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Can new genes arise from junk DNA?

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From Quanta Magazine:

Emerging data suggests the seemingly impossible — that mysterious new genes arise from “junk” DNA.

Genes, like people, have families — lineages that stretch back through time, all the way to a founding member. That ancestor multiplied and spread, morphing a bit with each new iteration.

For most of the last 40 years, scientists thought that this was the primary way new genes were born — they simply arose from copies of existing genes. The old version went on doing its job, and the new copy became free to evolve novel functions.

Certain genes, however, seem to defy that origin story. They have no known relatives, and they bear no resemblance to any other gene. They’re the molecular equivalent of a mysterious beast discovered in the depths of a remote rainforest, a biological enigma seemingly unrelated to anything else on earth.

The mystery of where these orphan genes came from has puzzled scientists for decades. But in the past few years, a once-heretical explanation has quickly gained momentum — that many of these orphans arose out of so-called junk DNA, or non-coding DNA, the mysterious stretches of DNA between genes. “Genetic function somehow springs into existence,” said David Begun, a biologist at the University of California, Davis. More.

Hmmm. Whenever scientists use terms like “somehow springs into existence,” find your boots, your bicycle lock key, or your car keys.

But this is a good conversation to be having.

Researchers are beginning to understand that de novo genes seem to make up a significant part of the genome, yet scientists have little idea of how many there are or what they do. What’s more, mutations in these genes can trigger catastrophic failures. “It seems like these novel genes are often the most important ones,” said Erich Bornberg-Bauer, a bioinformatician at the University of Münster in Germany.

Evolution isn’t what we used to think.

See also: The Myth of Junk DNA

and

Talk to the fossils: Let’s see what they say back.

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114 Replies to “Can new genes arise from junk DNA?

  1. 1
    Mapou says:

    “Genetic function somehow springs into existence,” said David Begun, a biologist at the University of California, Davis.

    Not very Darwinian, I would say. Where is the natural selection? Where are the random mutations?

  2. 2
    JDH says:

    “For the invisible things of him from the creation of the world are clearly seen, being understood by the things that are made, even his eternal power and Godhead; so that they are without excuse:”

  3. 3
    PaV says:

    From Quanta:

    Some scientists say they may even be common. 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 at the Hospital del Mar Research Institute in Barcelona, who presented the research. “But people have started seeing it more and more.”

    This mirrors the dilemna that electrophoresis created for Darwinists in the 60’s, leading to Kimura’s “Neutral Theory.” NT is Darwinism without natural selection: an oxymoron.

    Now, the EVO’s can’t get away from the fact the de novo genes are abundant. This ought to, right now, without a second’s more delay, debunk Darwinism, population genetics, and the whole nine yards. But, don’t hold your breath.

    With the rise of whole genome analysis (WGA), with it becoming more prevalent, accurate, and cheaper, this was the risk the Darwinists were running: that de novo genes would appear, not allowing them to any longer rationalize how new genes (and functions) could arise via gene duplication. The day of reckoning is upon them. They’re running out of “just-so” stories (although I might be very wrong in underestimating their ability to imagine implausible scenarios, and then swallow them. For example, the NT was first vilified before being swallowed up into Darwinian lore.). We’re living in interesting times.

  4. 4
    PaV says:

    Some more from Quanta:

    Yet if life’s toolkit is so limited, how could evolution generate the vast menagerie we see on Earth today? “If new parts only come from old parts, we would not be able to explain fundamental changes in development,” Bornberg-Bauer said.

    The first evidence that a strict duplication model might not suffice came in the 1990s, when DNA sequencing technologies took hold. Researchers analyzing the yeast genome found that a third of the organism’s genes had no similarity to known genes in other organisms. At the time, many scientists assumed that these orphans belonged to families that just hadn’t been discovered yet. But that assumption hasn’t proven true. Over the last decade, scientists sequenced DNA from thousands of diverse organisms, yet many orphan genes still defy classification. Their origins remain a mystery.

    Ouch!!! This has gotta hurt.

  5. 5
    PaV says:

    The article that keeps on giving:

    Scientists also want to understand how de novo genes get incorporated into the complex network of reactions that drive the cell, a particularly puzzling problem. It’s as if a bicycle spontaneously grew a new part and rapidly incorporated it into its machinery, even though the bike was working fine without it. “The question is fascinating but completely unknown,” Begun said.

    A human-specific gene called ESRG illustrates this mystery particularly well. Some of the sequence is found in monkeys and other primates. But it is only active in humans, where it is essential for maintaining the earliest embryonic stem cells. And yet monkeys and chimps are perfectly good at making embryonic stem cells without it. “It’s a human-specific gene performing a function that must predate the gene, because other organisms have these stem cells as well,” McLysaght said.

    “A human-specific gene performing a function that must predate the gene . . .”

    So, if the ancestral organisms don’t have the gene, then where did it come from? Yet, even if they didn’t have the gene, they must have had the function, else the stem cells would have been affected. However, if the ancestors have the function, then advantage can NS use to “evolve” the gene? [What came first, the chicken or the egg?]

    The EVO’s must not be sleeping well at night these days.

  6. 6
    bFast says:

    The development of gene families seems potentially darwinian. We still, of course, have to wrestle with where the first gene in the family came from. If there were a single gene family — if all genes could be traced back to a single ancestor gene, then Darwinism would be writing a compelling story.

    I remember dialoguing a few years back on a different site. I was dialoguing about de novo genes with what appeared to be a biologist. He suggested that the human lineage should have no more than one or two de novo genes, and that those genes should play a minor role. This smacked of a message that wasn’t too inconsistent with Darwinian prediction.

    However, the ID scientists have been talking for a long time about the statistical chance of a gene arising from junk. They would suggest that even the “one or two” position is painfully implausible. That de novo genes are common, and important, is just so very “not predicted” by the Darwinian model.

    I see de novo genes to be a major challenge to the theory.

  7. 7
    tjguy says:

    Researchers are beginning to understand that de novo genes seem to make up a significant part of the genome, yet scientists have little idea of how many there are or what they do. What’s more, mutations in these genes can trigger catastrophic failures. “It seems like these novel genes are often the most important ones,” said Erich Bornberg-Bauer, a bioinformatician at the University of Münster in Germany.

    “De novo genes make up a significant part of the genome.”

    This was NOT predicted by evolution. The opposite was predicted. In other words, the whole theory of evolution was based upon false assumptions about the genome and now we see that the genome does not support their claims.

