eldridge. Well now you see, I was aware of a number of examples of where evolutionary intermediates were cited. This was brought up as soon as people began to make the connection and question the (Darwinian) profession about their theory in light of the controversy. But the examples of claimed evolutionary transitionals, oddly enough, come from the area of the fossil record where fossilization is rarest. Where it is least likely to happen.,,,
    One of things that amused me is that there are so many fossil candidates for human ancestorship, and so very few fossils that are candidates for the great apes.,, There should be just as many. But why not? Any economist can give you the answer to that. Human ancestors have a great American value and so they are produced at a much greater rate.,,
    These also were grounds to be suspicious of what was going on,,,
    ,,,if the problem is the greatest where the fossil record is most complete and if the confirming examples are found where fossils are rarest, that doesn’t sound like it could be the explanation.”
    – Phillip Johnson – April 2012 – audio/video 15:05 minute mark to 19:15 minute mark
    http://www.youtube.com/watch?v.....age#t=903s

    O’ Leary comments on some of the many failed attempts by Darwinists to find the supposed ‘missing links’ for humans here:

    What Questions About Evolution Come Down to Is, “Who ARE We?” – Denyse O’Leary – August 18, 2014
    Excerpt: ,,, “human evolution” is now so integral to our culture that demand outpaces authenticity. The disappointing history of Sahelanthropus, Orrorin, and Ardi, all hailed in 2001 as human ancestors, attests to the frustrating search for “missing links.” Sediba, another supposed ancestor, fared no better in 2013. A science writer at Wired, not known for intelligent-design sympathies, derides the ceaseless buzz as “ancestor worship.”,,,
    “Flores Man” is an example. Supposedly, a new diminutive species of humans (discovered in 2004) arose, flourished, and died out from earlier than 18,000 years ago,,,
    The latest article I’m aware of charges that “Homo floresiensis” is an invalid species classification, and the principal skeleton may have been of a woman who suffered from a genetic disorder, Down syndrome.
    It hardly sounds like settled science to an observer.,,,
    ,,,Current humans have some Neanderthal genes and it is unclear that the group lived differently from the rest of ancient mankind. So any decisions about them are bound to be political or theological at this point.
    Commenting on a dispute over a supposed human ancestor, Smithsonian paleoanthropologist Richard Potts told the Wall Street Journal, “Evolution is wonderfully messy.” Few would dispute it, but a multitude of conflicting speculations does not add up to progress.
    http://www.evolutionnews.org/2.....89051.html

    Only a ‘true believer’ in common descent could find any comfort in such a failed track record to find supposed missing links for humans by Darwinists.

    Here are a few more notes that clearly establish the poverty of any real fossil evidence for the supposed common descent of humans from some hypothetical chimp-like creature:

    Human/Ape Common Ancestry: Following the Evidence – Casey Luskin – June 2011
    Excerpt: So the researchers constructed an evolutionary tree based on 129 skull and tooth measurements for living hominoids, including gorillas, chimpanzees, orangutans and humans, and did the same with 62 measurements recorded on Old World monkeys, including baboons, mangabeys and macaques. They also drew upon published molecular phylogenies. At the outset, Wood and Collard assumed the molecular evidence was correct. “There were so many different lines of genetic evidence pointing in one direction,” Collard explains. But no matter how the computer analysis was run, the molecular and morphological trees could not be made to match15 (see figure, below). Collard says this casts grave doubt on the reliability of using morphological evidence to determine the fine details of evolutionary trees for higher primates. “It is saying it is positively misleading,” he says. The abstract of the pair’s paper stated provocatively that “existing phylogenetic hypotheses about human evolution are unlikely to be reliable”.[10]
    http://www.evolutionnews.org/2.....nt-9266481

    Human Origins, and the Real Reasons for Evolutionary Skepticism – Jonathan M. – December 9, 2012
    Excerpt: “Cladistic analysis of cranial and dental evidence has been widely used to generate phylogenetic hypotheses about humans and their fossil relatives. However, the reliability of these hypotheses has never been subjected to external validation. To rectify this, we applied internal methods to equivalent evidence from two groups of extant higher primates for whom reliable molecular phylogenies are available, the hominoids and paionins. We found that the phylogenetic hypotheses based on the craniodental data were incompatible with the molecular phylogenies for the groups. Given the robustness of the molecular phylogenies, these results indicate that little confidence can be placed in phylogenies generated solely from higher primate craniodental evidence. The corollary of this is that existing phylogenetic hypotheses about human evolution are unlikely to be reliable.”
    http://www.evolutionnews.org/2.....67181.html

    No Known Hominin Is Common Ancestor of Neanderthals and Modern Humans, Study Suggests – Oct. 21, 2013
    Excerpt: The article, “No known hominin species matches the expected dental morphology of the last common ancestor of Neanderthals and modern humans,” relies on fossils of approximately 1,200 molars and premolars from 13 species or types of hominins — humans and human relatives and ancestors. Fossils from the well-known Atapuerca sites have a crucial role in this research, accounting for more than 15 percent of the complete studied fossil collection.,,,
    They conclude with high statistical confidence that none of the hominins usually proposed as a common ancestor, such as Homo heidelbergensis, H. erectus and H. antecessor, is a satisfactory match.
    “None of the species that have been previously suggested as the last common ancestor of Neanderthals and modern humans has a dental morphology that is fully compatible with the expected morphology of this ancestor,” Gómez-Robles said.
    http://www.sciencedaily.com/re.....153202.htm

    Skull “Rewrites” Story of Human Evolution — Again – Casey Luskin – October 22, 2013
    Excerpt: “There is a big gap in the fossil record,” Zollikofer told NBC News. “I would put a question mark there. Of course it would be nice to say this was the last common ancestor of Neanderthals and us, but we simply don’t know.” –
    http://www.evolutionnews.org/2.....78221.html

  106. 106
    EugeneS says:

    Zachriel again confuses the issue. I repeat, please provide a Darwinian mechanism for the hypothetical emergence of the gene duplication cell machinery. You don’t have to explain how it works.

    Again, explain in detail showing a plausible selectable path from “no gene duplication machinery” to “gene duplication machinery”.

    In your task, gene duplication is not a given but what is required.

  107. 107
    Zachriel says:

    EugeneS: I repeat, please provide a Darwinian mechanism for the hypothetical emergence of the gene duplication cell machinery.

    If there is replication, there is duplication. Evolution presupposes the existence of replication. You were interposing in a discussion of the evolution of aerobic citrate utilization in E. coli. As it is a discussion concerning evolution, it presupposes bacterial reproduction.

  108. 108
    Virgil Cain says:

    Zachriel:

    And yet we can show that mutations are random with respect to fitness, …

    OK we are waiting for such a demonstration.

  109. 109
    Virgil Cain says:

    Zachriel:

    It’s a consequence of arithmetic. If a neutral mutation represents 0.01% of the population, there’s a 0.01% chance of fixation by chance alone. Also, the rate of fixation of new neutral mutation is equal to the rate of introduction of such mutations.

    OK we are waiting for such a demonstration.

  110. 110
    Mapou says:

    I strongly suspect that Zachriel is really a group of people posting comments of significantly varying level of error in them.

    No. Zachriel is … [Deleted for privacy-related reasons]

  111. 111
    computerist says:

    DELETED for privacy-related reasons.

  112. 112
    daveS says:

    Are attempts at “outing” allowed here? Not a good idea, IMO.

  113. 113
    Virgil Cain says:

    It is also not a good idea to come here and posts lies, equivocations, misrepresentations and strawmen.

  114. 114
    Dr JDD says:

    So someone is a liar. Does that give us the right to stoop to the levels other people do and make it personal and bring out personal details and identities into it? Of course not – it doesn’t matter what they say or do, we should be above that.

    Deal with the lies and strawmen like a wise man – with wise words – not like a child does.

  115. 115
    Mapou says:

    Outing? Anybody who hides behind a pseudonym in order to spread lies is a gutless swine and should be outed, among other things.

  116. 116
    Mapou says:

    Dr. JDD:

    Does that give us the right to stoop

    The right? This is not about rights. It’s about the freedom to defend oneself against jackasses.

  117. 117
    Virgil Cain says:

    Deal with the lies and strawmen like a wise man – with wise words – not like a child does.

    You can only do that for so many years. Then it becomes the time to put a stop to it. Also Courts put people in jail for lying- are judges just children to you?

  118. 118
    JoeCoder says:

    @vjtorley and @zachriel

    Per comments 70 and 71 and since I’m a programmer I decided to take a look at the source code of Mendel’s Accountant. The code Zachriel refers to is in selection.f (Fortran version) and selection.c (C version). Both versions look like the same logic. Presuming the c version is newer and what’s being used (and because I know C), I took a look at that one. Starting on line 474 of selection.c, you can see there are three different modes of selection:

    Probability Selection (selection_scheme == 2)

    This is a selection mode deliberately designed to be mostly random. As the Mendel authors describe: “Under probability selection, the probability of an individual’s reproduction is directly proportional to that individual’s phenotypic fitness, such that even individuals with relatively low phenotypic fitness still have some likelihood of reproducing. It is generally understood that probability selection corresponds most closely to what occurs under natural circumstances.”

    This is the code Zachriel says “eliminates the vast majority of the signal from genetic or phylogenetic fitness”, but that’s also what it’s designed to do.

    Truncation Selection (selection_scheme == 3)

    This mode resembles artificial selection. The Mendel authors describe: “Probability selection contrasts strongly with truncation selection wherein there is no element of randomness. Under truncation selection, all individuals above a specific phenotypic value have a 100% probability of reproduction, while all individuals below that value have zero probability of reproduction… Such full truncation selection is almost never realized, even under the highly controlled conditions of artificial plant or animal breeding”

    Partial Truncation Selection (selection_scheme == 4)

    This is a blend between probability selection and truncation selection. Contrary to Zachriel’s statement “nor is it a tunable parameter,” this allows a parameter to specify the ratio.

    Zachriel, did you see these other modes when you looked at the Mendel source code?

    Which modes to the authors of Mendel’s accountant use in these simulations:

    1. In Using Computer Simulation to Understand Mutation, 2007, the Mendel authors used probability selection: “type of selection = probability” although the paper says all three modes were supported at that time.

    2. In Can Purifying Natural Selection Preserve Biological Information?, 2011, the authors used all three modes, but most of the runs were “partial truncation (unless otherwise specified)” with “partial truncation input parameter = 0.5”. They show declining fitness even with truncation selection. Note that this study used “no beneficial mutations” in order to specifically test natural selections preserving ability, since long linkage blocks cause a beneficial mutation will pick up deleterious hitchhikers on its way to fixation. Other papers on Mendel’s accountant have included beneficial mutations and still show decline.

    Finally, back in 2009 this person suggested Zachriel should plug his own randomization algorithm into Mendel to see what would happen. Zachriel, have you tried this? Given that we see fitness decline even under partial truncating selection (that uses reduced randomization), I doubt it could help?

  119. 119
    JoeCoder says:

    I also took a look at Zachriel’s own from-scratch simulation, Gregor’s Bookkeeper. It seems not to take linkage blocks into account at all, but assumes all genes are perfectly recombined every generation. That alone makes selection in the simulation far more efficient than any real mammal population. Second, it’s only simulating 20 genes. The population genetics being simulated are much closer to an RNA virus than anything like a human. To be fair, Mendel’s accountant also makes simplifying assumptions for the sake of simulation, but nothing that would remove it this far from reality.

    Zachriel I realize you’re trying to keep it simple for the sake of reproducability, but I think there’s good reason for Mendel’s complexity in simulating these items. Large genomes and long linkage blocks are the basis for why microbes evolve primarily through selection but evolution can do nothing better than drift in higher animals–the whole basis for neutral theory.

    Beyond that, I think both Mendel and Gregor are too generous in other matters:

    1. They assume all beneficial mutations sum together additively (Mendel) or multipicatively (Gregor) when many times you need two or more mutations to confer a selectable benefit.
    2. They assume beneficial mutations never interact negatively with one another.
    3. They track the total beneficial or deleterious effect of each allele, instead of individual mutations. This leads to situations where an allele with specific sequences may be largely replaced with random noise, but is seen by the simulation as equally fit because it has a few larger beneficial mutations still holding it up.

    It’s reasonable to omit these factors because would be difficult to simulate these accurately, but they make me think that even Mendel’s Accountant produces results better than the real world. Based on Mendel’s Accountant I am still convinced genetic entropy is an accurate understanding of real-world population genetics.

    In Gregor’s Bookkeeper, I’m also not clear what parameters are being used for the average effects of deleterious and beneficial mutations? Beneficial mutations happen at a rate of 0.00001 per beneficial, but is the average beneficial assumed to be as helpful as the average deleterious mutation is harmful? There are plenty of deleterious mutations that end in stillbirth, but few if any beneficial mutations that double reproductive fitness.

    Finally, I hope I haven’t made any mistakes in this my analysis here or the previous comment. It’s certainly possible and I am open to correction if so. Hoping we can all work together to find truth.

  120. 120
    JoeCoder says:

    @vjtorley

    Can you remove computerist’s comment at 111? I value my own anonymity and I am reluctant to participate on any forum where doxing is allowed and the same could happen to me.

  121. 121
    Mapou says:

    I, for one, believe that computerist’s comment at 111 should stay. It is a fair and legal comment.

  122. 122
    computerist says:

    I personally don’t mind if it’s deleted, so please go right ahead. The info was exposed on darwins-god.blogspot.com on several threads and it’s still up, found with a simple google search.

  123. 123
    JoeCoder says:

    To add to my comment at 118:

    In Mendel’s Accountant when partial truncating selection is used with a parameter of 0.5, the fitness of each individual will be divided by a random number between 0.5 and 1.0, before those with the lowest fitness are culled. This can be seen in selection.c line 529. The 2011 paper I linked above still shows declining fitness with this parameter.

  124. 124
    bornagain says:

    Thanks JoeCoder for the behind the scenes peek.

    Of related note is Behe’s work:

    Biological Information – Loss-of-Function Mutations by Paul Giem 2015 – video
    (Behe – Loss of function mutations are far more likely to fix in a population than gain of function mutations)
    https://www.youtube.com/watch?v=hzD3hhvepK8&index=20&list=PLHDSWJBW3DNUUhiC9VwPnhl-ymuObyTWJ

    Of off topic note, Paul Giem has a new video up:

    Miracles (Part 1) 10-17-2015 by Paul Giem – A look at Eric Metaxas’s best selling book ‘Miracles’ – video
    https://www.youtube.com/watch?v=VJCuOOmAczY

  125. 125
    bFast says:

    I’m with Joe Coder (120) Please remove comment 111. Individuals need to be in control of their level of anonymity.

  126. 126
    Mapou says:

    Everyone knows who I am (just click on my username). I believe that anonymity is a form of cowardice. A person should be ready to stand behind his or her words. If you’re afraid of something, just don’t comment until you can do something about the source of your fear.

  127. 127
    bFast says:

    JoeCoder et. el. This is a very fun thread. As a programmer myself, I will (if I find time) look into Mendel’s accountant.

    Zachriel, your link critiquing Mendel’s Accountant is interesting. You are suggesting a simple bug in the program. Please apply a simple fix, and demonstrate that the rest of the algorithm then works correctly.

    JoeCoder, “Zachriel I realize you’re trying to keep it simple for the sake of reproducability, but I think there’s good reason for Mendel’s complexity in simulating these items.”

    JC, I have seen this from Zachriel before — the theory that if it works in the small, it’ll work in the huge. This is a poor extrapolation. (Of course the entire theory of naturalistic evolution is one huge extrapolation.) I have often questioned whether there is enough signal in any positive mutation to overcome the noise of all of the other genes involved in the organism. Larry Moran suggests that Natural Selection will ignore “slightly beneficial” mutations. In the real world, in systems with 20,000 genes, and 100,000 kinds of proteins, how notable of a mutation is required for natural selection to promote reasonably ahead of drift?

  128. 128
    Zachriel says:

    JoeCoder: This is the code Zachriel says “eliminates the vast majority of the signal from genetic or phylogenetic fitness”, but that’s also what it’s designed to do.

    If it’s designed to do so, then it is not a bug, but a feature. Largely eliminating natural selection from the working fitness, then declaring natural selection to be impotent is not a valid argument.

    JoeCoder: To be fair, Mendel’s accountant also makes simplifying assumptions for the sake of simulation, but nothing that would remove it this far from reality.

    The main purpose of Gregor’s Bookkeeper was to use it as a scratchpad to determine why Mendel’s Accountant couldn’t simulate even simple instances of natural selection as observed in biological cases. However, we’ll take another look in light of your comments.

    bFast: I have often questioned whether there is enough signal in any positive mutation to overcome the noise of all of the other genes involved in the organism.

    We can can directly observe selection in nature and in the lab.

  129. 129
    computerist says:

    Mapou, I agree but also disagree. Many ID supporters have had their careers destroyed because an evomat Internet troll was hellbent on exposing their personal information, and in many cases contacting their employers demanding disciplinary action. This was revealed in the movie Expelled, but I believe it has also happened on this very forum and others. This also sort of happened to me at work, I work as a software developer and a staunch evomat systems administrator also the lead manager found out I was an ID supporter (not only from internal logs, ie: sites visited, but also from friendly conversations I had with him over my period), needless to say overtime it became a very hostile environment since I had to deal directly with this system admin with work related material and I decided it was best to simply quit. One thing is for sure, it will not happen in reverse, the evomats career is never in jeopardy. They may go around and spew chaos->order all day long, that cannot go under scrutiny. Thankfully, these days I run my own business in software.

  130. 130
    bornagain says:

    “We can can directly observe selection in nature and in the lab.”

    And the observations do not support evolution. Selection eliminates information or maybe maintains it. Selection certainly does not create information:

    “…but Natural Selection reduces genetic information and we know this from all the Genetic Population studies that we have…”
    Maciej Marian Giertych – Population Geneticist – member of the European Parliament – EXPELLED
    https://www.youtube.com/watch?v=6z5-15wk1Zk

    Genetic Mutations and the Theory of Evolution – Maciej Giertych, PhD – video
    https://www.youtube.com/watch?v=Za1nbINxdP8
    “Impact of Research on Race Formation and Mutations on the Theory of Evolution.” Biologist Maciej Giertych (who was interviewed in Ben Stein’s Expelled: No Intelligence Allowed) speaks on the various scientific problems with Darwinian evolution.