    “Scientists have little idea of how many there are or what they do.” Or, for that matter, of where they came from!

    Yet, evolution is a fact and the genome is evidence for evolution???

    I see. I wonder if the text books will be changed to reflect this fact/reality or if kids will simply continue to be snowed with evolutionary claims that are not supported by the data.

    Mutations in these genes can cause catastrophic failures – and these are the genes that are least understood! Yet evolution is a fact???

    It seems these mysterious genes are the most important ones yet no one knows how many there are, where they came from, or what they really do.

    Yet evolution is a fact. There is no need to sweat the minor details.

    And these evolutionists complain when people don’t believe them and swallow their ad hoc explanations whole.

    It seems to me that they aren’t as bright as they seem to think they are. Or perhaps, we are not as dumb as they think/hope we are.

  8. 8
    Mapou says:

    PaV:

    Now, the EVO’s can’t get away from the fact the de novo genes are abundant. This ought to, right now, without a second’s more delay, debunk Darwinism, population genetics, and the whole nine yards. But, don’t hold your breath.

    Darwinian evolution has been debunked many times over. One more humiliation will neither hurt it nor help it. But this fight was never about science, right?

  9. 9
    Box says:

    “How does novel gene become functional? How does it get incorporated into actual cellular processes?” McLysaght said. “To me, that’s the most important question at the moment.”

    Exactly my question. Assume that a perfect new gene is offered by random mutation. What is the next step towards expression / function? Where does the regulation come from? Without regulation there is no function. Will there be some random placement of transcription factors — a blind search for the starting and end position? Preceded by nucleosome / histone modifications?
    If a new protein is produced, what regulates its concentration so that it can be tolerated by the organism? How does the protein get to its proper position? And so forth.

    IOW how do you build gene- and protein-regulation from scratch?

    And how does all the experimenting stay within the boundaries of homeostasis? How can an unregulated (or even poorly regulated) new gene not be a huge threat to the organism?

  10. 10
    Box says:

    // follow up #9 //

    The irony is killing. A novel gene from junk-DNA, it sure is every atheist’s dream, right? Okay, now we find de novo genes in abundance — let’s assume, arguendo, that they magically appear from junk-DNA.

    Only now they start to realize that — given materialism — there is (still) absolutely no way forward from here:

    Scientists also want to understand how de novo genes get incorporated into the complex network of reactions that drive the cell, a particularly puzzling problem. It’s as if a bicycle spontaneously grew a new part and rapidly incorporated it into its machinery, even though the bike was working fine without it. “The question is fascinating but completely unknown,” Begun said.

    “How does novel gene become functional? How does it get incorporated into actual cellular processes?” McLysaght said. “To me, that’s the most important question at the moment.”

    It makes one wonder what the big idea was all along.

  11. 11
    bornagain77 says:

    Moreover, the essential genes were somehow incorporated into the ‘bicycle’ while the bicycle was being peddled, i.e. while the cell was busy being alive.

  12. 12
    Silver Asiatic says:

    Cue wd400:

    “Why do you think this is a problem for evolution”?

    Then days later.

    “We knew about all of this decades ago.”

  13. 13

    the logic! the logic!
    It’s a good thing we had that junk DNA around because it provides us with de novo genes…

    It’s a good thing my parents named me Rob, because that’s what everyone calls me…

  14. 14
    Silver Asiatic says:

    This one is beyond belief. I would have thought it was a satire.

    “Genetic function somehow springs into existence,” said David Begun, a biologist at the University of California, Davis.

    He obviously doesn’t understand evolution. First we have junk. Then we have new genes. He’s confused. They don’t “spring” into existence. They “arise” or in some cases “emerge”.

    Ahhhh – even better. They don’t “spring into existence”, they’re actually “selected” from junk. 🙂

    They might be able to salvage Darwin that way.

  15. 15
    Dr JDD says:

    Actually, I see this one being spun around to fit the narrative.

    Complex organisms can gain complexity through De novo gene arisal…which needs junk DNA…which complex organisms have more of…which is WHY they are complex…which is why junk DNA has pervaded NS despite being such an expense to the organism to replicate….but the junk DNA provides benefit as it allows complexity through novel gene appearance.

    Just what was predicted all along.

  16. 16
    PaV says:

    But Begun and collaborators found several genes that were present in only one or two species and not others, suggesting that these genes weren’t the progeny of existing ancestors. Begun proposed instead that random sequences of junk DNA in the fruit fly genome could mutate into functioning genes.

    Yet creating a gene from a random DNA sequence appears as likely as dumping a jar of Scrabble tiles onto the floor and expecting the letters to spell out a coherent sentence. The junk DNA must accumulate mutations that allow it to be read by the cell or converted into RNA, as well as regulatory components that signify when and where the gene should be active. And like a sentence, the gene must have a beginning and an end — short codes that signal its start and end.

    You’ll notice that this is exactly how IDers approach these types of questions. Yet, when we do, we’re told we don’t understand probabilities, we don’t understand evolution, etc., etc. But, then, when it comes to analyzing how novel genes come about, they use it to rule out the possibility of the new gene arising from nowhere. So, I guess we do understand evolution, and we do understand probabilities.

  17. 17
    PaV says:

    Dr JDD:

    Will the tautologies ever end? No need answering.

  18. 18
    wd400 says:

    Complex organisms can gain complexity through De novo gene arisal…which needs junk DNA…which complex organisms have more of…which is WHY they are complex…which is why junk DNA has pervaded NS despite being such an expense to the organism to replicate

    That’s not possible, of course. But something not so far from it might well be.

    For a big hulking multicellular creature the cost of one more ALU/SINE/repeat/transcript is so small as to make little difference. So such junk accumulates. There is good evidence for this by the way. All else being equal, creatures with high energetic needs (bats and birds for instance) for which selection agaist junk would be stronger have smaller genomes than those with little eneregetic constraint (salamanders have huge genomes). Likewise, organisms with large effective population sizes(and therefore strong selection) generally have smaller genomes. Multicellular creates of course generally have low effective population sizes.

    So, if de novo genes do indeed play an important role in evolutoin, complexity could indeed beget complexity. Complex organisms, by their nature, are more likely to accrue junk. That junk is more likely to generate new complexity and away we go. Something not unlike the idea of constructive neutral evolution.

    I have to admit I don’t quite understant the glee in the rest of the thread. It is certainly true that we didn’t think de novo genes would play a big role in evolution. But if they do it seems that biological function is easier to find in sequence space than we had previously thought. It’s hard to imagine, for instance, that humans are carrying around a Poldi because it was designed to later become a gene in mice!