    “We found an enormous amount of diversity within and between the African populations, and we found much less diversity in non-African populations,” Tishkoff told attendees today (Jan. 22) at the annual meeting of the American Association for the Advancement of Science in Anaheim. “Only a small subset of the diversity in Africa is found in Europe and the Middle East, and an even narrower set is found in American Indians.”
    Tishkoff; Andrew Clark, Penn State; Kenneth Kidd, Yale University; Giovanni Destro-Bisol, University “La Sapienza,” Rome, and Himla Soodyall and Trefor Jenkins, WITS University, South Africa, looked at three locations on DNA samples from 13 to 18 populations in Africa and 30 to 45 populations in the remainder of the world.-

    New analysis provides fuller picture of human expansion from Africa – October 22, 2012
    Excerpt: A new, comprehensive review of humans’ anthropological and genetic records gives the most up-to-date story of the “Out of Africa” expansion that occurred about 45,000 to 60,000 years ago.
    This expansion, detailed by three Stanford geneticists, had a dramatic effect on human genetic diversity, which persists in present-day populations. As a small group of modern humans migrated out of Africa into Eurasia and the Americas, their genetic diversity was substantially reduced.
    http://phys.org/news/2012-10-a.....nsion.html

    Moreover, there is a rarely mentioned pattern of degradation that is found in the younger human fossils, where the fossil record is clearest to read:

    Are brains shrinking to make us smarter? – February 2011
    Excerpt: Human brains have shrunk over the past 30,000 years,
    http://www.physorg.com/news/20.....arter.html

    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/20.....-shrinking

    The same pattern of deterioration is found in the genetic evidence

    Human Genetic Variation Recent, Varies Among Populations – (Nov. 28, 2012)
    Excerpt: Nearly three-quarters of mutations in genes that code for proteins — the workhorses of the cell — occurred within the past 5,000 to 10,000 years,,,
    “One of the most interesting points is that Europeans have more new deleterious (potentially disease-causing) mutations than Africans,”,,,
    “Having so many of these new variants can be partially explained by the population explosion in the European population. However, variation that occur in genes that are involved in Mendelian traits and in those that affect genes essential to the proper functioning of the cell tend to be much older.” (A Mendelian trait is controlled by a single gene. Mutations in that gene can have devastating effects.) The amount variation or mutation identified in protein-coding genes (the exome) in this study is very different from what would have been seen 5,000 years ago,,,
    The report shows that “recent” events have a potent effect on the human genome. Eighty-six percent of the genetic variation or mutations that are expected to be harmful arose in European-Americans in the last five thousand years, said the researchers.
    The researchers used established bioinformatics techniques to calculate the age of more than a million changes in single base pairs (the A-T, C-G of the genetic code) that are part of the exome or protein-coding portion of the genomes (human genetic blueprint) of 6,515 people of both European-American and African-American decent.,,,
    http://www.sciencedaily.com/re.....132259.htm

    Human Genome in Meltdown – January 11, 2013
    Excerpt: According to a study published Jan. 10 in Nature by geneticists from 4 universities including Harvard, “Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants.”,,,:
    “We estimate that approximately 73% of all protein-coding SNVs [single-nucleotide variants] and approximately 86% of SNVs predicted to be deleterious arose in the past 5,000 -10,000 years. The average age of deleterious SNVs varied significantly across molecular pathways, and disease genes contained a significantly higher proportion of recently arisen deleterious SNVs than other genes.”,,,
    As for advantageous mutations, they provided NO examples,,,
    http://crev.info/2013/01/human-genome-in-meltdown/

  131. 131
    Mapou says:

    Computerist,

    The way I see it, a man does what he has to do. However, when someone accuses you of “stooping” to some lower level for unmasking the liars, it is like accusing David of acting like a Philistine after he just chopped off the head of that jackass, Goliath.

  132. 132
    Vy says:

    That is incorrect. Adaptation is evolution resulting in phenotypic advantageous changes.

    You’ve certainly outdone yourself there. Pure equivocated nonsense.

    Adaptation, a pre-Darwinian (and I’m talking pre-grandpa Darwin) mechanism, is a valid readily observable phenomenon, evolution is an unobservable, blindly selective randomness surviving off equivocations.

    With that I say, carry on.

    This can occur on a microevolutionary scale or a macroevolutionary scale. Nor is all evolution adaptive.

    So this is the kind of stuff you have to believe to settle the effect of the mental gymnastics going on in your brain(s) to during such equivocations, eh? Awesome. And some might wonder why I say evodelusion, sheesh!

    Next, I’m gonna hear stasis, speciation, variation etc. are all evolution or evolutionary mumbo jumbo.

    And yet we can show that mutations are random with respect to fitness, and that they can lead to adaptation.

    Are you listening to yourself (or is that “selves”)?

    Adaptation can be demonstrated, blindly selective randomness cannot. The only way the latter can be demonstrated is via deluding one’s self into believing there’s any validity in equivocating evolution and adaptation, something you’ve shown yourself to be immensely capable of.

    Which contradicts your statement “eat citrate aerobically or die.” They couldn’t eat citrate for 30 thousand generations, but didn’t die. That’s because the Davis minimal broth had another resource, glucose. Citrate is only added as an chelating agent.

    For a guy that talks like a multitude, you are pretty blind:

    Lenski started off with a single microbe. It divided a few times into identical clones, from which Lenski started 12 colonies. He kept each of these 12 lines in its own flask. Each day he and his colleagues provided the bacteria with a little glucose, which was gobbled up by the afternoon. The next morning, the scientists took a small sample from each flask and put it in a new one with fresh glucose. And on and on and on, for 20 years and running.

    Lenski and his colleagues have also shown how natural selection has demanded trade-offs from the bacteria; while they grow faster on a meager diet of glucose,they’ve gotten worse at feeding on some other kinds of sugars.

    I wish I could say I hope it’s clear enough for you now but considering it’s become pretty obvious that you’re selectively blind, no such luck.

    Math.random is (pseudo) random.

    Yup, much like the mutations observed in these kind of experiments.

    We can show mutations are random with respect to fitness. We can show that the bacteria simply try mutations randomly.

    Correction: pseudorandomly. They don’t spontaneously try mutating for no reason due to nothing.

    It’s not like the bacteria are reading from a “How To Go From Anaerobic Citrate Gobbler to An Aerobic Citrate Gobbler For Dummies” manual.

    If one works, great.

    And my some naturamagic, they almost always find one that works (where almost is simply being benefit of the doubt). Whudda thunk it?

    You can say it’s goal-oriented, but there’s no evidence of that.

    Really?

    – Did they or did they not have a perfectly working mechanism to use citrate albeit under anaerobic conditions?
    – Were they or were they not put in a medium that had little glucose and more citrate?
    – Did they or did they not initially become very efficient in using glucose as an energy thus temporarily increasing their survival rate?
    – Did they or did they not finish up the glucose before the next day leaving them starving in the presence of something they could very well use if not for one variable for several hours before the next “lunch break”?
    – Did they or did they not gain the ability to transport citrate under anaerobic conditions by breaking a switch responsible for repressing the expression of citT under aerobic conditions?

    They weren’t forced to take citrate. The Cit+ strain lived in the same Davis minimal broth as its last 30 thousand ancestors had.

    Already dealt with though I doubt it’ll take.

    No, the results are consistent with random mutation.

    It’s very consistent with goal-oriented trial and error.

    It’s like claiming you were meant to roll a natural in Craps, when the house makes money every day on the odds.

    I haven’t got the slightest idea what “Craps” is although I think that it relates to gambling based on the “roll” part which I have 0 experience with.

  133. 133
    Vy says:

    Evolution presupposes the existence of replication.

    Naturalistic “popping up” of replication? Absolutely.

    Evidence for such? None.

    And that’s not the only thing this mutant theory presupposes.

  134. 134
    Vy says:

    And the observations do not support evolution. Selection eliminates information or maybe maintains it. Selection certainly does not create information.

    You’d think the name, “selection”, would be self-explanatory but it’s pretty clear he’s managed to convince himself everything and anything supports evolution.

    That is pretty much the norm with people like him.

  135. 135
    Box says:

    “…but Natural Selection reduces genetic information and we know this from all the Genetic Population studies that we have…”
    Maciej Marian Giertych

    Vy: You’d think the name, “selection”, would be self-explanatory but it’s pretty clear he’s managed to convince himself everything and anything supports evolution.

    “Colin Patterson’s description highlights something very easily overlooked—the fact that natural selection is not creative. As he says, it is a ‘weeding out process’ that leaves the stronger progeny. The stronger progeny must be already there: it is not produced by natural selection. Indeed the very word ‘selection’ ought to alert our attention to this: selection is made from already existing entities. This is an exceedingly important point because the words ‘natural selection’ are often used as if they were describing a creative process, for instance, by capitalizing their initial letters. This is highly misleading (…)”

    [John C. Lennox, ‘God’s Undertaker: Has Science Buried God?’, p.102]

  136. 136
    JoeCoder says:

    Zachriel wrote:

    Largely eliminating natural selection from the working fitness, then declaring natural selection to be impotent is not a valid argument.

    Take a look at figures 6.1B and 6.2B from the original Mendel’s Accountant paper in 2007. In 6.1B, the population recovers and increases in fitness once new mutations stop arriving. In 6.2B, the fitness declines with a population bottleneck and then recovers again afterward. If natural selection was largely ignored I do not think there would be a recovery in either graph. Both cases use the probability selection mode, which is the most random.

    I also tried Mendel’s Accountant myself with these parameters:

    Starting pop = 1000
    Mutation rate = 0
    Selection = Unrestricted Probability Selection

    I then set the starting population so that 25 individuals had alleles that gave them -10% fitness. Here are the results: http://i.imgur.com/xMluHMk.png

    Over time you can see that even with Unrestricted Probability Selection, all the deleterious alleles were removed from the population.

    I then tried another simulation to model beneficial allele fixation with similar parameters:

    Starting pop = 2000
    Mutation rate = 0
    Selection = Unrestricted Probability Selection

    I seeded the population with five individuals each having an allele that gives them a 10% fitness bonus. Here are the results, two of those five alleles fixed across the entire population: http://i.imgur.com/OSHQEOe.png

    Based on your math I thought that using Unrestricted Probability Selection would indeed “Largely eliminate natural selection from the working fitness” but it seems otherwise. Please check me on this.

  137. 137
    Dr JDD says:

    Mapou: I’m not sure how you can compare discussions on an Internet forum to a nation facing extermination and that nation being God’s chosen nation to dwell in the land He had for them. You like to quote the OT a lot yet seemingly ignore the wealth of personal examples and commandments written in the NT such as Jesus pronouncing forgiveness on the greatest liars of the day as they crucified Him and the fact He said we would be known for our love. Now I have no problem with calling out people’s lies and motives but it adds nothing to an argument or discussion (which this is) to start getting personal and creating an environment where someone could infiltrate and disrupt one’s personal life off this discussion board. Many people here have had that happen to them and it is not pleasant but that does not justify us doing it back.

    Secondly, the majority of ID supporters that firm this board desire to see ID supported as mainstream science. To do that requires actual Biologists on board and pro-ID. In biology such a view is mocked, looked down on, and unless you have tenure pretty much is career suicide. Quite frankly until there are enough people together who don’t have to stand as individuals people are not going to speak up unless they are directly asked and even then many fear the ramifications. You are transparent with who you are but I doubt in your career that you have this worry to the same degree a biologist does. Quite frankly if a biologist came on to read this thread and saw such behaviour where people link to personal info about posters here they would run for miles. I am a biologist and it is one of the biggest things that puts me off this site, not that I add much myself, but this is going to put off people who would be very valuable to ID.

    Finally such behaviour quite frankly puts off people in general – why would they want to participate in a place where if you disagree someone goes on a hunt for your personal info and plasters it over a public board for all to see?

    So yes, I stand by the word “stoop” as this “outing” to me does nothing to add to the argument and is a bit immature in the grand scheme of things quite frankly. Sadly, if this is what UD thinks is acceptable it’s not a place I would want to associate with personally for much longer.

  138. 138
    Zachriel says:

    Vy: Adaptation, a pre-Darwinian (and I’m talking pre-grandpa Darwin) mechanism, is a valid readily observable phenomenon,

    Yes, the word adaptation predates Darwin, and meant modification of something to a new condition.

    Vy: evolution is an unobservable, blindly selective randomness surviving off equivocations.

    Actually, we can directly observe how random mutations lead to evolutionary (heritable) adaptation.

    Vy: So this is the kind of stuff you have to believe to settle the effect of the mental gymnastics going on in your brain(s) to during such equivocations, eh?

    It’s not equivocation. Not all evolution is adaptive, and adaptation can occur on both microevolutionary and macroevolutionary scales.

    Vy: Adaptation can be demonstrated, blindly selective randomness cannot.

    That is incorrect. It has been shown that mutations leading to adaptation are random with respect to fitness. See Lederberg & Lederberg, Replica Plating and Indirect Selection of Bacterial Mutants, Journal of Bacteriology 1952.

    Vy: Lenski and his colleagues have also shown how natural selection has demanded trade-offs from the bacteria; while they grow faster on a meager diet of glucose,they’ve gotten worse at feeding on some other kinds of sugars.

    So you cite a study that says that natural selection resulted in adaptation to a glucose-rich environment. Glad you agree.

    Vy: They don’t spontaneously try mutating for no reason due to nothing.

    Actually, it has been shown that the mutations occur regardless of any benefit to the organism. See Lederberg & Lederberg, Replica Plating and Indirect Selection of Bacterial Mutants, Journal of Bacteriology 1952.

    Vy: And my some naturamagic, they almost always find one that works (where almost is simply being benefit of the doubt).

    The Lenski experiments shows that only some lineages found the pathway to Cit+, and that the chance of finding that pathway was consistent with mutation random with respect to fitness.

    Vy: – Did they or did they not gain the ability to transport citrate under anaerobic conditions by breaking a switch responsible for repressing the expression of citT under aerobic conditions?

    No. Cit+ was due to a novel pathway when a gene which had already been mutated was duplicated and put under the control of another regulator. Nothing was broken.

    Box: but Natural Selection reduces genetic information and we know this from all the Genetic Population studies that we have

    That’s correct. Natural selection tends to reduce genetic diversity. Mutation generally increases genetic diversity.
    http://www.adonline.id.au/plan.....raph-1.png

    JoeCoder: Based on your math I thought that using Unrestricted Probability Selection would indeed “Largely eliminate natural selection from the working fitness” but it seems otherwise.

    The key word there is “largely”. It does not completely eliminate selection, just dilutes it in a very odd manner. Dividing by a random number from 0-1 has no biological counterpart.

    It’s been several years, however. We’ll take another look at some point.

  139. 139
    Virgil Cain says:

    Actually, we can directly observe how random mutations lead to evolutionary (heritable) adaptation.

    Actually that is a lie.

    It has been shown that mutations leading to adaptation are random with respect to fitness. See Lederberg & Lederberg, Replica Plating and Indirect Selection of Bacterial Mutants, Journal of Bacteriology 1952.

    That study did not show that mutations are random with respect to fitness. It showed that the variation that allowed for fitness in the presence of anti-biotics was already present.

    The Lenski experiments shows that only some lineages found the pathway to Cit+, and that the chance of finding that pathway was consistent with mutation random with respect to fitness.

    Only ignorance can make such a determination.

    Natural selection tends to reduce genetic diversity. Mutation generally increases genetic diversity.

    Natural selection includes mutation.

  140. 140
    Vy says:

    So Zach prefers babbling the same things over and over again rather than answering the questions, great!

    It’s not equivocation. Not all evolution is adaptive, and adaptation can occur on both microevolutionary and macroevolutionary scales.

    Still as nonsensical a statement as it was the first time but enjoy the gymnastics. 😀

    So you cite a study that says that natural selection resulted in adaptation to a glucose-rich environment.

    Your selective blindness is your undoing. Prior to your out-of-context quote:

    Each day he and his colleagues provided the bacteria with a little glucose, which was gobbled up by the afternoon. The next morning, the scientists took a small sample from each flask and put it in a new one with fresh glucose. And on and on and on, for 20 years and running.

    Even a child can see that reality contradicts your “adaptation to a glucose-rich environment” assertion.

    And here are the questions you oh so blindly missed:

    – Did they or did they not have a perfectly working mechanism to use citrate albeit under anaerobic conditions?
    – Were they or were they not put in a medium that had little glucose and more citrate?
    – Did they or did they not initially become very efficient in using glucose as an energy thus temporarily increasing their survival rate?
    – Did they or did they not finish up the glucose before the next day leaving them starving in the presence of something they could very well use if not for one variable for several hours before the next “lunch break”?

    __

    No. Cit+ was due to a novel pathway when a gene which had already been mutated was duplicated and put under the control of another regulator. Nothing was broken.

    Damn! You gotta do something about those eyes!

    But a mutation in the citrate-eaters allowed them to make an “antiporter” protein, CitT, that allows citrate to cross the membrane and enter the cell. The gene for this protein already existed, but it’s usually switched off when oxygen is present.

    What really happened? A switch that normally represses expression of CitT under oxic conditions was broken, so the citrate-uptake pathway got turned on. This isn’t the evolution of a new molecular feature. It’s the breaking of a molecular feature — a repressor switch.

    The only “novel pathway” is the one in your imagination.

  141. 141
    Virgil Cain says:

    It is so awesome having other people see Zachriel for what it is- an insipid troll.

  142. 142
    Vy says:

    As for your allusions to the fact that because antibiotic resistant bacteria exist, it somehow puts your absurd assumptions on solid ground, please, you gotta let reality in once in a while.

    @Virgil: A massive seemingly D.I.Ded troll!

  143. 143
    Zachriel says:

    Vy: Still as nonsensical a statement as it was the first time but enjoy the gymnastics.

    Your inability to understand doesn’t make the statement nonsensical. More simply, while evolutionary adaptation is a subset of evolution, not all evolution is adaptation.

    Vy: that reality contradicts your “adaptation to a glucose-rich environment” assertion.

    “while they grow faster on a meager diet of glucose, they’ve gotten worse at feeding on some other kinds of sugars.”

    In other words, they adapted to the glucose environment, but lacking in other sugars (except citrate, which was added as an chelating agent).

    Vy: – Did they or did they not have a perfectly working mechanism to use citrate albeit under anaerobic conditions?

    Only in anaerobic conditions, yes.

    Vy: – Were they or were they not put in a medium that had little glucose and more citrate?

    The broth had glucose, as well as citrate added as a chelating agent.

    Vy: – Did they or did they not initially become very efficient in using glucose as an energy thus temporarily increasing their survival rate?

    Yes, per the researchers, they evolved to adapt to the laboratory conditions.

    Vy: – Did they or did they not finish up the glucose before the next day leaving them starving in the presence of something they could very well use if not for one variable for several hours before the next “lunch break”?

    Yes, it’s typical to allow the bacteria to fill the flask before cloning it.

    Vy: A switch that normally represses expression of CitT under oxic conditions was broken, so the citrate-uptake pathway got turned on. This isn’t the evolution of a new molecular feature. It’s the breaking of a molecular feature — a repressor switch.

    That’s not what happened. That’s what Behe and other ID proponents had supposed before the genomic analysis had been completed.

    Rather, a new “switch” was created. This required potentiating mutations and a duplication, then this was followed by optimizing mutations.

    Vy: The only “novel pathway” is the one in your imagination.

    Blount, Genomic analysis of a key innovation in an experimental Escherichia coli population, Nature 2012: “Our findings highlight the less-appreciated capacity of duplications to produce new functions by promoter capture events that change gene regulatory networks.”

    Vy: please, you gotta let reality in once in a while.

    Antibiotics, and therefore antibiotic resistance, occur in nature, and probably have for billions of years. Indeed, the first antibiotic was discovered in mold.

  144. 144
    Mapou says:

    JDD:

    So yes, I stand by the word “stoop” as this “outing” to me does nothing to add to the argument and is a bit immature in the grand scheme of things quite frankly. Sadly, if this is what UD thinks is acceptable it’s not a place I would want to associate with personally for much longer.

    I don’t care. You got your opinion and I got mine. People like Zachriel are not here to discuss or argue anything. The jackass is a dishonest troll. He’s here to bog us down in interminable and worthless debates when we should be working on expanding ID in order to come up with serious scientific predictions. If this site belonged to me, I would have kicked his arse off this forum a long time ago, along with his buddies. Heck I would not even allow people like Larry Moran to comment here. Know thine enemy.

  145. 145
    Dr JDD says:

    Mapou:

    Free will is a beautiful thing and we are all entitled to our opinion and we have each stated ours, so that is that. I’m not one to argue simply for the sake of it. I just sincerely hope certain behaviours (trolls or not) do not put off the type of crowd that UD wishes to draw.

    Best Wishes.

  146. 146
    Upright BiPed says:

    Moderators, comments #110 and #111 need to be removed from this thread.

  147. 147
    Vy says:

    Your inability to understand doesn’t make the statement nonsensical.

    Your illusory view that the statement is not nonsensical doesn’t make it so*.

    More simply, while evolutionary adaptation is a subset of evolution, not all evolution is adaptation.

    * – this being a case-in-point.

    The fact that you’ve successfully deceived yourself into believing that simply because evodelusionists have taken up adaptation as an evolutionary mechanism, it makes it one doesn’t affect reality.

    .. .they adapted to the glucose environment, but lacking in other sugars (except citrate, which was added as an chelating agent).

    They adapted to the glucose-deficient environment they were kept to get the most out or the little glucose they had till the next “lunch-break”.

    Only in anaerobic conditions, yes

    Redundant. A simple yes would’ve sufficed.

    The broth had glucose, as well as citrate added as a chelating agent.

    Not what I asked. Read before you respond.

    Yes, per the researchers, they evolved to adapt to the laboratory conditions

    False, they adapted, nothing evolves to do anything despite your assumptions in the other thread that evolution is purposeful and has goals.

    Yes, it’s typical to allow the bacteria to fill the flask before cloning it.

    What? That is not what I asked.
    Are you talking to an imaginary image in front of you?

    That’s what Behe and other ID proponents had supposed before the genomic analysis had been completed.

    Whoops, sorry. You’ve used so many numbers I taught you understood math. Is 2015 later or earlier than 2012?

    Rather, a new “switch” was created.

    Truth from constantly repeated lies, carry on. In reality-ville, Blount says:

    One possibility is that the Cit+ lineage activated a ‘cryptic’ [preexisting but dormant] transporter, that is, some once-functional gene that has been silenced by mutation accumulation …

    2. A more likely possibility, in our view, is that an existing transporter has been coopted for citrate transport under oxic conditions. This transporter may previously have transported citrate under anoxic conditions or, alternatively, it may have transported another substrate in the presence of oxygen. …

    Neither of those involve the creation of anything, in fact, it’s quite the opposite as already explained in the ENV article.

    More from Anderson and Purdom:

    Each of these mutant strains has an antagonistic pleiotropy characteristic. An existing system is traded for an altered phenotype that is better suited to survive the specific stressful environment. Regulation is reduced to enable overexpression. DNA repair and DNA polymerase fidelity are reduced to enable increased mutation rates (increasing the probability of a “beneficial” mutation). A gene is inactivated by a process that concurrently activates a silent gene. Such trade-offs provide a temporary benefit to the bacterium, increasing its chances of surviving specific starvation conditions. However, these mutations do not account for the origin of the silenced genes, as their prior existence is essential for the mutation to be beneficial.

    So far, you have been unable to understand simple English and answer simple questions directly. Do you need me to dumb it down with crayons and shiny graphics so that your selective blindness, mental gymnastics and delusions will be reduced to a fairer minimum?

  148. 148
    Mapou says:

    Does anybody know who Upright BiPed is? LOL.

  149. 149
    Zachriel says:

    Vy: The fact that you’ve successfully deceived yourself into believing that simply because evodelusionists have taken up adaptation as an evolutionary mechanism, it makes it one doesn’t affect reality.

    We can directly observe evolutionary adaptation.

    Zachriel: Yes, per the researchers, they evolved to adapt to the laboratory conditions

    Vy: False, they adapted

    Maybe the title of the project is a clue to the researchers’ thinking: E. coli long-term evolution experiment. See Blount et al., Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli, PNAS 2008: “All twelve populations underwent rapid improvement in fitness that decelerated over time. All evolved higher maximum growth rates on glucose, shorter lag phases upon transfer into fresh medium, reduced peak population densities, and larger average cell sizes relative to their ancestor.” It’s clear that, per the researchers, they evolved to adapt to the laboratory conditions.

    Vy: Neither of those involve the creation of anything

    Your claim was that Cit+ was due to the “breaking of a molecular feature — a repressor switch”. Instead, it was cooption of an existing transporter. That the new trait evolved by modification of an existing system is exactly how evolution is posited to work.

  150. 150
    EugeneS says:

    Zachriel,

    “If there is replication, there is duplication.”

    What I mean by a working gene duplication machinery is specific protein-protein interactions achieving controlled gene duplication such that one copy is there for integrity, the other is for alleged unguided exploration of the search space. How did a protein machinery that achieves no less than that function ever appear?

    Show in detail how you think such a system arose.

  151. 151
    EugeneS says:

    Zachriel,

    “We can directly observe evolutionary adaptation.”

    We can directly observe effects of adaptation. Whether it is evolutionary (e.g. Darwinian) or pre-programmed is open for discussion. No evolution is capable of producing a program together with a processor taking the program as input.

  152. 152
    Zachriel says:

    EugeneS: We can directly observe effects of adaptation. Whether it is evolutionary (e.g. Darwinian) or pre-programmed is open for discussion.

    Evolution refers to hereditary changes. In the case of many adaptations, we can show they are random with respect to fitness.

  153. 153
    Virgil Cain says:

    In the case of many adaptations, we can show they are random with respect to fitness.

    So something that aids fitness is random with respect to it? Really?

  154. 154
    Vy says:

    We can directly observe evolutionary adaptation.

    In your daydreams? Absolutely.
    In reality? We observe adaptation and evodelusionary twisting of adaptation, like all your comments on the issue.

    Maybe the title of the project is a clue to the researchers’ thinking

    Oh yes, I’m fully aware of the fact that they happen to be evodelusionists like you but that doesn’t affect reality.

    Just because I see a madman on TV because of a sloppily positioned video camera saying madmen matchsticks ignite when you strike them” doesn’t mean I should believe the nonsense. No way, I take the “non-“, “madmen” in this case, and keep the sense, which is the rest of the statement. It’s easy.

    Instead, it was cooption of an existing transporter. That the new trait evolved by modification of an existing system

    Again:

    More from Anderson and Purdom:

    Each of these mutant strains has an antagonistic pleiotropy characteristic. An existing system is traded for an altered phenotype that is better suited to survive the specific stressful environment. Regulation is reduced to enable overexpression. DNA repair and DNA polymerase fidelity are reduced to enable increased mutation rates (increasing the probability of a “beneficial” mutation). A gene is inactivated by a process that concurrently activates a silent gene. Such trade-offs provide a temporary benefit to the bacterium, increasing its chances of surviving specific starvation conditions. However, these mutations do not account for the origin of the silenced genes, as their prior existence is essential for the mutation to be beneficial.

    Sheesh!

    is exactly how evolution is posited to work.

    Correction: That’s how adaptation works. The evolution part is more twisting.

  155. 155
    Vy says:

    We can directly observe evolutionary adaptation.

    In your daydreams? Absolutely.
    In reality? We observe adaptation and evodelusionary twisting of adaptation, like all your comments on the issue.

    Maybe the title of the project is a clue to the researchers’ thinking

    Oh yes, I’m fully aware of the fact that they happen to be evodelusionists like you but that doesn’t affect reality.

    Just because I see a madman on TV because of a sloppily positioned video camera saying madmen matchsticks ignite when you strike them” doesn’t mean I should believe the nonsense. No way, I take the “non-“, “madmen” in this case, and keep the” sense”, which is the rest of the statement. It’s easy.

    Instead, it was cooption of an existing transporter. That the new trait evolved by modification of an existing system

    Again:

    More from Anderson and Purdom:

    Each of these mutant strains has an antagonistic pleiotropy characteristic. An existing system is traded for an altered phenotype that is better suited to survive the specific stressful environment. Regulation is reduced to enable overexpression. DNA repair and DNA polymerase fidelity are reduced to enable increased mutation rates (increasing the probability of a “beneficial” mutation). A gene is inactivated by a process that concurrently activates a silent gene. Such trade-offs provide a temporary benefit to the bacterium, increasing its chances of surviving specific starvation conditions. However, these mutations do not account for the origin of the silenced genes, as their prior existence is essential for the mutation to be beneficial.

    Sheesh!

    is exactly how evolution is posited to work.

    Correction: That’s how adaptation works. The evolution part is more twisting.

  156. 156
    computerist says:

    Dr JDD, you said:

    Finally such behaviour quite frankly puts off people in general – why would they want to participate in a place where if you disagree someone goes on a hunt for your personal info and plasters it over a public board for all to see?

    The way I see it this is the Internet, and it’s now more social than ever. If you expose any sort of details and you’re a person of interest, there is a chance someone will do some detective work, trace it to the source and expose it to the public. Ironically, this is also similar to how ID investigation works! 🙂

    This is exactly what happened to Zachriel, he probably said more than he should have in some online exchanges somewhere sometime ago (at ATBC or wherever), and/or gave too many clues pertaining to his identity. In that case, maybe he just doesn’t care about anonymity?

    I pasted a link pertaining to existing information posted a while back on a sub-blog (darwins-god.blogspot.com) to UD. Who knows if it’s even accurate, but the question of singular vs. plural Zachriel/s came up, and since I read much of Zachriels material for many years now as an ID supporter, I will admit I was a bit curious to know who/what Zachriel even is, whether it’s really some paid group of Darwin lobby trolls etc…and confirm here.

    I’m completely for taking down the link and understand privacy controls and concerns, but it’s still really weird that people are annoyed when this information is freely available online with a simple google search. That’s all I really have to say on this matter.

  157. 157
    Zachriel says:

    OFF TOPIC

    Mapou: we should be working on expanding ID in order to come up with serious scientific predictions.

    Thought this site was for general discussion. Perhaps that should be clarified in the comment policy, right next to the policies about germaneness, politeness, and tolerance.
    http://www.uncommondescent.com/comment-policy/

    Mapou: People like Zachriel are not here to discuss or argue anything.

    Actually, we are here to discuss ID and evolutionary biology, and try to support our position with relevant facts and argument. However, you seem to be more concerned with other issues. Good luck with that.

  158. 158
    Zachriel says:

    EugeneS: What I mean by a working gene duplication machinery is specific protein-protein interactions achieving controlled gene duplication such that one copy is there for integrity, the other is for alleged unguided exploration of the search space.

    Mistakes in duplication are intrinsic to the replication process, so inhere to the origin of replication.

    Vy: We observe adaptation and evodelusionary twisting of adaptation, like all your comments on the issue.

    No. We can observe that mutations are random with respect to fitness. We can observe how selection causes heritable changes in populations. One experiments showing mutation is random with respect to fitness is Lederberg & Lederberg, Replica Plating and Indirect Selection of Bacterial Mutants, Journal of Bacteriology 1952.

    Vy: I’m fully aware of the fact that they happen to be evodelusionists like you but that doesn’t affect reality.

    No, but it does support the claim that “per the researchers, they evolved to adapt to the laboratory conditions”.

    Vy: However, these mutations do not account for the origin of the silenced genes, as their prior existence is essential for the mutation to be beneficial.

    Evolution largely works by incremental change of existing structures.

  159. 159
    computerist says:

    Zachriel,

    The way I see it, biology is composed of multiple interdependent systems.
    If the mutation can occur in any arbitrary position affecting any of those systems, you cannot constructively or positively “evolve” anything.
    Now, the only way this can be circumvented, is if there are specific restrictions and controls in the cell similar to object oriented software design, where you have limited access to certain methods/properties, ie: public/protected/private.
    The evidence shows (for example dog breeds) that there are key mutational hot spots that are common and are responsible for determining a wide range of characteristics including size, color etc…aka: variation.
    These hot spots would be analogous to public properties/methods. They can be accessed and modified but also have modifier restrictions in place. This however still preserves the underlying functionality, and evolution can move forward, but in a limited way, that’s good.

  160. 160
    computerist says:

    This is why it’s more in-line with Evoillusion than Evolution.
    or maybe “pseudo-Evolution”? sounds good to me.

  161. 161
    Vy says:

    Computerist, how about evodelusion?

  162. 162
    computerist says:

    There is definitely a strong degree of delusion with respect to evolution, so in that case I would say it would be in a way synonymous with evoillusion and/or pseudo-evolution. Whichever one sounds better I guess 🙂

  163. 163
    Zachriel says:

    computerist: The way I see it, biology is composed of multiple interdependent systems.

    Organisms are organized at many levels throughout. They can be modeled as networks which have been built through preferential attachment.

    computerist: If the mutation can occur in any arbitrary position affecting any of those systems, you cannot constructively or positively “evolve” anything.

    Changes in a complex network can occur at most places within such networks without disrupting the entire network.

  164. 164
    computerist says:

    Changes in a complex network can occur at most places within such networks without disrupting the entire network.

    Networks operate within restrictions in the form of protocols. If you’re saying biology is like a network, it’s governed by strict protocols. I do not modify the transport control protocol when I send a message or make a request. The arbitrary message is “encapsulated” within the OSI layers (in the case of computer networks). If you’re saying ANYTHING can be modified, then the underlying protocols would be subsequently affected sooner rather than later, rendering the network non-functional.

  165. 165
    Zachriel says:

    computerist: If you’re saying ANYTHING can be modified, then the underlying protocols would be subsequently affected sooner rather than later, rendering the network non-functional.

    No, but largely robust to changes, contrary to your statement above. Nearly every single sexually reproducing organism is a unique combination of traits, and nearly all carry a number of mutations, yet the vast majority are viable.

  166. 166
    Vy says:

    No. We can observe that mutations are random with respect to fitness. We can observe how selection causes heritable changes in populations. One experiments showing mutation is random with respect to fitness is Lederberg & Lederberg, Replica Plating and Indirect Selection of Bacterial Mutants, Journal of Bacteriology 1952.

    Still the same rapping as last time and it is still false. Moving along, nothing new to see . . .

    No

    So they’re not evodelusionists like yourself? Are you even reading your comments???

    but it does support the claim that “per the researchers, they evolved to adapt to the laboratory conditions”.

    Do you have reading comprehension issues? The level of inanity in your comments is at a critical level, damn! You saw this:

    Maybe the title of the project is a clue to the researchers’ thinking

    Oh yes, I’m fully aware of the fact that they happen to be evodelusionists like you but that doesn’t affect reality.

    Just because I see a madman on TV because of a sloppily positioned video camera saying “madmen matchsticks ignite when you strike them” doesn’t mean I should believe the nonsense. No way, I take the “non-“, “madmen” in this case, and keep the” sense”, which is the rest of the statement. It’s easy.

    and you still had the audacity to post the comment? Come on!
    What do the claims of seemingly madmen, as per the analogy, have to do with a logical interpretation of said claims?

    Evolution largely works by incremental change of existing structures.

    I lost interest in any of your other redefinitions of what evolution is and isn’t two redefinitions ago so that your statement is as logical as “blahita maggiooop dd kd smiggles we worldiia tak overrrrr” and as useful as a stain on the wall.

    ___

    It was all nice and good in the beginning but having to repeat myself over and over has made this discussion become quite tiresome.

    You have shown, to me as well as others and even across threads, that the only thing you’re capable of doing is being consistently inconsistent (and I’m not even joking), selectively blind, ignore questions and/or give non-answers to simple yes/no questions, repeat the same refuted things over and over, bait-and-switch, and make comments that contradict your very own words and the inner workings of your pet theories.

    I guess I should have listened to Mapou and Virgil earlier on, whew!

  167. 167
    Zachriel says:

    Vy: You can refer to that same reference as many times as you want.

    And you can ignore the same reference as many times as you want, but it doesn’t go away. The Lederberg experiment shows that mutations are random with respect to fitness.

  168. 168
    Vy says:

    And you can ignore the same reference as many times as you want

    Is this coming from the same guy that ignored:

    In the case of many adaptations, we can show they are random with respect to fitness.

    Virgil: So something that aids fitness is random with respect to it? Really?

    ???

    The Lederberg experiment shows that mutations are random with respect to fitness.

    My, my, my. A few umpteen comments ago, it was the Lenski experiments that showed it and now it’s this one.

    Uh uh, you may like to move around in circles but not me.

  169. 169
    Virgil Cain says:

    Zachriel:

    Actually, we are here to discuss ID and evolutionary biology, and try to support our position with relevant facts and argument.

    And yet you refuse to learn what ID is and you equivocate when you talk about evolutionary biology. That means to don’t know the relevant facts and you don’t have an argument.

  170. 170
    Virgil Cain says:

    Zachriel:

    The Lederberg experiment shows that mutations are random with respect to fitness.

    In what way did that experiment show that mutations are random with respect to fitness? Be specific or go home.

  171. 171
    Mapou says:

    So random mutations are no longer random. They are now only random with respect to fitness, whatever that means. This is a favorite tactic of liars: when you’re caught in a lie, change the names in order to confuse people. This is why global warmists change “global warming” to “climate change” and why Darwinists are renaming random mutations. It’s called science by relabeling which is no better than the previous science by labeling. To explain something you are clueless about just give it a name. My favorite example so far is “convergence”.