  19. 19
    wd400 says:

    SA,

    “Why do you think this is a problem for evolution”?

    Then days later.

    “We knew about all of this decades ago.”

    It’s certainly very common for IDers to make a bigfuss about some new finding without saying why it’s relevant to evolution. News here, for instance, has dedicated many column inches to HGT without ever explaining why it a problem for evolutionary biology.

    Likewise, people frequently make a lot of noise about topics that are actually core evolutionary biology. My favorite is that radical idea that the environment influences gene expression (i.e. quantitative genetics).

    Those points seem relevant, so I often point them out.

  20. 20
    REW says:

    bFast

    However, the ID scientists have been talking for a long time about the statistical chance of a gene arising from junk. They would suggest that even the “one or two” position is painfully implausible. That de novo genes are common, and important, is just so very “not predicted” by the Darwinian model.

    I’d say that if we take the calculations of Doug Axe and Steven Meyer seriously, we’d have to conclude that if we looked at 10,000 proteins in each of the 20 million species on earth and then looked at a trillion identical planets each with 20,000,000 species with 10,000 proteins its extremely unlikely we’d find a single de novo protein. After all, he calculated the likeliness of coming up with a single folded protein domain as 1 in 10^70.
    So ID is proven or is completely demolished on this one observation

  21. 21
    Mapou says:

    Deep down, all Darwinists know that the combinatorial explosion, aka the curse of dimensionality, kills Darwinian evolution dead. After all, the mathematical argument against DE designing just one gene is simple and brutally unforgiving. The average human gene consists of about 23,000 nucleotides. The search space for a single gene is 4^23000! That’s 4 raised to 23000!

    No stochastic search algorithm has a chance of finding anything in such a huge space. Having a massively parallel computer as big as trillions upon trillions of universes would be no better than a wooden abacus.

    The “Scrabble tiles dumped onto the floor” metaphor is a joke in comparison. And that’s just for one little gene. Now imagine how big is the search space of an entire genome with its thousands of genes.

    All Darwinists are certifiably insane. As Feyerabend once wrote, “it’s time to cut them down to size and give them a lower position in society.”

  22. 22
    Mapou says:

    wd400:

    It is certainly true that we didn’t think de novo genes would play a big role in evolution. But if they do it seems that biological function is easier to find in sequence space than we had previously thought.

    Even if the size of the sequence space is 4^23000 ? Not a chance if all you have is Darwinian RM+NS. The math never lies. Your lying soul is the problem.

  23. 23
    wd400 says:

    What’s the average size of a de novo gene? What functions to they play?

  24. 24
    Mapou says:

    wd400 @23,

    You are certifiably insane.

  25. 25
    wd400 says:

    In case anyone was wondering, new genes are usually smaller than old ones, so the space is not so large. It’s not clear exactly what they do, without knowing that it’s hard to know what proportion of that space generates functional proteins.

  26. 26
    ppolish says:

    This TED talk on Quantum Biology is getting attention. Quantum Woo. Evowootion: http://www.ted.com/talks/jim_a....._questions

  27. 27
    Mapou says:

    wd400:

    In case anyone was wondering, new genes are usually smaller than old ones, so the space is not so large.

    Even a gene with just 100 nucleotides kills Darwinian evolution dead. But the size of a single gene is not a true indicator of its search space. It’s much bigger than that. The search space of a gene is always as huge as the size of the entire genome. Why? Because it must be fully compatible with the entire genome.

    Darwinists are math-challenged crackpots with bad will. You people have made a mockery of science. Shame on you. It’s time for you people to don sackcloths and ashes and start wailing and beating your chests on street corners. You have been a curse upon the surface of the earth.

    LOL

  28. 28
    PaV says:

    That HGT negates the basic assumptions of Mendelian genetics, and, hence, population genetics by extension, is rather obvious.

    That you want to equate epigenetic effects (environmental influences) with “quantitative genetics” is a bit disingenuous, since again, it is non-Mendelian.

  29. 29
    wd400 says:

    I do sometimes wonder if certain UD commenters are not actually extremely dedicated trolls

  30. 30
    daveS says:

    All Darwinists are certifiably insane. As Feyerabend once wrote, “it’s time to cut them down to size and give them a lower position in society.”

    QOTD.

  31. 31
    Mapou says:

    wd400:

    I do sometimes wonder if certain UD commenters are not actually extremely dedicated trolls

    Yeah, yeah, yeah. Man, go pack it where the sun don’t shine. 😀

  32. 32
    bornagain77 says:

    As to the comparative mental health issues between atheists and Theists, it is shown that religious belief is physically and psychologically beneficial

    Are atheists mentally ill? – August 14th, 2013 – Sean Thomas
    Excerpt: “Let’s dispense with the crude metric of IQ and look at the actual lives led by atheists, and believers, and see how they measure up. In other words: let’s see who is living more intelligently. And guess what: it’s the believers. A vast body of research, amassed over recent decades, shows that religious belief is physically and psychologically beneficial – to a remarkable degree.,,,
    [I hope this next part doesn’t upset too many people, but…] the evidence today implies that atheism is a form of mental illness. And this is because science is showing that the human mind is hard-wired for faith… religious people have all their faculties intact, they are fully functioning humans. Therefore, being an atheist – lacking the vital faculty of faith – should be seen as an affliction, and a tragic deficiency: something akin to blindness. Which makes Richard Dawkins the intellectual equivalent of an amputee, furiously waving his stumps in the air, boasting that he has no hands.”
    http://blogs.telegraph.co.uk/n.....tally-ill/

    As well, Christians respond better to psychiatric treatment than atheists

    Christians respond better to psychiatric treatment than atheists: – July 21, 2013
    Excerpt: “Our work suggests that people with a moderate to high level of belief in a higher power do significantly better in short-term psychiatric treatment than those without, regardless of their religious affiliation. Belief was associated with not only improved psychological well-being, but decreases in depression and intention to self-harm,” explained Rosmarin.
    The study looked at 159 patients, recruited over a one-year period. Each participant was asked to gauge their belief in God as well as their expectations for treatment outcome and emotion regulation, each on a five-point scale. Levels of depression, well being, and self-harm were assessed at the beginning and end of their treatment program.
    http://www.uncommondescent.com.....are-crazy/

    Atheists claim that life has no rhyme, reason, or purpose for its being. To the extent that atheists are able to live consistently within that worldview, they would be considered psychopathic:

    The Heretic – Who is Thomas Nagel and why are so many of his fellow academics condemning him? – March 25, 2013
    Excerpt:,,,Fortunately, materialism is never translated into life as it’s lived. As colleagues and friends, husbands and mothers, wives and fathers, sons and daughters, materialists never put their money where their mouth is. Nobody thinks his daughter is just molecules in motion and nothing but; nobody thinks the Holocaust was evil, but only in a relative, provisional sense. A materialist who lived his life according to his professed convictions—understanding himself to have no moral agency at all, seeing his friends and enemies and family as genetically determined robots—wouldn’t just be a materialist: He’d be a psychopath.
    http://www.weeklystandard.com/.....tml?page=3

    Moreover, this psychopathic characteristic inherent to the atheistic philosophy is born out empirically, in that people who do not believe that they are real ‘persons’, i.e. are a ‘conscious soul’, tend to be more psychopathic than the majority of normal people in America who do believe they are real persons, i.e. are ‘conscious souls’.
    You can pick that psychopathic study of atheists around the 14:30 minute mark of this following video with the paper of the study following the video:

    Anthony Jack, Why Don’t Psychopaths Believe in Dualism? – video – 14:30 minute mark
    http://www.youtube.com/watch?l.....zOk#t=862s

    A scientific case for conceptual dualism: The problem of consciousness and the opposing domains hypothesis. – Anthony I. Jack – 2013
    Excerpt page 18: we predicted that psychopaths would not be able to perceive the problem of consciousness.,,
    In a series of five experiments (Jack, in preparation), we found a highly replicable and robust negative correlation (r~-0.34) between belief in dualism and the primary psychopathic trait of callous affect7.
    Page 24: Clearly these findings fit well with the hypothesis (Robbins and Jack, 2006) that psychopaths can’t see the problem of consciousness8. Taking these finding together with other work on dehumanization and the anti-social effects of denying the soul and free will, they present a powerful picture. When we see persons, that is, when we see others as fellow humans, then our percept is of something essentially non-physical nature. This feature of our psychology appears to be relevant to a number of other philosophical issues, including the tension between utilitarian principles and deontological concerns about harming persons (Jack et al., accepted), the question of whether God exists (Jack et al., under review-b), and the problem of free will9.
    http://tonyjack.org/files/2013.....281%29.pdf
    Caveat: Anthony Jack is a physicalist. In trying to develop a physical theory of consciousness he proposes that for most people the problem of consciousness, the appearance of dualism, is caused by different brain networks used for thinking about mechanisms (ie how the brain works) and for understanding social situations (ie how people feel). According to Jack, it isn’t a natural gap but a gap due to brain physiology and psychopaths lack social thinking (are callous) so they don’t see the problem.

    To state what is overwhelmingly obvious for most theists who have interacted with atheists on the internet, most atheists harbor an irrational, and emotionally based, hated of God:

    When Atheists Are Angry at God – 2011
    Excerpt: I’ve never been angry at unicorns. It’s unlikely you’ve ever been angry at unicorns either.,, The one social group that takes exception to this rule is atheists. They claim to believe that God does not exist and yet, according to empirical studies, tend to be the people most angry at him.
    http://www.firstthings.com/ont.....gry-at-god

    Study explores whether atheism is rooted in reason or emotion – Jan. 2015
    Excerpt: “A new set of studies in the Journal of Personality and Social Psychology finds that atheists and agnostics report anger toward God either in the past or anger focused on a hypothetical image of what they imagine God must be like. Julie Exline, a psychologist at Case Western Reserve University and the lead author of this recent study, has examined other data on this subject with identical results. Exline explains that her interest was first piqued when an early study of anger toward God revealed a counterintuitive finding: Those who reported no belief in God reported more grudges toward him than believers.”
    http://www.uncommondescent.com.....r-emotion/

    Verse and Music:

    Luke 8:35
    and the people went out to see what had happened. When they came to Jesus, they found the man from whom the demons had gone out, sitting at Jesus’ feet, dressed and in his right mind; and they were afraid.

    You Love Me Anyway – Sidewalk Prophets – video
    https://www.youtube.com/watch?v=y8BBCYFAYRI

  33. 33
    PaV says:

    Ad hominems usually start when facts can’t be contested.

  34. 34
    wd400 says:

    If you’d like me to put it directly I can PaV. I find if very hard to believe anyone could honestly believe that the mere existence of HGT put an end to population genetics (as if horizontally transferred genes became immune to selection mutation and the rest) or that an environmental influence of gene expression is somehow counter to Mendalism (!).

    Perhaps you are that ignorant or deluded, perhaps you are a troll. I’m not going to waste time working out which.

  35. 35
    Mapou says:

    daveS:

    All Darwinists are certifiably insane. As Feyerabend once wrote, “it’s time to cut them down to size and give them a lower position in society.”

    QOTD.

    Well, I was just being polite. They’re either insane, stupid or they’re plain jackasses. Or all of the above. Many of them are also malignant narcissists. I can name names, too: Richard Dawkins, Jerry Coyne, Paul Z Myers, etc. Oh, don’t forget Charles Darwin, the first patient in the asylum.

  36. 36
    bornagain77 says:

    population genetics itself put an end to population genetics

    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

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

    Biological Information – Mutation Count & Synergistic Epistasis (mutation accumulation) 1-17-2015 by Paul Giem – video
    https://www.youtube.com/watch?v=6gdoZk_NbmU

    Calling all Darwinists, where is your best population genetics simulation? – September 12, 2013
    Excerpt: So Darwinists, what is your software, and what are your results? I’d think if evolutionary theory is so scientific, it shouldn’t be the creationists making these simulations, but evolutionary biologists! So what is your software, what are your figures, and what are your parameters(?) And please don’t cite Nunney, who claims to have solved Haldane’s dilemma but refuses to let his software and assumptions and procedures be scrutinized in the public domain. At least Hey was more forthright, but unfortunately Hey’s software affirmed the results of Mendel’s accountant.
    http://www.uncommondescent.com.....imulation/

    Panda’s Thumb Richard Hoppe forgot about Humpty Zombie – April 15, 2014
    Excerpt: I discovered if you crank up Avida’s cosmic radiation parameter to maximum and have the Avida genomes utterly scrambled, the Avidian organisms still kept reproducing. If I recall correctly, they died if the radiation was moderate, but just crank it to the max and the creatures come back to life!
    This would be like putting dogs in a microwave oven for 3 days, running it at full blast, and then demanding they reproduce. And guess what, the little Avida critters reproduced. This little discovery in Avida 1.6 was unfortunately not reported in Nature. Why? It was a far more stupendous discovery! Do you think it’s too late for Richard Hoppe and I to co-author a submission?
    Hoppe eventually capitulated that there was indeed this feature of Avida. To his credit he sent a letter to Dr. Adami to inform him of the discovery. Dr. Adami sent Evan Dorn to the Access Research Network forum, and Evan confirmed the feature by posting a reply there.
    http://www.creationevolutionun.....idcs/?p=90

    Avida, when using realistic biological parameters as its default settings, instead of using highly unrealistic default settings as it currently does, actually supports Genetic Entropy instead of Darwinian evolution:

    Biological Information – Mendel’s Accountant and Avida 1-31-2015 by Paul Giem
    https://www.youtube.com/watch?v=cGd0pznOh0A&list=PLHDSWJBW3DNUUhiC9VwPnhl-ymuObyTWJ&index=14

    Using Numerical Simulation to Better Understand Fixation Rates, and Establishment of a New Principle – “Haldane’s Ratchet” – Christopher L. Rupe and John C. Sanford – 2013
    Excerpt: We then perform large-scale experiments to examine the feasibility of the ape-to-man scenario over a six million year period. We analyze neutral and beneficial fixations separately (realistic rates of deleterious mutations could not be studied in deep time due to extinction). Using realistic parameter settings we only observe a few hundred selection-induced beneficial fixations after 300,000 generations (6 million years). Even when using highly optimal parameter settings (i.e., favorable for fixation of beneficials), we only see a few thousand selection-induced fixations. This is significant because the ape-to-man scenario requires tens of millions of selective nucleotide substitutions in the human lineage.
    Our empirically-determined rates of beneficial fixation are in general agreement with the fixation rate estimates derived by Haldane and ReMine using their mathematical analyses. We have therefore independently demonstrated that the findings of Haldane and ReMine are for the most part correct, and that the fundamental evolutionary problem historically known as “Haldane’s Dilemma” is very real.
    Previous analyses have focused exclusively on beneficial mutations. When deleterious mutations were included in our simulations, using a realistic ratio of beneficial to deleterious mutation rate, deleterious fixations vastly outnumbered beneficial fixations. Because of this, the net effect of mutation fixation should clearly create a ratchet-type mechanism which should cause continuous loss of information and decline in the size of the functional genome. We name this phenomenon “Haldane’s Ratchet”.
    http://media.wix.com/ugd/a704d.....fa9c20.pdf

  37. 37
    bFast says:

    Wd400, “But if they do it seems that biological function is easier to find in sequence space than we had previously thought.”

    Or the theory is wrong. ‘Seems like its time for scientists to accept the challenge, and prove that biological function is VASTLY easier to find in sequence space than is currently understood.

  38. 38
    Mapou says:

    bFast:

    Wd400, “But if they do it seems that biological function is easier to find in sequence space than we had previously thought.”

    Seems like its time for scientists to accept the challenge, and prove that biological function is VASTLY easier to find in sequence space than is currently understood.

    Like almost everything else in Darwinism, it’s a pseudoscientific conjecture since it cannot be falsified. Also, the use of a fictitious historical narrative in science, especially one that begins with “it seems that” already has one foot squarely planted in the pseudoscience bin. It’s not even wrong.

  39. 39
    bornagain77 says:

    as to:

    Can new genes arise from junk DNA? – August 24, 2015
    Excerpt: The first evidence that a strict duplication model might not suffice came in the 1990s, when DNA sequencing technologies took hold. Researchers analyzing the yeast genome found that a third of the organism’s genes had no similarity to known genes in other organisms. At the time, many scientists assumed that these orphans belonged to families that just hadn’t been discovered yet. But that assumption hasn’t proven true. Over the last decade, scientists sequenced DNA from thousands of diverse organisms, yet many orphan genes still defy classification. Their origins remain a mystery.
    http://www.uncommondescent.com.....ent-577361

    Paul Nelson has been following this ORFan argument for a while now:

    ,,,”Typical bacterial species. The smallest part of the pie are the genes that all bacteria share. 8% roughly. This second and largest slice (of the pie, 64%) are the genes that are specialized to some particular environment. They call them character genes. By far the biggest number of genes are the ones that are unique. This big green ball here (on the right of the illustration). These are genes found only in one species or its near relatives. Those are the ORFans (i.e. Genes with no ancestry). They said, on the basis of our analysis the genetic diversity of bacteria is of infinite size.”
    Paul Nelson – quoted from 103:48 minute mark of the following video
    Widespread ORFan Genes Challenge Common Descent – Paul Nelson – video
    https://youtu.be/9UTrZX47e00?t=3820

    You can see the pie chart that Dr. Nelson used in his talk here on page 108 (figure 2) of this following article:

    Estimating the size of the bacterial pan-genome
    Excerpt Figure 2 pg. 108: At the genomic level, a typical bacterial genome is composed of _8% of core genes, 64% of character genes and 28% of accessory genes,,,
    http://www.paulyu.org/wp-conte.....genome.pdf

    Estimating the size of the bacterial pan-genome – Pascal Lapierre and J. Peter Gogarten – 2008
    Excerpt: We have found greater than 139 000 rare (ORFan) gene families scattered throughout the bacterial genomes included in this study. The finding that the fitted exponential function approaches a plateau indicates an open pan-genome (i.e. the bacterial protein universe is of infinite size); a finding supported through extrapolation using a Kezdy-Swinbourne plot (Figure S3). This does not exclude the possibility that, with many more sampled genomes, the number of novel genes per additional genome might ultimately decline; however, our analyses and those presented in Ref. [11] do not provide any indication for such a decline and confirm earlier observations that many new protein families with few members remain to be discovered.
    http://www.paulyu.org/wp-conte.....genome.pdf

  40. 40
    Box says:

    WD400,

    WD400: It is certainly true that we didn’t think de novo genes would play a big role in evolution. But if they do it seems that biological function is easier to find in sequence space than we had previously thought.

    Let’s assume, arguendo, that de novo genes arise from junk-DNA. Could you take us through the next steps? How do we get to a regulatory system?

    Scientists also want to understand how de novo genes get incorporated into the complex network of reactions that drive the cell, a particularly puzzling problem. It’s as if a bicycle spontaneously grew a new part and rapidly incorporated it into its machinery, even though the bike was working fine without it. “The question is fascinating but completely unknown,” Begun said.