  172. 172
    computerist says:

    Nearly every single sexually reproducing organism is a unique combination of traits, and nearly all carry a number of mutations, yet the vast majority are viable.

    So? Have you not read what I stated about public/private/protected regions? That allows your scenario to be viable, without it your scenario would not be viable.

  173. 173
    mike1962 says:

    Zechriels: The Lederberg experiment shows that mutations are random with respect to fitness.

    You should have put “many” in front of “mutations.”

    In 1952, Esther and Joshua Lederberg performed an experiment that helped to show that many mutations are random, not directed.

    http://www.evolution.berkeley......berg.shtml

    They did not evolve resistance in response to exposure to the antibiotic.

    Which leaves up in the air how the little beasts managed to “evolve resistance” in the first place and maintain that resistance in a subset of the population when no need existed for it.

    http://www.uncommondescent.com.....ent-584909

  174. 174
    Zachriel says:

    Zachriel @152: Evolution refers to hereditary changes. In the case of many adaptations, we can show they are random with respect to fitness.

    That statement should read “In the case of many mutations, we can show they are random with respect to fitness.”

  175. 175
    Zachriel says:

    Vy: “In the case of many adaptations, we can show they are random with respect to fitness.

    That was a misstatement. It should read “In the case of many mutations, we can show they are random with respect to fitness.” We appended a correction.

    Vy: A few umpteen comments ago, it was the Lenski experiments that showed it and now it’s this one.

    Thousands of experiments show that mutations are random with respect to fitness. The Lederbergs Experiment happens to be one that is easy to understand, and easy to replicate.

    mike1962: You should have put “many” in front of “mutations.”

    Or: The Lederberg experiment shows that the specific mutations in the study are random with respect to fitness. Of course, many other experiments have been done to confirm this applies to mutations generally.

    mike1962: Which leaves up in the air how the little beasts managed to “evolve resistance” in the first place and maintain that resistance in a subset of the population when no need existed for it.

    Antibiotic resistance degrades over time. However, antibiotics are common in the natural environment as well as in human society, so many forms of resistance persist.

  176. 176
    wd400 says:

    Having only just seen comments 110 and 111 here, can I join the list of commenters who would like to see those posts deleted and a clear policy of that people outing real-world identities should expect to be banned in future?

    I don’t know (or care) if the information is true, but allowing this sort of behviour is dangerous (people value their anonymity for any number of good reasons) and will see many comenters leave.

  177. 177
    Vy says:

    That was a misstatement.

    Nope, it’s pretty much standard Zachriel.

    We appended a correction.

    We did, eh?

    Thousands of experiments show that mutations are random with respect to fitness. The Lederbergs Experiment happens to be one that is easy to understand, and easy to replicate.

    *yawn*

    The park is closed. No more going around circles with you, especially someone like you.

    Who knows what next you’re gonna bring up, fruit flies? Rats?? Uh uh, I have better things to do.

  178. 178
    Mapou says:

    wd400 @176 whining about the right to be anonymous:

    I don’t know (or care) if the information is true, but allowing this sort of behviour is dangerous (people value their anonymity for any number of good reasons) and will see many comenters leave.

    You, too, should be outed since you’re nothing but a troll. And good riddance.

  179. 179
    Zachriel says:

    Vy: Who knows what next you’re gonna bring up, fruit flies? Rats??

    Turns out that fruit flies and rats are biological organisms, hence, relevant to a discussion biology. Notably, you have to response to how the Lederberg Experiment shows that mutations are random with respect to fitness.

  180. 180
    Mung says:

    Upright BiPed:

    Moderators, comments #110 and #111 need to be removed from this thread.

    I second that motion. And Mapou should be warned and if it happens again, banned. This should not be tolerated.

  181. 181
    JoeCoder says:

    @Mapou at 178

    As an ID proponent I very much appreciate wd400’s participation here. When I have an interesting idea there’s nobody here who is as knowledgeable yet still friendly as he/she is for me to test it against. And testing against critics is IMHO the best way to tell whether an idea is true.

    In contrast, we have several other ignorant but friendly critics, and perhaps a couple other knowledgeable but rude critics.

  182. 182
    Mapou says:

    Does anybody know the identities of Mung and JoeCoder? LOL

    Anonymous cowards calling for banning me from UD? You must be joking. I don’t care. UD is mostly recreation for me when I need a break from my work. I enjoy bashing atheists and Darwinists.

  183. 183
    computerist says:

    Come on guys, if the comments need to be taken down, take them down already.

  184. 184
    Mung says:

    Mapou:

    Does anybody know the identities of Mung and JoeCoder?

    I know the identity of Mung.

  185. 185
    Vy says:

    Turns out that fruit flies and rats are biological organisms

    Ya think? :/

    Normally, I’d say the mental gymnastics (MGs) in your brain settled down to realize this oh so obvious fact but I remembered you’re a multi-person entity so the version that posted that must’ve done a Google search on what rats and fruitflies are.

    Congrats, Zachriel XY v.2.0. 🙂

    Notably, you have to response [sic] to how the Lederberg Experiment shows that mutations are random with respect to fitness.

    Yup, at this point, it’s obvious Zachriel XY v.2.0 was talking to another Zachriel because of the reactivation of the MGs.

    The mental gymnastics caused a “too_much_reality” overload as that’ll explain why you’re asking yourself a very good question concerning a delusional idea proposed by another Zachriel which BTW Mike has already refuted in the other thread.

  186. 186
    JoeCoder says:

    @Mapou

    Even though I’m on your side (ID), you are now calling for me to be doxed because I think ideas within ID should be subjected to review from knowledgeable but friendly critics to help test their validity?

  187. 187
    Virgil Cain says:

    JoeCoder, Lighten up, Mapou was joking. The “LOL” should have been a clue.

    Also doxing insipid trolls should be mandatory.

  188. 188
    Zachriel says:

    JoeCoder: The Mendel authors describe: “Probability selection contrasts strongly with truncation selection wherein there is no element of randomness.

    While we haven’t reviewed the entire project, this statement is false due to the division of working fitness by a random number from zero to one.

  189. 189
    Virgil Cain says:

    Right, now the authors don’t know what they are talking about.

    Nice “argument”, Zachriel.

  190. 190
    Zachriel says:

    Z: the division of working fitness by a random number from zero to one.

    We haven’t devised a definitive test, but a quick experiment shows that when fitnesses vary only slightly, as with nearly neutral mutations, then the divide-by-random function tends to scramble the ranking more than when fitnesses vary widely, as with strong selection.

  191. 191
    JoeCoder says:

    @Zachriel

    Sorry I didn’t respond sooner. I had thought this thread was dead and hadn’t checked it. In the Mendel source code, take a look at selection.c lines 516 through 530:

    if (selection_scheme == 4) { // partial truncation selection
    // …
    work_fitness[i] /= partial_truncation_value + (1. – partial_truncation_value) * randomnum();

    randonnum() is defined in ranlib.c line 6:

    #define randomnum() (float)(rand()/(float)RAND_MAX).
    The built in function rand() returns a number between 0 and RAND_MAX (a very large integer), so the randomnum() function returns a random number between 0 and 1 with a uniform distribution.

    In the 2011 paper the authors used “partial truncation (unless otherwise specified)” with “partial truncation input parameter = 0.5?.

    So if you plug that into the formula above, the fitness is divided by:

    (0.5 + (0.5 * randomnum()))

    So when partial truncation selection is used (most runs), they are dividing by a random number uniformly distributed between 0.5 and 1.0 and still have the declining fitness shown in figure 6.

    However in a few cases they do use unrestricted probability selection (selection_scheme == 2) for comparison,and there they do divide between 0 and 1. I think it’s very biologically realistic to scramble the ranking more when the differences in fitness are smaller. I don’t know how to calculate whether unrestricted probability selection is biologically realistic, but partial truncation selection is overly generous and still shows decline.

    The Mendel authors summarize:

    With a [deleterious] mutation rate of 10, almost half of all deleterious mutations were retained, with a nearly constant accumulation rate of 4.5 mutations per individual per generation.

    In other words, we can’t have more than 10 – 4.5 = 5.5 deleterious mutations per generation. This seems consistent with estimates of various evolutionists. Forty-three years ago Susumu Ohno calculated that no more than 6% of our DNA could be nucleotide-specific functional:

    the moment we acquire 10^5 gene loci, the overall deleterious mutation rate per generation becomes 1.0 which appears to represent an unbearably heavy genetic load… at the most, only 6% of our DNA base sequences is utilized as genes

    If you read the context you can see that by “genes” he means functional entities, not necessarily only protein coding exons. If I’m reading him right, Larry Moran seems to prefer an even smaller number:

    if the deleterious mutation rate is too high, the species will go extinct… It should be no more than 1 or 2 deleterious mutations per generation.

    Ford Doolittle, Dan Graur, and T. Ryan Gregory have made similar comments.

  192. 192
    Zachriel says:

    JoeCoder: So if you plug that into the formula above, the fitness is divided by:

    (0.5 + (0.5 * randomnum()))

    So when partial truncation selection is used (most runs), they are dividing by a random number uniformly distributed between 0.5 and 1.0

    If the parameter is 0.5, then the value is 0.5 to 1.0
    If the parameter is 0.1, then the value is 0.1 to 0.2
    If the parameter is 0.9, then the value is 0.9 to 1.8
    If the parameter is 1.0, then the value is 1.0 to 2.0

    Selection is by ranking, so what is the effect of the parameter?

    JoeCoder: The Mendel authors describe: “Probability selection contrasts strongly with truncation selection wherein there is no element of randomness.

    Still don’t see the justification for this statement.

  193. 193
    JoeCoder says:

    If the parameter is 0.1, then the value is 0.1 to 0.2
    If the parameter is 0.9, then the value is 0.9 to 1.8
    If the parameter is 1.0, then the value is 1.0 to 2.0

    These calculations are incorrect. The second term is 1 minus the parameter. If the parameter is 0.1, then you get (0.1 + 0.9 * randomnum()) and fitness is divided by a random number from 0.1 to 1.0. If the parameter is 0.9, then it’s divided by a random number from 0.9 to 1.0

    JoeCoder: The Mendel authors describe: “Probability selection contrasts strongly with truncation selection wherein there is no element of randomness.

    Maybe you’ve got the modes mixed up? We have:

    probability selection – very random (selection_state == 2)
    truncaction selection – non-random (selection_state == 1)
    partial truncation selection – a blend between the two modes above. (selection_state == 4)

    The formula I worked out above is partial truncation selection. If you use Chrome’s web inspector on Mendel’s user interface, you can verify that truncation selection is selection_state==1. So in selection.c it doesn’t execute any of those three “if (selection_state == ?)” paths that add randomness to the fitness.

    There’s also strict proportionality probability selection (selection_state == 3), but I haven’t seen the Mendel authors report using this mode. Although i haven’t read all their other papers.

  194. 194
    Zachriel says:

    JoeCoder: The second term is 1 minus the parameter.

    Okay. It dropped out in your shortened formula.

    p+(1-p)*randnum()

    We haven’t looked at the code in several years (2009). We’ll take another look at some point.

  195. 195
    Zachriel says:

    Assuming a parameter of 0.5, the result will still be essentially scrambled when the selection coefficient is small. It’s also dependent on population size, and the founder effect.

  196. 196
    Mung says:

    Zachriel: We haven’t looked at the code in several years (2009). We’ll take another look at some point.

    Do you remember my asking you the last time you had looked at the code and you telling me that it had not changed?

  197. 197
    JoeCoder says:

    Zachriel, Kimura showed that when selection coefficients are sufficiently small, selection treats beneficial alleles as if they are neutral. So greater scrambling with smaller coefficients is exactly what Mendel’s Accountant should be doing.

    Based on the experiments I reported in comment #136, even probability selection (the most random mode) looks to me to be at least within the realm of what’s biologically realistic. All 25 deleterious mutations were removed and 40% of the beneficial mutations fixed. Do you have a way to exactly quantify how much randomness is too much or not enough in the selection process?

  198. 198
    Zachriel says:

    Had some troubles with the new version (2.0.2). Apparently, the old version (1.4.7) had to be deinstalled first.

    JoeCoder: Kimura showed that when selection coefficients are sufficiently small, selection treats beneficial alleles as if they are neutral.

    That is correct. And everyone agrees that if mutations occur too quickly, it will lead to extinction. On the other hand, mice have been around for a very large number of generations, and there is no sign of mutational meltdown — not to mention yeast, rabbits, and beetles. Notably, organisms have evolved to survive even high radiation environments.

    One of the problems with the model is the ratio of deleterious to beneficial mutations. While selectively significant mutations are mostly deleterious, nearly neutral but beneficial mutations are much more frequent. Consider an optimized structure. The peak of the fitness curve has a slope, and small changes can occur on either side of the peak with only small effect. Consequently, the fitness will meander around the peak, with fitness sometimes being slightly degraded, and other times slightly improved.

    Another problem is that heritability varies with trait, and depends on the particular environment, as well as the amount of variation in the population. This factor is in addition to the randomization, so further degrades the signal.

  199. 199
    JoeCoder says:

    Mice and rabbits have less time and fewer cell divisions between generation, which likely gives them a lower mutation rate. They also have a lot more offspring per female than humans. And their larger population sizes make selection better able to filter slightly deleterious alleles. If I remember, any selection coefficient less than the inverse of the population size is seen as completely neutral by selection. But I don’t have a source handy for this or remember if there’s a constant to multiply by in there.

    So if anything these factors would allow mice and rabbits to outlast us. Generally it seems like the larger animals are the most prone to extinction. Lining up with this prediction (or retrodiction) they also have smaller populations, lower reproductive rates, and more cell divisions between generation. I don’t know if large animal extinction risk is a result of genetic entropy or if it’s due to other factors.

    nearly neutral but beneficial mutations are much more frequent.

    How frequent are you proposing? I’ve seen some experiments propose beneficial rates of up to 5 to 13%, but these are often just knocking out genes not needed in lab conditions.

    Here are a couple sources I’ve seen with perhaps better estimates. In bacterial ribosomal genes:

    We used a bacterial system in which the fitness effects of a large number of defined single mutations in two ribosomal proteins were measured with high sensitivity… most mutations (120 out of 126) are weakly deleterious and the remaining ones are potentially neutral. The DFEs [Distribution of Fitness Effects] for synonymous and nonsynonymous substitutions are similar, suggesting that in some genes, strong fitness constraints are present at the level of the messenger RNA.

    From a review paper on exploring fitness landscapes via directed evolution:

    “Statistically, random mutations tend to be quite harsh, usually decreasing activity and sometimes destroying it altogether. 30–50% of single amino acid mutations [within protein coding regions] are strongly deleterious, 50–70% are neutral or slightly deleterious and 0.01–1% are beneficial.”

    John Sanford and Wolf Ekkard Lonnig have each argued that if beneficial mutations were more common (or at least detectable) then the mutagenic breeding experiments involving billions of plants would’ve been more successful.

    The 2007 paper from the Mendel team I linked above used a beneficial rate of 1% which I think is unrealistically high. But that paper used probability selection (the mostly random one).

    The 2011 paper did not use any beneficial mutations, but they were specifically testing the preserving ability of Mendel’s accountant. Just as deleterious mutations interfere with the selection of beneficials, having beneficials can interfere with selection against deleterious mutations.

    There’s at least half a dozen other papers from the Mendel team I haven’t had time to look at.

    I admit I haven’t looked at how Mendel simulates heritability, if at all. Do you think different distributions have a significant effect on the simulation outcome?

  200. 200
    vjtorley says:

    I only just found about posts 110 and 111. I have deleted any confidential information.

  201. 201
    Mung says:

    thank you

  202. 202
    Zachriel says:

    JoeCoder: Mice and rabbits have less time and fewer cell divisions between generation, which likely gives them a lower mutation rate.

    Yes. Mammals have about the same mutation rate per year, not per generation. See Kumar & Subramanian, Mutation rates in mammalian genomes, PNAS 2002.

    JoeCoder: Generally it seems like the larger animals are the most prone to extinction.

    Sure, but that’s usually due to other causes, at least until they reach too low a population to be sustainable.

    JoeCoder: “We used a bacterial system in which the fitness effects of a large number of defined single mutations in two ribosomal proteins were measured with high sensitivity… most mutations (120 out of 126) are weakly deleterious and the remaining ones are potentially neutral.”

    Bacteria tend to have highly optimized genomes. The selection coefficient of these mutations are on the order of -0.005. However, consider that once these mutations have occurred, assuming they aren’t purged by selection, they likely will undone by a future mutation, in which case they would be beneficial. In other words, a natural population will exhibit significant variation, with traits drifting about the maximum for each trait.

    JoeCoder: The 2007 paper from the Mendel team I linked above used a beneficial rate of 1% which I think is unrealistically high. But that paper used probability selection (the mostly random one).

    Our own efforts were in response to the 2007 paper. Division by random(1) is ill-considered, and doesn’t properly represent randomness in nature. As important, it dilutes most of the signal from selection, especially with small variations in selection coefficients.

    That paper led to claims that the human genome was melting down, which is odd considering their rapid expansion in population over the last few centuries. Humans seem rather fecund, and hear-tell, they have resorted to artificial means to limit their reproduction.

    We’re running some experiments with 0.5 partial truncation…

  203. 203
    JoeCoder says:

    Division by random(1) is ill-considered, and doesn’t properly represent randomness in nature. As important, it dilutes most of the signal from selection, especially with small variations in selection coefficients.

    I think we need a way to quantify what amount of randomness is biologically realistic. Without that I don’t see us advancing past this point. I see selection as pretty random to begin with, but I am open to having my view amended in light of data.

    Small variations in selection coefficients SHOULD be the most diluted (per Kimura), so I see no problem there.

    I agree selection can keep bacterial genomes more efficient. I’m just sharing the data I’ve come across.

    That paper led to claims that the human genome was melting down, which is odd considering their rapid expansion in population over the last few centuries.

    Populations expand when the strength of selection is decreased. In the last few thousand years technological progress (beginning with farming) has allowed us to decrease our own selective pressures. So I think grown is expected any time selective pressures decrease faster than the deleterious load increases. Although decreased selective pressures also lead to faster deleterious accumulation.

    Out of curiosity, who is “we”? I don’t care about names, I value my privacy, and I have no desire to dox you. An answer like “me and my flatmate” would be fine.

  204. 204
    Zachriel says:

    JoeCoder: Small variations in selection coefficients SHOULD be the most diluted (per Kimura), so I see no problem there.

    Sure, but even strong selection is strongly diluted when working fitness is derived by division with a random number between zero and one. It also creates a strange skew of working fitness, from small to infinity.