    BA77: Moreover, the essential genes were somehow incorporated into the ‘bicycle’ while the bicycle was being peddled, i.e. while the cell was busy being alive.

    “How does novel gene become functional? How does it get incorporated into actual cellular processes?” McLysaght said. “To me, that’s the most important question at the moment.”

  41. 41
    Silver Asiatic says:

    Box

    Let’s assume, arguendo, that de novo genes arise from junk-DNA. Could you take us through the next steps? How do we get to a regulatory system?

    Once you have genes, you’ll need a regulatory system. So that arises also. 🙂

  42. 42
    Silver Asiatic says:

    wd400

    So, if de novo genes do indeed play an important role in evolutoin, complexity could indeed beget complexity.

    Simplicity begat complexity then complexity begat complexity. Abraham begat Isaac; and Isaac begat Jacob.

    That junk is more likely to generate new complexity and away we go.

    Away we go. Or perhaps we go away. I’d like to see a model of the process. We start with lots of random, junk detritus. Then randomize further. Increase the complexity. Then watch the functional, specified order ‘arise’ from it.

    I have to admit I don’t quite understant the glee in the rest of the thread.

    Clearly, there’s quite a lot you don’t understand.

    It is certainly true that we didn’t think de novo genes would play a big role in evolution.

    As above, there’s a lot you didn’t think of. I admit having quite a lot of glee looking at this thread, but I’m also a bit sad to see you in this condition. You either have to keep lying to yourself or keep trying to pump up your feeling of superiority over everyone else, or perhaps just try to ignore this and wait for a new evolutionary fairy-tale to come along to weasel out of it. You’ll certainly need something more than your attempt below, which is pathetic, really.

    But if they do it seems that biological function is easier to find in sequence space than we had previously thought.

    “I never realized it, but levitation is quite a lot easier than we had previously thought”, he said, after watching David Copperfield rise off the floor and fly across the stage.

    It’s hard to imagine, for instance, that humans are carrying around a Poldi because it was designed to later become a gene in mice!

    It might be a good spiritual exercise for you to work on imagining design and the potential of a designer.

  43. 43
    bornagain77 says:

    Box @ 40

    “How do we get to a regulatory system?”

    That is just the right question Box.

    First off, genes are turning out to be fantastically complex. Far more complex that Darwinists had ever dared imagine they would be.

    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

    “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

    And even though neo-Darwinists have failed to demonstrate the origin of even a single one of those fantastically complex novel genes/proteins by unguided material processes,,,

    HISTORY OF EVOLUTIONARY THEORY – WISTAR DESTROYS EVOLUTION
    Excerpt: A number of mathematicians, familiar with the biological problems, spoke at that 1966 Wistar Institute,, For example, Murray Eden showed that it would be impossible for even a single ordered pair of genes to be produced by DNA mutations in the bacteria, E. coli,—with 5 billion years in which to produce it! His estimate was based on 5 trillion tons of the bacteria covering the planet to a depth of nearly an inch during that 5 billion years. He then explained that the genes of E. coli contain over a trillion (10^12) bits of data. That is the number 10 followed by 12 zeros. *Eden then showed the mathematical impossibility of protein forming by chance.
    http://www.pathlights.com/ce_e.....hist12.htm

    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

    “Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds” 2004: – Doug Axe
    Excerpt: ,,,this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences.”
    http://www.mendeley.com/resear.....yme-folds/

    “Charles Darwin said (paraphrase), ‘If anyone could find anything that could not be had through a number of slight, successive, modifications, my theory would absolutely break down.’ Well that condition has been met time and time again. Basically every gene, every protein fold. There is nothing of significance that we can show that can be had in a gradualist way. It’s a mirage. None of it happens that way.”
    – Doug Axe PhD – Nothing In Molecular Biology Is Gradual – video
    http://www.metacafe.com/watch/5347797/

    “In light of Doug Axe’s number, and other similar results,, (1 in 10^77), it is overwhelmingly more likely than not that the mutation, random selection, mechanism will fail to produce even one gene or protein given the whole multi-billion year history of life on earth. There is not enough opportunities in the whole history of life on earth to search but a tiny fraction of the space of 10^77 possible combinations that correspond to every functional combination. Why? Well just one little number will help you put this in perspective. There have been only 10^40 organisms living in the entire history of life on earth. So if every organism, when it replicated, produced a new sequence of DNA to search that (1 in 10^77) space of possibilities, you would have only searched 10^40th of them. 10^40 over 10^77 is 1 in 10^37. Which is 10 trillion, trillion, trillion. In other words, If every organism in the history of life would have been searching for one those (functional) gene sequences we need, you would have searched 1 in 10 trillion, trillion, trillionth of the haystack. Which makes it overwhelmingly more likely than not that the (Darwinian) mechanism will fail. And if it is overwhelmingly more likely than not that the (Darwinian) mechanism will fail should we believe that is the way that life arose?”
    Stephen Meyer – 46:19 minute mark – Darwin’s Doubt – video
    https://www.youtube.com/watch?v=Vg8bqXGrRa0&feature=player_detailpage#t=2778

  44. 44
    bornagain77 says:

    Nor have Darwinists ever even demonstrated the transition of any existing protein into another another protein of a similar sequence but of a slightly different function.

    “Enzyme Families — Shared Evolutionary History or Shared Design?” – Ann Gauger – December 4, 2014
    Excerpt: If enzymes can’t be recruited to genuinely new functions by unguided means, no matter how similar they are, the evolutionary story is false.,,,
    Taken together, since we found no enzyme that was within one mutation of cooption, the total number of mutations needed is at least four: one for duplication, one for over-production, and two or more single base changes. The waiting time required to achieve four mutations is 10^15 years. That’s longer than the age of the universe. The real waiting time is likely to be much greater, since the two most likely candidate enzymes failed to be coopted by double mutations.
    http://www.evolutionnews.org/2.....91701.html

    Yet, even though Darwinists have dramatically failed to demonstrate the origin of a single new gene/protein by neo-Darwinian processes, or even the transition of a protein to a similar protein of a slightly different function, neo-Darwinists, as you pointed out with your question in 40 Box, have completely ignored the larger question of “How do we get to a regulatory system?”