    JoeCoder: So I think grown is expected any time selective pressures decrease faster than the deleterious load increases.

    J Sandord (2008): “When biologically realistic parameters are selected, Mendel shows consistently that genetic deterioration is an inevitable outcome of the processes of mutation and natural selection. The primary reason is that most deleterious mutations are too subtle to be detected and eliminated by natural selection and therefore accumulate steadily generation after generation and inexorably degrade fitness.”

    Yet humans survived a bottleneck with very low population, and then survived rapid expansion.

  205. 205
    JoeCoder says:

    It also creates a strange skew of working fitness from small to infinity

    With a parameter of 0, the distribution is such that 50% are less than 2, 90% of them are less than 10, and 99% of them are less than 100. randonmum() has to return a value less than 0.01 to go above 100.

    This seems realistic because every now and then super-unfit guy still has lots of kids. Maybe he woos women with good poetry? Mendel realistically makes the rareness of this event proportional to his unfitness.

    So it’s a realistic distribution. I don’t know if it’s an absolutely correct distribution or how to determine that. I also don’t know how to determine whether a parameter of 0 or 0.5 is more biologically realistic.

    Yet humans survived a bottleneck with very low population, and then survived rapid expansion.

    Under the genetic entropy model being proposed, by extrapolation humans would’ve had far fewer deleterious alleles back at that bottleneck. Thus the negative effect of such a bottleneck would be much less.

    Also how rapid of an expansion are you suggesting? Even the YECs who want to fit everything within only 4350 yeas need need 2.23 reproducing offspring per female to go from 6 people to a world population of 1.7 billion in the year 1900AD:

    N1 = N0 * e ^ (r*t)
    1.7 billion people = 6 people * e^(r * 170 generations)
    r = 0.115
    2r = 0.230, since you need two people to reproduce

    While 2 reproducing offspring per female is required to maintain constant population size. I don’t thinks 2.23 versus 2.0 reproducing offspring is a very big difference in terms of selection.

  206. 206
    Mung says:

    Zachriel, are you intentionally ignoring my question @196?

    Did you or did you not tell me that the software had not changed? And how did you know that if you haven’t looked at it since 2009?

  207. 207
    Zachriel says:

    Mung: Zachriel, are you intentionally ignoring my question @196?

    Please provide a reference.

    JoeCoder: With a parameter of 0, the distribution is such that 50% are less than 2, 90% of them are less than 10, and 99% of them are less than 100.

    If working fitness includes reproductive potential, then there’s the obvious problem that one wouldn’t expect 1% of the population to produce a hundred times the offspring by accident. Sure it could happen — all the superior stags got wiped out by a lava flow —, but it’s very unlikely.

    If working fitness doesn’t include reproductive potential, then the working fitness is only used for ranking. Even then, with probability selection, small but significant selective advantages are lost at a rate higher than expected based on population genetics.

    JoeCoder: Maybe he woos women with good poetry?

    That would be a superior phenotype then.

    JoeCoder: I don’t thinks 2.23 versus 2.0 reproducing offspring is a very big difference in terms of selection.

    That figure doesn’t include all reproduction, which includes miscarriages, stillborns, and those who die before their own chance to reproduce. (About half of human conceptions end in miscarriage, often due to defects, the first step in natural selection, so the reproductive rate would be at least twice the population increase.) In any case, a low reproductive rate allows deleterious mutations to accumulate faster. Humans seem to be more than healthy enough to continue their existence into the foreseeable future. This is contrary to the claim made by Sanford.

    Truncated selection seems to work reasonably well, but because the method of randomization and the calculation of working fitness is non-biological, it’s hard to make sense of it. You can’t break it down to compare it to real examples. For instance, fitness doesn’t seem equivalent to selection coefficient.

  208. 208
    JoeCoder says:

    That figure doesn’t include all reproduction, which includes miscarriages, stillborns, and those who die before their own chance to reproduce.

    Right, I’m only counting those who survive and reproduce because that’s how you calculate population growth. Assume that each woman has on average 6 offpsring (or 12 if you count failed pregnancies) and either 2.0 or 2.23 survive to reproduce, based on the strength of selection.

    one wouldn’t expect 1% of the population to produce a hundred times the offspring by accident.

    It makes them 100 times more likely to survive to the point of producing offspring at all. Not produce 100 times more offspring. So it’s only used for ranking.

    probability selection, small but significant selective advantages are lost at a rate higher than expected based on population genetics

    What is the correct rate? I’ve been asking you for it through the last several comments now. I don’t know it either but you are the one claiming Mendel is using the wrong rate : )

  209. 209
    Zachriel says:

    JoeCoder: What is the correct rate?

    In a large population, the chance of fixation for a new beneficial mutation is about 2s.* If a variant has a selective advantage of 0.1, then it will fix 20% of the time. Neutral or near neutral variants will fix at a rate equal to their proportion in the population. If there is a new mutant in a population of a thousand, then the chance of fixation is one in a thousand.

    With probability selection, the result tends to resemble the latter rather than the former. Sure, luck is a factor, but in the long run, selection does play out.

    * 2s(Ne/N), where s is the selection coefficient, N is the population size, and Ne is the effective population size. Effective population varies, but is important in organisms with harem breeding strategies, or organisms that have experienced population bottlenecks.

  210. 210
    JoeCoder says:

    Zachriel: If a variant has a selective advantage of 0.1, then it will fix 20% of the time.

    In my comment #136 above, I used probability selection and seeded a population of 2000 with 5 beneficial mutations each having a selective advantage of 0.1. The mutation rate was 0. 2 out of 5 of those beneficials fixed–40%. Doesn’t that make even probability selection in Mendel’s accountant twice as generous as your formula?

    Also, do you have a link so I can read how the 2s(Ne/N) formula is derived? I’m surprised it doesn’t have a “dumb luck” coefficient in there somewhere, that would vary according to how efficient selection is in various populations. Maybe that somehow cancels out but I don’t see how?

  211. 211
    Mung says:

    Mung:

    Zachriel, are you intentionally ignoring my question @196?

    Did you or did you not tell me that the software had not changed? And how did you know that if you haven’t looked at it since 2009?

    Zachriel:

    Please provide a reference.

    Well, to be honest I was sort of hoping we could avoid all that. But I do enjoy a challenge. May take some digging. We can start here though.

    Zachriel December 1, 2014 at 10:03 am:

    Mendel’s Accountant has a demonstrable flaw which virtually eliminates the known empirical effects of selection.

    Zachriel now:

    We haven’t looked at the code in several years (2009).

    Now even if you last looked at the code at the end of 2009, that’s still five years.

  212. 212
    Zachriel says:

    Mung: Well, to be honest I was sort of hoping we could avoid all that.

    Sorry. Don’t want to be a bother.

    We have looked at the code briefly in the discussion with JoeCoder. We have not studied the code in detail in several years. As there is a new version, some of the code is undoubtedly changed. However, the code concerning probability selection and division by random(0,1) is still there.

  213. 213
    Mung says:

    Zachriel,

    http://www.uncommondescent.com.....tic-codes/

    Comments 48, 56, 58, 60

    Does that refresh your memory?

  214. 214
    JoeCoder says:

    Zachriel, it looks like we have three options:

    1. The formula you provided in comment #209 is wrong.
    2. I somehow made a mistake in the parameters when running Mendel’s Accountant in comment #136. I don’t think I did.
    3. There never was any bug in Mendel’s Accountant to begin with, even back in 2009 when you first looked at it.

    Thoughts?

  215. 215
    Zachriel says:

    JoeCoder: I used probability selection and seeded a population of 2000 with 5 beneficial mutations each having a selective advantage of 0.1.

    Fitness in Mendel’s Accountant doesn’t necessarily translate into the selection coefficient. A selection coefficient of 0.1 means the organism will, on average, leave 10% more fertile offspring. (The use of sign may vary with context.)

    JoeCoder: Also, do you have a link so I can read how the 2s(Ne/N) formula is derived?

    Here’s a review. If you want more details, you can follow the citations to Kimura’s original diffusion model.
    http://www.ncbi.nlm.nih.gov/pm.....MC2607448/

    JoeCoder: I’m surprised it doesn’t have a “dumb luck” coefficient in there somewhere, that would vary according to how efficient selection is in various populations.

    Take the simple model of accidental death. Because death is random, as long as there are a substantial number of survivors, the survivors will have variations similar in proportion to the larger population. The survivors will still be subject to selection, and those survivors with a selective advantage will still tend to leave more offspring.

  216. 216
    JoeCoder says:

    Zachriel: Fitness in Mendel’s Accountant doesn’t necessarily translate into the selection coefficient. A selection coefficient of 0.1 means the organism will, on average, leave 10% more fertile offspring. (The use of sign may vary with context.)

    Right, but I don’t think this will have any significant effect on the outcome when simulating the consequences of deleterious load.

    Mendel also has a “Fitness-dependent fecundity decline” option in the advanced selection parameters, but I have not studied it.

    Zachriel: http://www.ncbi.nlm.nih.gov/pm.....MC2607448/

    Ah, I recognize that paper from having it saved in my notes with a “need to read” tag. All the more reason I should do so. Thank you nonetheless. I will have to think more about the model for accidental death. I think you may be right that there is not a need for a “dumb luck” coefficient since fitness is equivalent to number of offspring.

    Still, per comment #214 I don’t see a reason to doubt the results of Mendel’s Accountant. The inevitability of fitness decline also seems consistent with the claims of Susumu Ohno, Larry Moran, and others per comment #191. That’s one of the main reasons Larry Moran argues that so much DNA is junk–so that the deleterious mutation rate can be decreased far enough to avoid the problem.

  217. 217
    Zachriel says:

    JoeCoder: The inevitability of fitness decline also seems consistent with the claims of Susumu Ohno, Larry Moran, and others per comment #191

    Fitness decline can certainly occur, but typically with much smaller population sizes than claimed by Sanford. As already pointed out, humans have been around for thousands of generations, and are happily fecund. There’s clearly something wrong with his model, actually many things.

  218. 218
    JoeCoder says:

    As you know, John Sanford is a young earth creationist and uses genetic entropy as an argument against long ages. However, I’m not sure genetic entropy would prevent humans from existing for thousands of generations. Genomes are very redundant with one system kicking in to compensate for when another is knocked out. The ENCODE team noted the difficulty this caused in testing for functions via knockout:

    Loss-of-function tests can also be buffered by functional redundancy, such that double or triple disruptions are required for a phenotypic consequence. Consistent with redundant, contextual, or subtle functions, the deletion of large and highly conserved genomic segments sometimes has no discernible organismal phenotype, and seemingly debilitating mutations in genes thought to be indispensible have been found in the human population

    Zachriel: Fitness decline can certainly occur, but typically with much smaller population sizes than claimed by Sanford.

    Take a look at Figure 9 from the 2011 Can Purifying Natural Selection Preserve Biological Information paper. The Mendel authors write:

    Figure 9 shows the effect of population size on percent retention after 10,000 generations. Within this limited amount of time, there was only a trivial advantage in having population sizes greater than 5,000. With a population size of 5,000, the rate of mutation accumulation was 89.38%. Doubling the population size to 10,000 resulted in 89.05% accumulation, and doubling the population size again to 20,000 resulted in no further improvement (89.05% accumulation). It is clear that the advantage of larger population size beyond 1000 is only realized in deep time, which seems to imply the need for some type of very long-term selection equilibrium, which may be conceptually problematic.

    Granted 20,000 still isn’t a very large population, but that graph makes it look like there won’t be much benefit to going larger and computational resources make it difficult. We can try simulating larger populations if you think it would help.

    Zachriel: There’s clearly something wrong with his model, actually many things.

    Do you likewise disagree with Larry Moran’s view that anything more than a small number of deleterious mutations will lead to extinction? You’re departing from the majority of biologists knowledgeable in population genetics who argue against ID. That’s OK because I sometimes also take minority positions. But I do want to point that out.

    Mendel’s Accountant is a simulation and does not model reality perfectly. But if you want to win me to your position then I will need a reason why the results are not reliable enough.

  219. 219
    Zachriel says:

    JoeCoder: Granted 20,000 still isn’t a very large population, but that graph makes it look like there won’t be much benefit to going larger and computational resources make it difficult.

    The effective population size of humans is only about 100,000 due to a bottleneck in the recent past.

    JoeCoder: Do you likewise disagree with Larry Moran’s view that anything more than a small number of deleterious mutations will lead to extinction?

    Sure. However, most mutations are neutral.

    JoeCoder: Mendel’s Accountant is a simulation and does not model reality perfectly.

    That’s fine. All models are wrong, but some are useful. If it were presented as a general model, then it might have some value, but it’s presented as an accurate model of biological evolution. That’s where it fails.

  220. 220
    JoeCoder says:

    Zachriel: it’s presented as an accurate model of biological evolution. That’s where it fails.

    In using a deleterious rate of 10, the Mendel authors are already assuming about 90% of mutations are neutral. I don’t think there are any reasons left for me to believe that Mendel is not an accurate-enough simulation of genetic load in humans. Do you have any other ideas?

  221. 221
    Zachriel says:

    JoeCoder: In using a deleterious rate of 10, the Mendel authors are already assuming about 90% of mutations are neutral.

    You cited Larry Moran. He suggests “there are fewer than 2 detrimental mutations per generation and this is an acceptable genetic load.”
    http://sandwalk.blogspot.com/2.....stand.html

    JoeCoder: I don’t think there are any reasons left for me to believe that Mendel is not an accurate-enough simulation of genetic load in humans.

    Sure there are. We have strong evidence that humans have been around for thousands of generations and are still happily making babies by the millions.

  222. 222
    JoeCoder says:

    Larry Moran’s view requires that mutations falling within 98% of the genome be functionally neutral. I don’t see how that’s possible given recent research. A few examples:

    1. Pheasant and Mattick, 2007 estimated that “the functional portion of the genome may exceed 20%” based on conserved sequences and those under purifying selection.

    2. ENCODE 2012 estimated “that at a minimum 20% (17% from protein binding and 2.9% protein coding gene exons) of the genome participates in… specific functions, with the likely figure significantly higher”

    3. ENCODE 2014 estimated that “12-15%” of DNA is evolutionarily conserved.

    4. Martin Smith et al, 2013 estimated that at least 13.6 – 30% of DNA is conserved in its RNA structure. This means that animals with different DNA sequences still produce RNA molecules that have the same shape. They report of their conserved RNA’s that “88% of which fall outside any known sequence-constrained element, suggesting that a large proportion of the mammalian genome is functional.”

    5. Additionally, we know at least 85.2% of the genome is transcribed, and John Mattick says there are usually functional consequences in disrupting those transcripts:

    where tested, these noncoding RNAs usually show evidence of biological function in different developmental and disease contexts, with, by our estimate, hundreds of validated cases already published and many more en route, which is a big enough subset to draw broader conclusions about the likely functionality of the rest.

    Granted conserved sequences rely on the assumption of common descent, but that and protein binding alone would make the deleterious rate at least 20 mutations per generation. And all of those are lower-bound measurements of the number of non-netural nucleotides. I don’t see how it’s reasonable to believe only 1 to 2% of nucleotides are non-neutral?

    Zachriel: humans have been around for thousands of generations and are still happily making babies by the millions.

    Supposing you agreed genetic entropy were true, how many generations do you think would be too many before humans go extinct? Given the levels of redundancy we see in genomes, and that the worst mutations are still selected against, I don’t think thousands of generations is too many. Unless you are able to quantify it?

  223. 223
    Zachriel says:

    JoeCoder: Pheasant and Mattick

    Looking at Pheasant and Mattick, they are including spacers, as well as other functions which are not sequence specific or otherwise relaxed in terms of sequence.

    The general claim that most of the genome is non-functional in terms of sequence is supported by the C-value paradox, a.k.a. onion text. It’s also supported by many experiments showing consistency in rates of neutral evolution in many different taxa and many different parts of the genome. Of course, much of the genome may have function which is relaxed in terms of sequence.

    JoeCoder: Given the levels of redundancy we see in genomes, and that the worst mutations are still selected against, I don’t think thousands of generations is too many. Unless you are able to quantify it?

    Sanford explicitly claims Mendel’s Accountant shows that the history of biological descent cannot be measured in millions of years.

  224. 224
    JoeCoder says:

    Zachriel: Pheasant and Mattick.. are including spacers, as well as other functions which are not sequence specific or otherwise relaxed in terms of sequence.

    Correct. But this is still strong evidence against the claim that only 1 to 2% is nucleotide-specific functional. The nucleic acids that make up RNA products connect to each other in very specific ways, which force RNA molecules to twist and loop into a variety of complicated 3D structures. John Mattick was quoted in a press release from one of the papers I cited above:

    We believe that RNA structures probably operate in a similar way to proteins, which are composed of structural domains that assemble together to give the protein a function.

    Even if only one fourth of the 85% transcribed RNA nucleotides are specific, that’s still a number 10 to 20 times higher than the 1 to 2% we were talking about above, and twice as much as the number the Mendel team is using.

    Zachriel: the C-value paradox, a.k.a. onion text.

    I’ve read much about what Dr. Moran, Graur, and others have written about C-values and I don’t find it convincing. I think there are good reasons for varying C-values that are still entirely compatible with design.

    1. On a very large scale, genome size is correlated with number of cell types. See figure 2B from this paper. More cell types would generally require more information. Although note that they only plot protostomia and deuterostomia animals as two points and we can’t see differences between individual clades.

    2. Take a look at this composite image I put together from this angiosperm paper and also a paper from T. Ryan Gregory in 2001. There seems to be a good correlation between cell size and genome size. The idea being that larger cells require more RNA’s. One textbook makes an analogy:

    The situation is like that of a car factory aiming for a steady output of cars: engines, wheels and doors must be made at the same rate; if overall output is to be increased the number of each must be increased by the same proportion. Moreover, if each robot, machine tool, and operative is already working at maximal rates, one can increase output only by increasing the number of assembly lines

    Although I’m sure it’s more complex than that, since I don’t think the number of protein coding genes increases. I have also seen papers reporting correlations between c-value and longevity, but I am hesitant to cite them because I have not yet read them. It makes sense that more DNA would bring more redundant systems against failure, leading to longevity.

    3. Genome size differences may represent tradeoffs between different forms of data storage. One ENCODE researcher commented on reddit:

    Organism introduce genetic variation in different ways. For instance, in Drosophila, a 100 kilobase gene (DSCAM) encode thousands of different proteins through a complex alternate splicing mechanism. One could envision copying each of these transcripts – without the alternate splicing – into the genome thus increasing the size of the genome by 10 million bases, or roughly 10%, but not changing the complexity at all.