    Box, your question is not a minor question for two reasons. First, it is found that ‘developmental Gene Regulatory Networks’ (dGRNs) are vastly different even among supposedly closely related species, i.e. chimps and humans. And the second reason is that mutations to dGRNs are ‘always catastrophically bad’

    “Where (chimps and humans) really differ, and they differ by orders of magnitude, is in the genomic architecture outside the protein coding regions. They are vastly, vastly, different.,, The structural, the organization, the regulatory sequences, the hierarchy for how things are organized and used are vastly different between a chimpanzee and a human being in their genomes.”
    Raymond Bohlin (per Richard Sternberg) – 9:29 minute mark of video
    http://www.metacafe.com/watch/8593991/

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

    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 the unfalsifiable ‘blind faith’ religion of atheists, this finding, by itself, should have been more than enough to falsify neo-Darwinian claims.

    Here is supplemental quote by Dr. Stephen Meyer commenting on the overt Theistic implications of the present genetic evidence as it now sits:

    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/

  45. 45
    Box says:

    WD400: But if they do it seems that biological function is easier to find in sequence space than we had previously thought.

    Exactly how difficult did you guys think it is to find biological function? I mean it is certainly not the case that not much biological function has been found ….

    In fact, it has been estimated that 99.9% of all species that have ever lived on Earth are now extinct.

    It doesn’t add up.

  46. 46
    wd400 says:

    Box,

    I have no clue how you think the two statements above relate to each other, so can’t answer you question.

    For your question about regulation, for the de novo genes we atually know about (the SMBE talk is not published so I don’t know if the same applies to these) it’s the onset of expression that marks the “birth” of the gene (e.g. sequences homologous to Poldi are found in other rodents and primates, but only expressed as a genein mice). Vertebrate genomes are full of LINES, SINES and other repetitive elements that (a) drive their own expression and (b) get copied around the genome. One way to get a new transcript expressed is to have one of these elements integrate upstream.

    In fact, the distribution of ages of genes (given in the linked piece) is such that we might expect only a few apparent de novo genes have any function. Most of them don’t stick around, so may just be transient patterns of expression arising from a process like that described above. It will be interesting to see the genes described in the SMBE talk.

    SA,

    Feel free to let me know what I’m missing.

  47. 47
    Silver Asiatic says:

    The arts of double-speak, misinformation and manipulative ambiguity are necessary skills for any budding evolutionary biologist to develop.

  48. 48
    bFast says:

    wd400, “In fact, the distribution of ages of genes (given in the linked piece) is such that we might expect only a few apparent de novo genes have any function.”

    “It seems like these novel genes are often the most important ones,” said Erich Bornberg-Bauer.

    Hmmm.

    If de novo genes rarely have any function, and if the function they do have is insignificant, then this line of reasoning has little power. If, however, de novo genes are playing significant roles in organisms, which it seems from the evidence I have been seeing, then your theory is in serious trouble. Right?

  49. 49
    wd400 says:

    Again, SA, feel free to point out specific examples.

  50. 50
    wd400 says:

    bFast, I think we already know that statement by Bornberg-Bauer is not generally true. Phylogenetic conservation and nothing else is a pretty good predictor of how important a protein is. If these genes were very important in diseases we would have found them back in the recombination mapping days.

    I would be surprised if de novo genes generally had very specific biochemical functions, and such a finding would make us change our understanding of the evolution of genes and genomes. But I should also point out all the other data we have on the evolution of genomes wouldn’t disappear. If de novo genes are indeed more important than we’d though, that doesn’t meant gene duplication and more traditional models of gene evolution aren’t also important.

  51. 51
    Silver Asiatic says:

    wd

    What you’re missing? I’d say you’ve got a bit of a gap between the grandiose claims of your theory and something we just read like this …

    Researchers are beginning to understand that de novo genes seem to make up a significant part of the genome, yet scientists have little idea of how many there are or what they do.

    You pretend to have a story of origins and you don’t even know how fundamental aspects of life work.

    I accept that you don’t see any incongruity there. For you, there’s no problem at all.

    Evolution means never having to say you’re sorry.

    You made it quite clear – no matter what is found, the evolutionary fairy tale persists. Whatever it is, it merely …

    would make us change our understanding of the evolution of genes and genomes

    Great theory. It predicts that you will adapt your understanding to whatever observations you encounter.

  52. 52
    wd400 says:

    Great theory. It predicts that you will adapt your understanding to whatever observations you encounter.

    How do you think science should work? Everytime we get new information we just forget everything we learned earlier?

  53. 53
    Mapou says:

    wd400:

    I would be surprised if de novo genes generally had very specific biochemical functions, and such a finding would make us change our understanding of the evolution of genes and genomes.

    How? By going from a (pathetically lame and stupid) stochastic search (RM+NS) to a non-stochastic search?
    How does that NOT falsify Darwinian evolution, pray tell? And how would that non-stochastic mechanism work?

    You can’t just reverse the most basic tenet of a theory and still cling to the pretense that it’s the same theory. It’s like the communist party in China clinging to the pretense of not being a bunch of capitalist roaders like everyone else. It’s weak.

  54. 54
    bFast says:

    wd400, “Phylogenetic conservation and nothing else is a pretty good predictor of how important a protein is.”

    Balderdash! That is Darwinistic theory driving research. Knock-out is by far the best way to test the importance of a gene. Even knock-out, however, isn’t universally effective. Sometimes a gene only proves important in specific circumstances.

    wd400, “How do you think science should work? Everytime we get new information we just forget everything we learned earlier?”

    Wd400, I contend that it is you who doesn’t get how science (is supposed to) work. When contrary information comes in, plausible explanations within the current theory are sought, yes. But then the plausible explanations ARE TESTED! Science is supposed to work on the belief that the validity of every theory can be challenged at any time by the data.

    Your method of science: oh, unexpected data. Hah! Here’s a possible explanation. No problem — done.

    Proper science: oh, unexpected data. Here’s a possible explanation. Lets test the explanation to see whether it holds water.

    This de novo issue is very much big enough to dethrone the darwistic paradigm. If de novos are happening outside the bounds of statistical reason, and they appear to be, then an explanation other than “chance” must be found.

  55. 55
    wd400 says:

    Balderdash! That is Darwinistic theory driving research…

    To be clear, I meant by “phylogenetic conservation and nothing else” I mean if all you know about a given site in a given protein is how conserved it is, that is a pretty good predictor of how important the site is. That’s the basis of scores like SIFT and PolyPhen which are used in labs to predict the severity of mutations every day.

    Your method of science: oh, unexpected data. Hah! Here’s a possible explanation. No problem — done.

    No. As I said, it will be interesting to read about these apparent de novo genes when the SMBE talk is published. Then we’ll be able to start testing ideas about their origin.