    This is similar to how our own compression algorithms operate–frequently used sequences are stored only once and re-referenced, as opposed to the same information being stored multiple times, at perhaps higher fidelity. A png image is not 90% junk just because it’s 10 times larger than an equivalent lossy jpeg.

    4. Finally, some taxonomically restricted cases of varying c-values (like onions) may be legitimate cases of junk through runaway transposon duplication. Perhaps these clades are simply more prone to transposition. However, I don’t think these can be used to then argue that most genomes in most organisms are junk.

    Our own genomes are very close to the same size as all other mammals, so I don’t think we or they are subject to excess transposition.

    Zachriel: [a highly neutral genome is] also supported by many experiments showing consistency in rates of neutral evolution in many different taxa and many different parts of the genome

    That depends on the assumption that evolution is what created our genomes, which is the very thing I am contesting here. The argument could be rephrased as “Most of the genome bust be functionally neutral because evolution could create no better”.

    Zachriel: Sanford explicitly claims Mendel’s Accountant shows that the history of biological descent cannot be measured in millions of years.

    Perhaps Sanford is overstating his case and not taking redundancy into account? This paper in the Journal of Creation estimates between 1200 and 1.5 million years to extinction based on the parameters used. It doesn’t look like something easy to pin down.

  225. 225
    Zachriel says:

    JoeCoder: That depends on the assumption that evolution is what created our genomes, which is the very thing I am contesting here.

    You are? Do you accept common descent?

    JoeCoder: More cell types would generally require more information.

    So onions have more cell types than humans.

    JoeCoder: There seems to be a good correlation between cell size and genome size. The idea being that larger cells require more RNA’s.

    Mutations that might have been deleterious are no longer so. Redundancy, such as polyploidism, results in huge flexibility in response to mutation.

    JoeCoder: The argument could be rephrased as “Most of the genome bust be functionally neutral because evolution could create no better”.

    Fast reproducing organisms, such as bacteria, have more compact genomes. Slow reproducing organisms, such as mammals, tend to accumulate genomic material, which can also have an evolutionary advantage. Retroviruses may be an important component of this process.

    JoeCoder: This paper in the Journal of Creation estimates between 1200 and 1.5 million years to extinction based on the parameters used. It doesn’t look like something easy to pin down.

    From a thousand to a million years. Quite the range. In any case, the average lifespan of a species is a few million years, but it’s not as if they don’t leave descendants — they often do.

  226. 226
    Alicia Cartelli says:

    “There seems to be a good correlation between cell size and genome size. The idea being that larger cells require more RNA’s.”

    That doesn’t make any sense, if more RNAs are needed, cells would increase transcription, not genome size. (Usually, I guess polytene chromosomes in Drosophila would be an exception)
    The smallest and largest human cells are the sperm and oocyte respectively, and both have the same amount of genetic information (half that of a typical cell.)

  227. 227
    JoeCoder says:

    I reject common descent. I also question the ages of life on earth, due to carbon-14 and soft tissue being found throughout the fossil record. Genetic entropy adds another point to this argument. But the ages of the rocks around the fossils argues against it. So I am unable to argue for a definitive position one way or the other, which is why I’ve avoided that topic so far. I think the earth itself and universe are billions of years old and do not question the conventional dates there.

    But saying that most DNA must be functionally neutral because of evolution, requires genomes to be created by unguided evolution. Behe for example, who accepts common descent, still thinks an intelligence is necessary to inject larges amounts of information.

    As I said above, I think junk DNA is a good explanation for taxonomically restricted cases of large C-value differences. Some onion genomes probably are mostly junk DNA. But that does not mean that most DNA in most organisms is junk.

    I also fully agree that larger genomes are more likely to accumulate excess DNA over time, due to weaker selection and because a deletion is more likely to be deleterious than an insertion. My point is that there are equally good explanations for C-value differences under design. Therefore C-value variation cannot be used to argue for junk DNA.

    One thing to keep in mind is that much functional redundancy is not due to duplications. From a paper in yeast:

    I used functional genomics data from the yeast Saccharomyces cerevisiae to test the hypotheses related to the following: if gene duplications are mostly responsible for robustness, then a correlation is expected between the similarity of two duplicated genes and the effect of mutations in one of these genes. My results demonstrate that interactions among unrelated genes are the major cause of robustness against mutations.

    This is good design, because having backup systems that operate in very different ways makes them less prone to the factors that made primary systems fail.

    So because of their uniqueness, these redundant systems should also be counted among the functional nucleotides that selection must maintain. They can’t be easily replaced simply through more duplications of existing systems.

  228. 228
    JoeCoder says:

    @Alicia Cartelli, Welcome to our friendly debate : )

    Larger cells could either increase transcription and copy number. But having increased copy number allows a faster response to changes. I use the term “copy number” extremely loosely, as not all copies need be the same sequence, per the principles of redundancy I outlined above.

    Granted this is speculative. But I think we have enough design-compatible reasons for varying C-values that we can’t say junk DNA is the only possible explanation for varying C-values.

    As you know, sperm and oocytes have the same amount of genetic information because cells within the same organism have the same haploid genome size. Perhaps due to a constraint of cell differentiation itself?–I’m not up to speed on those details.

  229. 229
    NickMatzke_UD says:

    4. Finally, some taxonomically restricted cases of varying c-values (like onions) may be legitimate cases of junk through runaway transposon duplication. Perhaps these clades are simply more prone to transposition. However, I don’t think these can be used to then argue that most genomes in most organisms are junk.

    Casey Luskin has been trying out this line of argument also, hoping that genome size variation can be brushed off as a few exceptional groups with bloated genomes. The problem is that it relies on wishful thinking rather than facts. Genome size variation is ubiquitous, and the size variations are over several orders of magnitude. There are plants and animals with small genomes and little that looks like junk (e.g. fruit flies and Arabidopsis), but they are exceptions. Unnecessarily huge genomes, with pretty huge variations in genome size, are normal and very common. Download T. Ryan Gregory’s genome size databases and plot the variation. I have. It’s everywhere — yet virtually all of these animals and plants have roughly the same number of genes, ~15000-30000.

  230. 230
    Alicia Cartelli says:

    Not looking to join, I was just curious what you’d say.
    I know my point didn’t really add anything to the topic at hand as you guys are comparing different species.
    But anyways gametes always have half the genome because they are produced via meiosis if that was what you weren’t sure about.

  231. 231
    JoeCoder says:

    @Nick Matzke, welcome : )

    Runaway transposition is only one of four design-compatible reasons I listed as to why we might see variation in genome size. As for plots, In my comment #224 already shared several between genome size and other features like cell size and cell types. They’re not perfect but we should not expect a plot against a single variable to be when there are likely multiple explanations at play.

    Also, is number of protein coding genes the correct metric to use when functional RNAs are also at play?

  232. 232
    Mung says:

    Nick M,

    Do you know what sequence space is yet?

  233. 233
    Mung says:

    Zachriel,

    Have you figured out what you knew and when you knew it yet?

    Were you all not talking to yourselves for a while?

  234. 234
    JoeCoder says:

    @Mung – Unlike most of the discussion on UD, I’m hoping to keep this a friendly and thus productive debate. Can you help me with that goal?

    @Alicia Cartelli – the part I wasn’t sure about was how feasible it would be to design cells so that after they differentiate into specific cell types, they jetison DNA only used by other cell types. But we both know the gametes can’t do that or else the offspring are in trouble!

  235. 235
    Zachriel says:

    JoeCoder: I reject common descent.

    If you reject the historical descent of life, then mechanisms of that change are ungrounded. We’ve always found it hard to imagine, in a world where dinosaur fossils are on display in museums across the world, how someone could reject that long history. Scientists make expeditions around the world to find predicted intermediate fossils. Lucky guessers?

    JoeCoder: This is good design, because having backup systems that operate in very different ways makes them less prone to the factors that made primary systems fail.

    Your analysis has no way to separate evolution from design.

  236. 236
    bornagain says:

    Zachriel, did not we discuss the fossil record the other day?

    http://www.uncommondescent.com.....ent-586453

    Would it hurt your feelings that much to mention the fact that the fossil record, according to leading experts, is severely discordant with Darwinian predictions, with only a handful of supposed intermediates which are all argumentative in their interpretation?

    Or are you just a pathological liar who can’t help yourself? And that you will never honestly admit anything that might cast doubt on Darwinism?

    Can you even answer that question honestly?

  237. 237
    Zachriel says:

    bornagain: did not we discuss the fossil record the other day?

    You mentioned that notochords still existed. We pointed out that you had one once, but outgrew it.

    bornagain: Would it hurt you to mention the fact that the fossil record, according to leading experts, is severely discordant with Darwinian predictions, with only a handful of supposed intermediates which are all argumentative in their interpretation?

    Because we don’t agree with your premise.

  238. 238
    bornagain says:

    Zachriel, it is not you not ‘agreeing with my premise’. It is about you living in complete delusional denial of the fact that the fossil record is severely discordant with what Darwin predicted., i.e. it is about you constantly lying!

    The discordant fossil record is a scientific fact, not a philosophical premise.

    Scientific study turns understanding about evolution on its head – July 30, 2013
    Excerpt: evolutionary biologists,,, looked at nearly one hundred fossil groups to test the notion that it takes groups of animals many millions of years to reach their maximum diversity of form.
    Contrary to popular belief, not all animal groups continued to evolve fundamentally new morphologies through time. The majority actually achieved their greatest diversity of form (disparity) relatively early in their histories.
    ,,,Dr Matthew Wills said: “This pattern, known as ‘early high disparity’, turns the traditional V-shaped cone model of evolution on its head. What is equally surprising in our findings is that groups of animals are likely to show early-high disparity regardless of when they originated over the last half a billion years. This isn’t a phenomenon particularly associated with the first radiation of animals (in the Cambrian Explosion), or periods in the immediate wake of mass extinctions.”,,,
    Author Martin Hughes, continued: “Our work implies that there must be constraints on the range of forms within animal groups, and that these limits are often hit relatively early on.
    Co-author Dr Sylvain Gerber, added: “A key question now is what prevents groups from generating fundamentally new forms later on in their evolution.,,,
    http://phys.org/news/2013-07-s.....ution.html

    In Allaying Darwin’s Doubt, Two Cambrian Experts Still Come Up Short – October 16, 2015
    Excerpt: “A recent analysis of disparity in 98 metazoan clades through the Phanerozoic found a preponderance of clades with maximal disparity early in their history. Thus, whether or not taxonomic diversification slows down most studies of disparity reveal a pattern in which the early evolution of a clade defines the morphological boundaries of a group which are then filled in by subsequent diversification. This pattern is inconsistent with that expected of a classic adaptive radiation in which diversity and disparity should be coupled, at least during the early phase of the radiation.”
    – Doug Erwin
    What this admits is that disparity is a worse problem than evolutionists had realized: it’s ubiquitous (throughout the history of life on earth), not just in the Cambrian (Explosion).
    http://www.evolutionnews.org/2.....00111.html

    disparity
    [dih-spar-i-tee] noun, plural disparities.
    1. lack of similarity or equality; inequality; difference:

    “It is hard for us paleontologists, steeped as we are in a tradition of Darwinian analysis, to admit that neo-Darwinian explanations for the Cambrian explosion have failed miserably. New data acquired in recent years, instead of solving Darwin’s dilemma, have rather made it worse. Meyer describes the dimensions of the problem with clarity and precision. His book is a game changer for the study of evolution and points us in the right direction as we seek a new theory for the origin of animals.”
    -Dr. Mark McMenamin – 2013
    Paleontologist at Mt. Holyoke College and author of The Emergence of Animals

    “The record of the first appearance of living phyla, classes, and orders can best be described in Wright’s (1) term as ‘from the top down’.”
    (James W. Valentine, “Late Precambrian bilaterians: Grades and clades,” Proceedings of the National Academy of Sciences USA, 91: 6751-6757 (July 1994).)

    “Darwin’s prediction of rampant, albeit gradual, change affecting all lineages through time is refuted. The record is there, and the record speaks for tremendous anatomical conservatism. Change in the manner Darwin expected is just not found in the fossil record.”
    Niles Eldredge and Ian Tattersall, The Myth of Human Evolution (New York: Columbia University Press, 1982), 45-46.

    In Explaining the Cambrian Explosion, Has the TalkOrigins Archive Resolved Darwin’s Dilemma? – JonathanM – May 2012
    Excerpt: it is the pattern of morphological disparity preceding diversity that is fundamentally at odds with the neo-Darwinian scenario of gradualism. All of the major differences (i.e. the higher taxonomic categories such as phyla) appear first in the fossil record and then the lesser taxonomic categories such as classes, orders, families, genera and species appear later. On the Darwinian view, one would expect to see all of the major differences in body plan appear only after numerous small-scale speciation events. But this is not what we observe.
    per ENV

    “The facts of greatest general importance are the following. When a new phylum, class, or order appears, there follows a quick, explosive (in terms of geological time) diversification so that practically all orders or families known appear suddenly and without any apparent transitions. Afterwards, a slow evolution follows; this frequently has the appearance of a gradual change, step by step, though down to the generic level abrupt major steps without transitions occur. At the end of such a series, a kind of evolutionary running-wild frequently is observed. Giant forms appear, and odd or pathological types of different kinds precede the extinction of such a line.”
    Richard B. Goldschmidt, “Evolution, as Viewed by One Geneticist,” American Scientist 40 (January 1952), 97.

    Problem 5: Abrupt Appearance of Species in the Fossil Record Does Not Support Darwinian Evolution – Casey Luskin January 29, 2015
    Excerpt: Rather than showing gradual Darwinian evolution, the history of life shows a pattern of explosions where new fossil forms come into existence without clear evolutionary precursors. Evolutionary anthropologist Jeffrey Schwartz summarizes the problem:
    “We are still in the dark about the origin of most major groups of organisms. They appear in the fossil record as Athena did from the head of Zeus — full-blown and raring to go, in contradiction to Darwin’s depiction of evolution as resulting from the gradual accumulation of countless infinitesimally minute variations. . .”98
    per ENV

    “With the benefit of hindsight, it is amazing that paleontologists could have accepted gradual evolution as a universal pattern on the basis of a handful of supposedly well-documented lineages (e.g. Gryphaea, Micraster, Zaphrentis) none of which actually withstands close scrutiny.”
    Christopher R.C. Paul, “Patterns of Evolution and Extinction in Invertebrates,” K.C. Allen and D.E.G. Briggs, eds., Evolution and the Fossil Record (Washington, D.C., Smithsonian Institution Press, 1989), 105.

    “It must be significant that nearly all the evolutionary stories I learned as a student from Trueman’s Ostrea/Gryphaea to Carruthers’ Zaphrentis delanouei, have now been ‘debunked’. Similarly, my own experience of more than twenty years looking for evolutionary lineages among the Mesozoic Brachiopoda has proved them equally elusive.’
    Dr. Derek V. Ager (Department of Geology & Oceonography, University College, Swansea, UK), ‘The nature of the fossil record’. Proceedings of the Geologists’ Association, vol.87(2), 1976,p.132.

    “The point emerges that if we examine the fossil record in detail, whether at the level of orders or of species, we find’ over and over again’ not gradual evolution, but the sudden explosion of one group at the expense of another.”
    Paleontologist, Derek V. Ager, “The Nature of the Fossil Record,” 87 Proceedings of the British Geological Association 87 (1976): 133. (Department of Geology & Oceanography, University College, Swansea, UK)

    “It is a feature of the known fossil record that most taxa appear abruptly. They are not, as a rule, led up to by a sequence of almost imperceptibly changing forerunners such as Darwin believed should be usual in evolution…This phenomenon becomes more universal and more intense as the hierarchy of categories is ascended. Gaps among known species are sporadic and often small. Gaps among known orders, classes and phyla are systematic and almost always large.”
    G.G.Simpson – one of the most influential American Paleontologist of the 20th century

    “A major problem in proving the theory has been the fossil record; the imprints of vanished species preserved in the Earth’s geological formations. This record has never revealed traces of Darwin’s hypothetical intermediate variants – instead species appear and disappear abruptly, and this anomaly has fueled the creationist argument that each species was created by God.”
    Paleontologist, Mark Czarnecki

    “There is no need to apologize any longer for the poverty of the fossil record. In some ways, it has become almost unmanageably rich and discovery is outpacing integration. The fossil record nevertheless continues to be composed mainly of gaps.”
    T. Neville George – Professor of paleontology – Glasgow University,

    “Evolution requires intermediate forms between species and paleontology does not provide them.”
    David Kitts – Paleontologist – D.B. Kitts, Paleontology and Evolutionary Theory (1974), p. 467.

    “The long-term stasis, following a geologically abrupt origin, of most fossil morphospecies, has always been recognized by professional paleontologists” –
    Stephen Jay Gould – Harvard

    “Now, after over 120 years of the most extensive and painstaking geological exploration of every continent and ocean bottom, the picture is infinitely more vivid and complete than it was in 1859. Formations have been discovered containing hundreds of billions of fossils and our museums now are filled with over 100 million fossils of 250,000 different species. The availability of this profusion of hard scientific data should permit objective investigators to determine if Darwin was on the right track. What is the picture which the fossils have given us? … The gaps between major groups of organisms have been growing even wider and more undeniable. They can no longer be ignored or rationalized away with appeals to imperfection of the fossil record.”
    Luther D. Sunderland, Darwin’s Enigma 1988, Fossils and Other Problems, 4th edition, Master Books, p. 9

    “The evidence we find in the geological record is not nearly as compatible with Darwinian natural selection as we would like it to be …. We now have a quarter of a million fossil species but the situation hasn’t changed much. The record of evolution is surprisingly jerky and, ironically, we have even fewer examples of evolutionary transition than in Darwin’s time … so Darwin’s problem has not been alleviated”.
    David Raup, Curator of Geology at Chicago’s Field Museum of Natural History

    “In virtually all cases a new taxon appears for the first time in the fossil record with most definitive features already present, and practically no known stem-group forms.”
    Tom S. Kemp, Fossils and Evolution (New York; Oxford University Press, 1999), 246. – Curator of Zoological Collections

    “The record certainly did not reveal gradual transformations of structure in the course of time. On the contrary, it showed that species generally remained constant throughout their history and were replaced quite suddenly by significantly different forms. New types or classes seemed to appear fully formed, with no sign of an evolutionary trend by which they could have emerged from an earlier type.”
    Peter Bowler, Evolution: The History of an Idea (Berkeley, CA: University of California Press, 1984), 187.

    “The lack of ancestral or intermediate forms between fossil species is not a bizarre peculiarity of early metazoan history. Gaps are general and prevalent throughout the fossil record.”
    R.A. Raff and T.C. Kaufman, Embryos, Genes, and Evolution: The Developmental-Genetic Basis of Evolutionary Change (Bloomington, IN: Indiana University Press, 1991), 34.

    “No one has found any such in-between creatures. This was long chalked up to ‘gaps’ in the fossil records, gaps that proponents of gradualism confidently expected to fill in someday when rock strata of the proper antiquity were eventually located. But all the fossil evidence to date has failed to turn up any such missing links . . . There is a growing conviction among many scientists that these transitional forms never existed.”
    Niles Eldredge, quoted in George Alexander, “Alternate Theory of Evolution Considered,” Los Angeles Times, November 19, 1978.

    “Gradualism is a concept I believe in, not just because of Darwin’s authority, but because my understanding of genetics seems to demand it. Yet Gould and the American Museum people [i.e., Eldredge] are hard to contradict when they say there are no transitional fossils. As a paleontologist myself, I am much occupied with the philosophical problems of identifying ancestral forms in the fossil record. You say that I should at least ‘show a photo of the fossil from which each type of organism was derived.’ I will lay it on the line – there is not one such fossil for which one could make a watertight argument.”
    Colin Patterson to Luther Sunderland, April 10, 1979, quoted in Luther .D. Sunderland, Darwin’s Enigma: Fossils and Other Problems, 4th ed. (El Cajon, CA: Master Book Publishers, 1988), 89.

    For the first decade after the paper was published, it was the most controversial and hotly argued idea in all of paleontology. Soon the great debate among paleontologists boiled down to just a few central points, which Gould and Eldredge (1977) nicely summarized on the fifth anniversary of the paper’s release. The first major discovery was that stasis was much more prevalent in the fossil record than had been previously supposed. Many paleontologists came forward and pointed out that the geological literature was one vast monument to stasis, with relatively few cases where anyone had observed gradual evolution. If species didn’t appear suddenly in the fossil record and remain relatively unchanged, then biostratigraphy would never work—and yet almost two centuries of successful biostratigraphic correlations was evidence of just this kind of pattern. As Gould put it, it was the “dirty little secret” hidden in the paleontological closet. Most paleontologists were trained to focus on gradual evolution as the only pattern of interest, and ignored stasis as “not evolutionary change” and therefore uninteresting, to be overlooked or minimized. Once Eldredge and Gould had pointed out that stasis was equally important (“stasis is data” in Gould’s words), paleontologists all over the world saw that stasis was the general pattern, and that gradualism was rare—and that is still the consensus 40 years later.
    Donald Prothero – American paleontologist, geologist, and author who specializes in mammalian paleontology.

    Leading Evolutionary Scientists Admit We Have No Evolutionary Explanation of Human Language – December 19, 2014
    Excerpt: Understanding the evolution of language requires evidence regarding origins and processes that led to change. In the last 40 years, there has been an explosion of research on this problem as well as a sense that considerable progress has been made. We argue instead that the richness of ideas is accompanied by a poverty of evidence, with essentially no explanation of how and why our linguistic computations and representations evolved.,,,
    (Marc Hauser, Charles Yang, Robert Berwick, Ian Tattersall, Michael J. Ryan, Jeffrey Watumull, Noam Chomsky and Richard C. Lewontin, “The mystery of language evolution,” Frontiers in Psychology, Vol 5:401 (May 7, 2014).)
    It’s difficult to imagine much stronger words from a more prestigious collection of experts.
    http://www.evolutionnews.org/2.....92141.html

    In fact Zach, I hold that if you can not bring yourself to admit the fact that the fossil record is discordant to Darwinism then you ought to rightly be banned from UD.

    Don’t worry though Zach, I am not a moderator. For some reason the moderators on UD feel it is OK to have a pathological liar such as yourself on UD.

    I guess they figure that you are so over the top in your intellectual dishonesty that you can only help ID.

  239. 239
    Zachriel says:

    bornagain: It is about you living in complete delusional denial of the fact that the fossil record is severely discordant with what Darwin predicted., i.e. it is about you constantly lying!

    As a general rule, if someone is delusional, they aren’t lying.

    bornagain: Contrary to popular belief, not all animal groups continued to evolve fundamentally new morphologies through time. The majority actually achieved their greatest diversity of form (disparity) relatively early in their histories.

    Meaning some don’t. In any case, Darwin posited that stasis would be prevalent in the historical record.

  240. 240
    bornagain says:

    Actually, whether someone is delusional or not does not negate whether the words coming from them or lies or not. (in fact, how we tell when a person is delusional is when their words (and actions) are grossly out of line with reality, i.e. when their words and actions are ‘lies’)

    Lies are lies, regardless of the mental state of the person uttering them. So which is it, or you lying purposely or are you lying because you are mentally ill?

    To give you the benefit of a doubt, I opt for mentally ill.

    Do you want to the see the studies proving that atheists are mentally ill?

  241. 241
    JoeCoder says:

    bornagain: lying purposely or are you lying because you are mentally ill?

    I’ve been having a good discussion with Zachriel so far. When this started I was interested in determining whether Mendel’s Accountant is an accurate simulation, and Zachriel has been helpful in probing my biases to raise objections I had not thought about. In the end I still think my view is correct, but I cannot have confidence in my own views unless I first expose them to scrutiny. If this discussion descends into insults it becomes much harder to do that. Sometimes I’m also wrong (and so are you) and I appreciate it when people don’t rub it in my face and call me names.

    I’m also not sure how you expect to convert anyone to your own view through insulting them. What is your end-goal here?

  242. 242
    JoeCoder says:

    Zachriel: in a world where dinosaur fossils are on display in museums across the world, how someone could reject that long history.

    I’m not a YEC and I’m not arguing for young ages. Rather–I’m arguing that there is enough conflicting data that we should be agnostic about the ages.

    There was a talk in 2012 by creationists at the American Geophysical Union/Asia Oceania Geosciences Society conference. In the laymanized version of their paper, they report 20 unmineralized samples of cretaceous and jurassic acrocanthosaurus, allosaurus, hadrosaur, triceratops, and apatosaur were C14 dated at the University of Arizona using both the AMS and beta-decay methods to 22-39k years old. They note, “Both [the triceratops and hadrosaur] bones were tested by a licensed lab for presence of collagen. Both bones did in fact contain some collagen.” Collagen is an animal protein so it can’t be a bacterial contaminant. At 13 minutes into the talk, several more lines of evidence are offered against contamination: AMS and beta-decay methods are in agreement, C14 concentrations decrease with distance from the fossils, and the C13 concentrations in the triceratops match expected values for an animal that consumes C3 carbon fixation system plants (those in temperate environments).

    The soft tissue itself with preserved DNA, osteocytes, and collagen should also not be in tact after millions of years. For a long time this was used as a (now failed) argument against Mary Schweitzer’s discoveries of soft tissue to insist that it could not be original.

    Yet the rocks around those bones strongly disagree! I wish I could just go one direction or the other in regard to the age of the fossil record, but because of things like this I’m stuck in cognitive dissonance. It’s frustrating.

    Zachriel: Scientists make expeditions around the world to find predicted intermediate fossils. Lucky guessers?

    I’m not going to overwhelm you with citations like BA has. But I do particularly like Don Prothero’s article in Skeptic Magazine where he says the fossil record is “vast monument to stasis, with relatively few cases where anyone had observed gradual evolution” It’s short and an easy read–would you have time to take a look? If I’m not mistaken, Darwin thought stasis might be an artifact of a poor record. In that article Prothero makes it a point that the stasis is real and confirmed by enough samples that it cannot be “bias in my sampling”.

    I’m also not impressed by the proposed fossil intermediates because of signal vs noise. As one example, take a look at this image of aardvarks, anteaters, and pangolins. Based on morphology we used to think the three were very close relatives. But genetics has now placed them within different orders of mammalia. For context: bats, whales, and humans are each a different order of mammals.

    But aardvarks, anteaters, and pangolins are MORE similar to one another than things like tiktaalik and its proposed fishapod cousins. The noise of homoplasy overwhelms any signal of transition. That and the Zachelmie prints show that animals were already leaving toe-prints on land 20 million years prior to tiktaalik splashing in the mud, at least according to the dates of nearby rocks.

    Zachriel: Your analysis [of redundant genes] has no way to separate evolution from design.

    I think it very much does separate evolution from design. The issue above highlighted by Mendel’s Accountant is that selection is not strong enough to preserve functional DNA. How could selection preserve sequences of backup systems that are only used in the rare cases when primary systems fail? And what there is not enough selective pressure to preserve, there’s certainly not enough to have created it.

    Yet in our own most fail-safe designs we commonly use redundant systems built in alternate ways from the primary systems. Check out this short comment about the Boeing 757, from Walter Bright who is one of my favorite engineers to follow.

    So I think this redundancy through disparate parts is one way that genomes are more like our own designs than they are like what we would expect evolutionary processes create. Tell me what you think?

  243. 243
    bornagain says:

    JoeCoder, I certainly don’t expect Zach to ever be ‘converted’ through my meek efforts and if he ever does become a Christian I will certainly consider it a bonafide miracle from God. Where God, in his mercy, changed Zach’s heart and revealed Himself to Zach in a personal way.

    I did not touch on your discussion with Zach regarding Mendel’s accountant and I only can comment on his dishonesty towards the fossil record which is what we were discussing. And that is exactly what I called his bluff on. i.e. He is being a dishonest liar in regards to the fossil record! That is a fact! It is not something that I purposely say to smear him! It is something I say primarily to state the fact that he is in fact a pathological liar in my dealings with him on the fossil record. It is why I requoted a few of the leading paleontologists on the fossil record from the other day. (I have many more quotes from many other paleontologists saying the same thing). He saw the quotes before, presented no evidence to the contrary, and repeated the same lies that the fossil record overwhelmingly supports Darwinism.

    This is not some nuanced programming language in a computer that is intelligently designed by a human to see whether Darwinism is feasible or not (a self-refuting proposition is ever there were one). These are stone cold hard fossils.

    I’m sure you are a sensitive soul and are open to reason. Yet, I’ve seen no such inclination in Zach. In fact Zach, in my dealings with him over several years, resolutely refuses to be honest on even the most trivial facts of empirical truth that I present.

    Your dealings in computer programming may be different with him, but I sincerely doubt that he is dealing completely straight with you in that area either.

    IMHO, he ought to be banned from UD for his repeated lying. But, like I said, the moderators on UD must think his over the top lies serve some purpose.

  244. 244
    JoeCoder says:

    I made a typo! Above I meant to say “bats, whales, and humans are each IN a different order of mammals”. For example humans are obviously not the only species of primate!

  245. 245
    Zachriel says:

    JoeCoder: I’ve been having a good discussion with Zachriel so far.

    Agreed, and we have already tentatively modified our position somewhat based on that discussion. While we don’t agree with Mendel’s methodology, partial truncation avoids at least some of the problems.

    JoeCoder: There was a talk in 2012 by creationists at the American Geophysical Union/Asia Oceania Geosciences Society conference.

    Carbon dating isn’t very useful on very old fossils, and there are a number of sources of error. Fossils are usually dated by looking at strata above and below that allow for other forms of radiometric dating. The great age of the Earth’s strata was determined long before radiometric dating, so geological methods provide an independent method.

    Darwin’s theory, of course, requires an old Earth. The greatest physicists of his time thought the Earth could only be a few million years old to still be hot inside. Geologists and biologists claimed otherwise. It was the discovery of radioactivity that explained why the Earth’s interior was still hot after billions of years. Lucky guess?

    JoeCoder: If I’m not mistaken, Darwin thought stasis might be an artifact of a poor record.

    Darwin: Many species when once formed never undergo any further change but become extinct without leaving modified descendents and the periods, during which species have undergone modification, though long as measured by years, have probably been short in comparison with the periods during which they retain the same form.

    JoeCoder: I’m also not impressed by the proposed fossil intermediates because of signal vs noise.

    So when Darwin predicted there would be fossils of hominids with small brains, and such organisms were found, it was luck? Or when Shubin led a successful expedition to the Canadian arctic to look in specific strata for a “fishapod”, it was luck?

    The geological record clearly shows a fossil succession, and the overall age is known to be ancient.

  246. 246
    Zachriel says:

    JoeCoder: As one example, take a look at this image of aardvarks, anteaters, and pangolins.

    Convergence is part of the theory of evolution.

    JoeCoder: The noise of homoplasy overwhelms any signal of transition.

    Genetics has helped resolve these discrepancies, as you point out.

    JoeCoder: The issue above highlighted by Mendel’s Accountant is that selection is not strong enough to preserve functional DNA.

    No. It purports to show that slightly deleterious mutations accumulate, not that strong selection doesn’t lead to adaptation.

    JoeCoder: How could selection preserve sequences of backup systems that are only used in the rare cases when primary systems fail?

    Because duplications continue to evolve and form new integrated networks. The difference is that with evolution, we predict and can often find evidence of how this occurred in a selectable, stepwise fashion.

  247. 247
    Mung says:

    JoeCoder:

    @Mung – Unlike most of the discussion on UD, I’m hoping to keep this a friendly and thus productive debate. Can you help me with that goal?

    Absolutely. Does Zachriel still claim there is a bug in the code of Mendel’s Accountant?

    That’s relevant, right?

  248. 248
    Zachriel says:

    Mung: Does Zachriel still claim there is a bug in the code of Mendel’s Accountant?

    Yes. Dividing fitness by a random number from zero to one (probability selection used in the original papers) to determine working fitness is non-biological and dilutes the signal from selection, especially when differences in fitness are small.

  249. 249
    JoeCoder says:

    I worry that we’re diverging into too many different topics for a productive discussion. But I’ll respond nonetheless.

    You say “carbon dating doesn’t work on very old fossils”, but how do you know their age unless you first date them? Based on the half life of carbon-14 there should be zero carbon-14 left after a couple hundred thousand years, except in some samples where a very small amount may be created through neutron capture from decaying uranium. But not nearly enough to give an age of 22-39 thousand years in samples of purified animal proteins.

    All radiometric dating is tricky. I think you could be equally skeptical of the dates from rocks. For example due to trapped argon or excess argon from lower layers.

    Zachriel: It was the discovery of radioactivity that explained why the Earth’s interior was still hot after billions of years. Lucky guess?

    As I said above, I think the Earth itself is billions of years old. For example, take a look at the graphs of ancient meteorite dates from a recent paper YEC geologist Andrew Snelling published in ARJ. They generally cluster around 4.55–4.57 Ga, and Snelling says they show no evidence of past rapid decay. That seems pretty unavoidable.

    Zachriel: Darwin: “Many species when once formed never undergo any further change”

    Darwin also said:

    Geology assuredly does not reveal any such finely-graduated organic chain; and this, perhaps, is the most obvious and serious objection which can be urged against the theory. (The Origin of Species). The explanation lies, as I believe, in the extreme imperfection of the geological record.

    So that is why I said Darwin believed missing species were an artifact of a poor record. Apparently we’re both right and Darwin believed gradations were missing due to a poor record, and because he thought evolution happens in bursts.

    Zachriel: when Shubin led a successful expedition to the Canadian arctic to look in specific strata for a “fishapod”, it was luck?

    Probably so, yes. I expect you could find fishapods in a wide variety of strata if you spent enough time looking. And the Zachelmie prints show he wasn’t looking in the correct strata to begin with.

    Zachriel: When Darwin predicted there would be fossils of hominids with small brains

    Again, probably so. If genetic entropy is true then selection primarily removes variation, so we should expect ancient organisms to be more varied than those alive today. For the record I do think sapiens, erectus, ergaster, neanderthals, and floresiensis share a common ancestor, and among most of those we have particularly good fossil transitions.

    Zachriel: “aardvarks, anteaters, and pangolins” – Convergence is part of the theory of evolution.

    If false links are better than “true” links then no argument can be made from the “true” links.

    Zachriel: Genetics has helped resolve these discrepancies, as you point out.

    We’re talking using fossils to place extinct species into a progression–there’s no genetic data available for them. Besides, while genetic data can show how similar or distant organisms are to one another, I don’t think it’s of much help either. Take a look at one of Sean B. Carroll’s papers on the topic, particularly figure 2. I’m not convinced those phylogenies are any clearer than what you’d get trying to build trees from designed objects.

    Zachriel: “Mendel’s Accountant [shows] selection is not strong enough to preserve functional DNA.” – No. It purports to show that slightly deleterious mutations accumulate

    Having deleterious mutations accumulate in functional DNA is the same thing as selection not preserving functional DNA.

    Zachriel: Because duplications continue to evolve and form new integrated networks.

    With an almost complete lack of selection to do so, since there are already primary systems performing the same task? I don’t find that compelling in the least.

  250. 250
    JoeCoder says:

    Zachriel: Dividing fitness by a random number from zero to one (probability selection used in the original papers) to determine working fitness is non-biological and dilutes the signal from selection

    Based on the formula you provided in comment #209, even probability selection in Mendel’s Accountant doesn’t dilute selection enough. If anything it looks like Mendel needs to dilute selection even MORE before it is biologically realistic. Why do you think it needs to be diluted less?

    Zachriel: especially when differences in fitness are small.

    We’ve already discussed why it is realistic for smaller differences to be more diluted than larger differences – see comment #198. I don’t understand why you still think this is an issue?

  251. 251
    Virgil Cain says:

    Shubin- Had Shubin had the knowledge of the Polish tetrapod tracks he would not have been looking for a fish-a-pod where he found Tiktaalik, You don’t go looking for evidence of a transition that happened millions of years earlier.

  252. 252
    Zachriel says:

    JoeCoder: You say “carbon dating doesn’t work on very old fossils”, but how do you know their age unless you first date them?

    Geological dating, due to fossil placement in strata, provides relative dating, as well as attesting to the great age of fossils. Radiometrically, by dating of volcanic layers above and below the fossil. Biologically, from the theory of evolution. That’s three independent means reaching the same conclusion.

    JoeCoder: Based on the half life of carbon-14 there should be zero carbon-14 left after a couple hundred thousand years, except in some samples where a very small amount may be created through neutron capture from decaying uranium.

    Other scientists who have looked at the study believe that contamination explains the results. In addition, it’s contradicted by several other independent tests.

    JoeCoder: As I said above, I think the Earth itself is billions of years old.

    As is the geology of the Earth.

    JoeCoder: So that is why I said Darwin believed missing species were an artifact of a poor record.

    As well as due to evolutionary stasis.

    Zachriel: when Shubin led a successful expedition to the Canadian arctic to look in specific strata for a “fishapod”, it was luck?

    JoeCoder: Probably so, yes.

    IDers never seem to be “lucky”. Odd that.

    JoeCoder: I expect you could find fishapods in a wide variety of strata if you spent enough time looking.

    Well, you might find fishapods after the divergence, but not before. While we can’t say exactly when that divergence occurred, it certainly happened after the evolution of lobed fish.

    JoeCoder: For the record I do think sapiens, erectus, ergaster, neanderthals, and floresiensis share a common ancestor, and among most of those we have particularly good fossil transitions.

    Why stop there?

    JoeCoder: If false links are better than “true” links then no argument can be made from the “true” links.

    Not sure what that means. It can be difficult to unravel specific branches of the tree, even though the overall tree is clearly evident.

    JoeCoder: We’re talking using fossils to place extinct species into a progression–there’s no genetic data available for them.

    Fossils show both a clear pattern of succession, and a clear tree.

    JoeCoder: I’m not convinced those phylogenies are any clearer than what you’d get trying to build trees from designed objects.

    In evolution, the closer organisms are related, the more difficult to distinguish. Therefore, the closer you come to the root, not only do you have only limited evidence, but they become more and more difficult to distinguish. That doesn’t mean that the tree isn’t clearly evident for other taxa, such as eukaryotes.

    JoeCoder: Having deleterious mutations accumulate in functional DNA is the same thing as selection not preserving functional DNA.

    No. That’s not the case, even in Mendel. If you have a strongly selective trait, it should propagate through the population.

    JoeCoder: With an almost complete lack of selection to do so, since there are already primary systems performing the same task? I don’t find that compelling in the least.

    Again, that is incorrect. In evolution, they continue to integrate with the overall network, providing robustness and novel functions.

    JoeCoder: Based on the formula you provided in comment #209, even the most random mode Mendel’s Accountant offers doesn’t dilute selection enough.

    We ran a simple simulator. It only tests the first generation, so we don’t have to worry about fecundity. The population is 1000, reproductive rate 5, fitness = 1.0, probability selection, 100 trials.

    There is a novel mutation in one individual. Here is the rate of extinction after one generation given the fitness of the mutant. (Fitness of 1.0 is neutral. It should go extinct 4/5 of the time in the first generation.)

    fitness 1.00, 80%
    fitness 1.05, 80%
    fitness 1.10, 73%
    fitness 1.15, 78%
    fitness 1.20, 79%
    fitness 1.25, 76%

    Here’s the top of the last trial. What was ranked 913 with a fitness of 1.0 is now ranked first with a working fitness over two thousand.

    913 – 2,673.66
    90 – 1,040.12
    879 – 881.11
    992 – 577.09
    750 – 354.32
    751 – 321.45
    308 – 257.87
    607 – 227.90
    760 – 193.95
    … …

    Sure, “time and chance happens to them all”, but it not usual for Barney Fife to get all the girls.

  253. 253
    JoeCoder says:

    Zachriel: We ran a simple simulator. It only tests the first generation.

    I think only running that simulation one generation is the problem. You’ll get a lot of noise as your results demonstrate. But over many generations that randomness averages out. For example, your person #913 is very unlikely to be ranked near the top again in the second generation.

    Selection in Mendel is already working more efficiently than you said it should according to the formula you cited in comment #209.

    Zachriel: Other scientists who have looked at the study believe that contamination explains the results. In addition, it’s contradicted by several other independent tests.

    Who? At the end of that talk I linked the guy is begging other researchers to perform the same tests on their own bones so their data can be checked. Jack Horner (Mary Schweitzer’s boss) was even [offered a $23k grant](http://kgov.com/files/museumoftherockiestrex2.jpg) to C14 date his own soft-tissue dinosaur bones. He agreed it was more than enough money but refused because [it would help creationists](http://www.youtube.com/watch?v=8T3rEX4zq_4).

    Other than Mark Armitage who has confirmed their results with dates from his own soft-tissue triceratops horn, who else is C14 dating soft tissue dinosaur bones? What is the evidence of contamination?

    Zachriel: IDers never seem to be “lucky”. Odd that.

    ID makes no prediction either way about where fishapods should be found. Evolutionary theory predicts the oldest fishapods should predate the oldest tetrapod tracks and at present we have the reverse. I’m not sure why that’s lucky? Shubin may have thought he was lucky but his luck has run out.

    Zachriel: “sapiens, erectus, ergaster, neanderthals, and floresiensis share a common ancestor” Why stop there?

    Because you can get a great deal of variation just through allele shuffling and loss. These are well documented phenomenon and probabilisticly easy. But phenotypic variation hits a hard limit once your population already has all the alleles that amplify a particular trait. To go beyond this, you need evolution to create new alleles with specific functions. Per our main topic of debate here, evolution shouldn’t even be able to preserve existing function. So positing it to create lots of new variation is very problematic.

    Zachriel: “Having deleterious mutations accumulate in functional DNA is the same thing as selection not preserving functional DNA.” No. That’s not the case, even in Mendel. If you have a strongly selective trait, it should propagate through the population.

    It sounds like we’re now talking about completely different things here. My original point that you contested was “Mendel’s Accountant shows selection is not strong enough to preserve functional DNA.” A highly beneficial allele will still spread through the population but more deleterious mutations will accumulate in other alleles as it does so–the total effect is still a net negative.

    Zachriel: Fossils show both a clear pattern of succession, and a clear tree.

    I disagree that it’s any clearer of a tree than a tree you’d get trying to build one from designed objects. iPhones and androids both share code for zlib, webkit, and openGL, while an ICBM missile is clearly the outgroup. Besides, I already cited aardvarks, anteaters, and pangolins of an example that clearly contradicts the expected tree:

    What fascinates me most is the tremendous incongruence between the morphological and molecular data,’ says Mark Springer, an evolutionary biologist at the University of California, Riverside. For example, grouping animals according to their anatomy alone puts physically similar species such as pangolins, anteaters and aardvarks in the same tight group, whereas molecular data shows that they belong to different orders.

    Also from Sean B. Carroll’s paper that I cited above:

    Molecular systematics has surmounted the confusion stemming from comparisons of morphologically disparate species to reveal unexpected evolutionary relationships such as the Afrotheria, a clade composed of strikingly different mammals including elephants, aardvarks, manatees, and golden moles

    Zachriel: “If false links are better than “true” links then no argument can be made from the “true” links.” – Not sure what that means.

    I want to stick to this point because I think it’s very important. Suppose all we have is morphological data–which is the truth when looking at fossils. Suppose morphological distance could be quantified into a single number. Aardvarks and anteaters have a morphological distance of perhaps 5, and tiktaalik and ichthyostega a distance of perhaps 12. Yet you conclude that distance of 12 is beyond a doubt evidence that either one evolved into the other or that they are close cousins in an evolutionary lineage? Even when two mammals with a distance of 5 are not closely related at all? That is being selective with data.

    Zachriel: In evolution, they continue to integrate with the overall network, providing robustness and novel functions.

    Without any selection? Having mutations (sans selection) building complex things is just storytelling and contrary to any reasonable probability. Even with selection operating and without the issue of deleterious load I think there are serious issues with evolution being able to craft sufficient amounts of specific functional sequences. But I have avoided talking about other arguments to avoid too many topics at once.

  254. 254
    Zachriel says:

    JoeCoder: I think only running that simulation one generation is the problem.

    Extinction is extinction. There’s no coming back. The problem is that Mendel’s method is non-biological. Unlike the standard biological selection coefficient, the parameter doesn’t relate to anything real. It may “look right”, but there’s no way to tell.

    Also, individual fertility seems to be based on average phenotypic fitness, not individual phenotypic fitness.

    do i=1,current_pop_size
    post_sel_fitness = post_sel_fitness + fitness(i)
    mean_pheno_fitness = mean_pheno_fitness + pheno_fitness(i)
    end do

    post_sel_fitness = post_sel_fitness/current_pop_size

    if(fitness_dependent_fertility) then
    fitness_adjusted_offspring =
    & num_offspring*sqrt(post_sel_fitness)

    Barney Fife has as many children as Genghis Khan (further diluting selection).

    Baumgardner et al., Mendel’s Accountant: A New Population Genetics Simulation Tool for Studying Mutation and Natural Selection 2008: Truncation selection eliminates those individuals in the new generation whose phenotypic fitness falls below an appropriate cutoff value.

    Truncation is based on what they call working fitness, not phenotypic fitness. Working fitness, of course, is only tenuously related to phenotypic fitness.

    JoeCoder: At the end of that talk I linked the guy is begging other researchers to perform the same tests on their own bones so their data can be checked.

    There’s too many other lines of evidence that contradict the carbon-testing. If they are convinced, then they have to find independent lines of evidence.

    JoeCoder: Evolutionary theory predicts the oldest fishapods should predate the oldest tetrapod tracks and at present we have the reverse.

    The oldest fishapods should predate the oldest tetrapods, which is not the same thing at all. Tiktaalik is probably not the oldest fishapod.

    JoeCoder: I’m not sure why that’s lucky?

    Because he said I will pull a fishapod out of the Arctic wasteland, and then pulled a fishapod out of the Arctic wasteland. Repeat this story a thousand times for all sorts of transitional fossils. A thousand lucky guesses.

    So unlike ID.

    Zachriel: Zachriel: “sapiens, erectus, ergaster, neanderthals, and floresiensis share a common ancestor” Why stop there?

    JoeCoder: Because you can get a great deal of variation just through allele shuffling and loss.

    But the tree structure is still there; and the closer you come to the common ancestor, the more difficult to distinguish, just as expected of branching descent. Once you agree there’s a common Homo ancestor, then there is no reason to stop.

    JoeCoder: A highly beneficial allele will still spread through the population but more deleterious mutations will accumulate in other alleles as it does so–the total effect is still a net negative.

    If Mendel’s doesn’t show that strong selection accumulates in a population, then it is clearly contrary to observation, and the discussion is over. What the authors will state is that strongly selective traits will tend to propagate in a population, but that they are simply too rare to compensate for the accumulation of slightly deleterious mutations.

    JoeCoder: I disagree that it’s any clearer of a tree than a tree you’d get trying to build one from designed objects.

    Go ahead. Try vehicles as an instance. Construct a nested hierarchy. It doesn’t have to be comprehensive, but should have at least a few levels. You will find that there are many different, equally rational nested hierarchies.

    JoeCoder: I already cited aardvarks, anteaters, and pangolins of an example that clearly contradicts the expected tree

    As Darwin pointed out, particular traits will defy the tree due to convergence, but that the entire structure will still show the pattern. In this case, the molecular evidence strongly supports the nested hierarchy.

    JoeCoder: Suppose all we have is morphological data–which is the truth when looking at fossils. Suppose morphological distance could be quantified into a single number. Aardvarks and anteaters have a morphological distance of perhaps 5, and tiktaalik and ichthyostega a distance of perhaps 12.

    The tree is not defined by distance, but by the nested hierarchy. Even though there are anomalies, the overall pattern objectively exists.

    JoeCoder: Without any selection?

    With selection. The typical pattern is a structure A, duplicated to A-A, then polar migration from specialization to A1-A2, which are now co-dependent. Duplicate this new superstructure A to AB, to A1′-A2′-B1-B2. And so on.

  255. 255
    Zachriel says:

    Here’s another source of randomness.

    noise = sqrt(geno_fitness_variance*(1. – heritability) /heritability + non_scaling_noise**2)

    do i=1,total_offspring
    pheno_fitness(i) = fitness(i) + random_normal() * noise + 1.d-15*i
    end do

    Currently, the default is heritability = 0.2, while non-scaling noise = 0.05. Low heritability adds a lot of noise to the phenotypic fitness even before we get to the divide by random problem.

  256. 256
    JoeCoder says:

    Zachriel: The problem is that Mendel’s method is non-biological. Unlike the standard biological selection coefficient, the parameter doesn’t relate to anything real. It may “look right”, but there’s no way to tell.

    In your comment #209 you wrote:

    In a large population, the chance of fixation for a new beneficial mutation is about 2s.* If a variant has a selective advantage of 0.1, then it will fix 20% of the time.

    That formula creates a relationship such that if a variant has a selective advantage of 0.01, its odds of fixation are 2%. Likewise, the scaling applied by Mendel’s Accountant in probability selection makes it so that if a variant’s selection coefficient is 10 times smaller, it is 10 times less likely to fix. So therefore it does follow the biologically realistic curve provided by your formula.

    Even still my own run showed Mendel’s probability selection is twice as efficient as what your formula predicts. Perhaps it should be scaling the randomness by another factor of two in order to compensate? Or perhaps my population size of 2000 was too small.

    In comment #136 I wrote about my simulation of fixing beneficial alleles:

    Starting pop = 2000
    Mutation rate = 0
    Selection = Unrestricted Probability Selection

    I seeded the population with five individuals each having an allele [heterozygous] that gives them a 10% fitness bonus.

    I wondered if this may be an anomaly, so I ran it with the same parameters three more times. All three times, two of the five beneficial mutations fixed.

    Zachriel: Currently, the default is heritability = 0.2, while non-scaling noise = 0.05.

    The Mendel manual states:

    0.2 is an extremely generous heritability value.

    For simplicity, the default value is 0.05, but reasonable values probably exceed 0.01 and might exceed 0.1.

    Do you have any sources that suggest different values should be used?

    Zachriel: If Mendel’s doesn’t show that strong selection accumulates in a population

    As you know selection doesn’t accumulate in a population. I think you’ve mistyped something in this sentence and that’s causing me to not understand what you mean.

    In the original 2007 Genetic Entropy paper, The Mendel team used a beneficial rate of 1%, which over-generously high.

  257. 257
    JoeCoder says:

    Zachriel: There’s too many other lines of evidence that contradict the carbon-testing. If they are convinced, then they have to find independent lines of evidence.

    Soft tissue throughout the fossil record and genetic entropy also support a young timeline. And as you say there are other lines of evidence that argue against. Hence I am agnostic about the ages instead of adopting a YEC perspective that would be more consistent with my Christian worldview.

    CMI has a list of 101 evidences for a young age of the earth and the universe, while RationalWiki has a list of 28 evidences against a recent creation. Both lists contain some rather strained arguments and the vast majority I’ve never explored in enough depth to have an informed view.

    Zachriel: Try vehicles as an instance… You will find that there are many different, equally rational nested hierarchies.

    I’m sure there would be. My point is we see the same thing in biology. Figure 2 from Sean Carrol’s Paper showed this. If you need more examples, take a look at this diagram that I annotated from figure 3 here. It shows the number of genes shared by humans, mice, chickens, and zebrafish. I underlined the gene counts that are shared by some but not all species–those that tell an evolutionary story. In green are the ones that match the expected progression, while in red are those that contradict it. Overall, 51% conflict. Mammals are more than twice as related to fish as they are to chickens (2059 vs 892 genes), which is the opposite of what evolutionary theory predicts.

    I don’t see how this is compatible with your statement that “the molecular evidence strongly supports the nested hierarchy.” Yet another example:

    [Michael] Syvanen recently compared 2000 genes that are common to humans, frogs, sea squirts, sea urchins, fruit flies and nematodes. In theory, he should have been able to use the gene sequences to construct an evolutionary tree showing the relationships between the six animals. He failed. The problem was that different genes told contradictory evolutionary stories. This was especially true of sea-squirt genes. Conventionally, sea squirts – also known as tunicates – are lumped together with frogs, humans and other vertebrates in the phylum Chordata, but the genes were sending mixed signals. Some genes did indeed cluster within the chordates, but others indicated that tunicates should be placed with sea urchins, which aren’t chordates. ‘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

    At this point you can posit reasons for the discordance such as incomplete lineage sorting, convergence, or horizontal transfers. But you can’t say trees support evolution while simultaneously trying to explain why there are no trees.

    Zachriel: Duplicate this new superstructure A to AB, to A1?-A2?-B1-B2.

    That ignores my citation above that redundancy is primarily NOT from duplication. As I cited in comment #227 about a study in yeast:

    I used functional genomics data from the yeast Saccharomyces cerevisiae to test the hypotheses related to the following: if gene duplications are mostly responsible for robustness, then a correlation is expected between the similarity of two duplicated genes and the effect of mutations in one of these genes. My results demonstrate that interactions among unrelated genes are the major cause of robustness against mutations.

    ————–

    Zachriel, I think I’ve lost interest in continuing our discussion any further. At first your comments made me doubt Mendel was being realistic, but we’ve already explored this in sufficient depth that my only remaining doubt is that Mendel may actually be TOO generous in regard to the strength of selection.

    If you’re the type of person that always has to have the last word, then go for it. This discussion has been very time consuming, but my questions have already been answered so I have no need to continue.

  258. 258
    Zachriel says:

    JoeCoder: Do you have any sources that suggest different values should be used?

    To make sure we are talking about the same thing, what is the heritability of a person having five fingers on each hand? What is the heritability of wearing lipstick?

    JoeCoder: Mammals are more than twice as related to fish as they are to chickens (2059 vs 892 genes), which is the opposite of what evolutionary theory predicts.

    No. That’s not what the diagram shows. A particular lineage can lose genes or gain genes, but when you look at sequences, especially silent substitutions, you can still reconstruct the expected phylogeny.

    JoeCoder: “At this point you can posit reasons for the discordance such as incomplete lineage sorting, convergence, or horizontal transfers.

    Tunicates may have arisen through hybridization. Again, just because the pattern isn’t perfect doesn’t mean the pattern doesn’t exist. Does the Earth follow an elliptical path around the Sun?

    JoeCoder: That ignores my citation above that redundancy is primarily NOT from duplication.

    That supports evolution even more strongly. Evolution often results in overlapping functions. It’s a consequence of network evolution, or as the author states, “This type of robustness is probably an evolved response of genetic networks to stabilizing selection.”

  259. 259
    Zachriel says:

    JoeCoder: my only remaining doubt is that Mendel may actually be TOO generous in regard to the strength of selection.

    Our simple and easily repeatable experiments with the parameters given show that the signal from selection is highly obscured. It’s a situation where Barney Fife and Genghis Khan have the same number of children.

  260. 260
    JoeCoder says:

    Zachriel, I had another thought about how to test this. See this simple simulation I put together that tests the outcome of Probability Selection in Mendel’s Accountant:

    http://jsfiddle.net/p1prvd4h/

    Barney Fife (fitness = 1.0) and Genghis Khan (fitness = 1.1) are sorted by Mendel’s probability selection algorithm 1 million times–dividing by a random number between one and infinity. Genghis Khan comes out ahead 20% of the time. Even though he should only come out ahead 10% of the time.

    Therefore Probability Selection in Mendel’s Accountant is TWICE as efficient as it should be. This also explains why exactly twice as many beneficial mutations are fixing as what should, according to your own formula. (As I explained in comment #210).

    To get correct results instead of having overly strong selection, Mendel actually needs to divide by a random number squared.

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