  56. 56
    Mapou says:

    wd400:

    Then we’ll be able to start testing ideas about their origin.

    Ha! What possible ideas could you have that do not do away with the Darwinian stochastic search mechanism? Why are you people so dishonest with yourselves and everyone else? The religious fervor of your conviction is duly noted.

    The end soon cometh. And sooner than y’all think. Wait for it. I’ve said it before. I’ll be watching the whole thing unravel with a beer in one hand, a bag of Cheetos in the other and a smirk on my face.

    ahahaha…AHAHAHA…ahahaha…

    PS. I think I’ll add a Havana cigar into the mix for good measure. ahahaha…

  57. 57
    REC says:

    bfast-

    “Proper science: oh, unexpected data. Here’s a possible explanation. Lets test the explanation to see whether it holds water.”

    Describe a formal test that intelligent design in biology.

    It is cute watching IDers, who generally haven’t a clue about what scientists do, moan over the mangled secondhand bits “news” harvests from other science writers.

  58. 58
    Mapou says:

    REC:

    Describe a formal test that intelligent design in biology.

    Here are 4 predictions of intelligent design:

    1. The species are organized in a mostly nested hierarchy (i.e., there are many instances of HGT).
    2. De novo genes are everywhere.
    3. There is no such thing as junk DNA.
    4. The genome is organized hierarchically.

    Falsify those, Mr. Dirt worshipper. And don’t bother telling us when you’re done. We don’t care.

    It is cute watching IDers, who generally haven’t a clue about what scientists do, moan over the mangled secondhand bits “news” harvests from other science writers.

    You can pack your science up you know where. A stochastic search mechanism (e.g., RM+NS) is useless against a search space as huge as 4^23000, the search space for a single gene. RM+NS is a stupid idea in the bozo category. You people are not scientists. You are all a bunch of freaking morons. Your time in the sun is almost at an end. Wait for it.

    ahahaha…

  59. 59
    Mapou says:

    To wd400 and REC et al. You people are traitors to your own species. You are the scum of the earth, AFAIC.

  60. 60
    ppolish says:

    “Describe a formal test that intelligent design in biology.”

    How about “appearance of design”. Mountains of evidence for “appearance”.

    Algorithm of Appearance of Design. Appearance lol:)
    https://m.youtube.com/watch?v=Yn_Xarm6Rj8

  61. 61
    bFast says:

    REC, “Describe a formal test that intelligent design in biology.”
    Begone with your “my theory is better than your theory” argument. It is stupid! Your theory must stand or fall, on its own, against the data. Why bother with a theory that doesn’t fit the facts? Because it is better than the other guy’s theory (a theory that you are determined not to understand)? The principle of falsification does not require an alternative theory — period.

  62. 62
    Dr JDD says:

    wd400 – this is where the deception comes in, when it is stated in such a way that conserved sequences are important to infer that if there is a lack of phylogenetic conservation it must not be functionally important. This line of thinking has polluted modem science and is false for 2 reasons:
    1) as above, non-conserved proteins demonstrate functional necessity
    2) only ~2% of the genome is protein coding yet there is more functional sequence that is non-codingthan thrthere is protein coding (so homology of 2% doesn’t say much tbh).

    No one denies that if something shows conservation it is likely to be of functional importance. However what is contended is that there are also non-conserved sequences which exhibit very important functions (often overlooked because…They are not conserved!).

    REC – you do realise many IDers are successful scientists with peer reviewed publications and fully understand how science works, don’t you?

  63. 63
    bFast says:

    wd400, “To be clear, I meant by “phylogenetic conservation and nothing else” I mean…”

    So you are taking back the “and nothing else” part then? Good, it needs to be gone. There certainly is some value in conservation analysis. We, over here, think its a lot less valuable than it is made out to be. (‘Seems that phylogenetic conservation confirms value to less than 10% of human dna, when the analysis done by the encode project suggests the number is more like 80%) However, I think that phylogenetic conservation is pretty much useless when analyzing de novo genes, as there is virtually no history to analyze for conservation.

    wd400, “Then we’ll be able to start testing ideas about their origin.”

    Good. Please test the theory! In the mean time please don’t inform me and mine that the theory is as clearly established as gravity.

  64. 64
    EugeneS says:

    REC,

    What kind of falsification are you talking about?

    The origin of life is a one-off event in the natural history of the Earth. Whatever the explanation, it is a matter of plausibility and inference that best fits the available data, not a matter of falsifiability as such. It cannot be falsified in the sense you imply because it was a singular event.

    The more science progresses, the more data will fit into the design explanatory mode. However, there will always be a loop-hole for believers in fluctuations and frozen accidents just because it was a singular event, despite all the evidence to the contrary: organisms being decision making systems may only have appeared as a result of decision making and nothing else.

  65. 65
    wd400 says:

    JDD,

    The questoin was wetherde novo genes are generally involved in important processes. Of course some non-conserved sequences will be involved in in biologically important process (but even they will be conserved at a population level if their function is sequence related).

    bFast,

    “and nothing else” only meant that using only phylogenetic data was helpful. There are other measures that also include biochemistry or population diversity data, which are would be “conservation and some other stuff”. The meme that ENCODE proved 80% of the genome has function is, I’m afraid, just rubbish. Even the ENCODE group don’t make that claim.

  66. 66
    Mapou says:

    Notice how the dirt worshippers steer away from the argument that a search space as large as 4^23000 (the search space for a single gene!) kills Darwinism dead?

    They have no answer to this simple yet devastating argument against their little dirt-worshipping religion. And you know why? They are morons and liars. That’s why.

  67. 67
    ppolish says:

    “The meme that ENCODE proved 80% of the genome has function is, I’m afraid, just rubbish. Even the ENCODE group don’t make that claim.”

    Even memes of rubbish serve a purpose WD400. Kind of like junk DNA.

  68. 68
    Box says:

    WD400: I have no clue how you think the two statements above relate to each other, so can’t answer you question.

    Really? Let me spell it out for you:
    If you guys thought that biological function is difficult to find in sequence space, how does that add up with the tremendous amount of species that once roamed the Earth – 99.9% of all species that have ever lived on Earth are now extinct.
    Seems to me that this shows that in fact a staggering amount of biological function has been found in sequence space and therefor there is no room for the (correct) belief that biological function is difficult to find in sequence space.

    WD400: For your question about regulation, for the de novo genes we atually know about (the SMBE talk is not published so I don’t know if the same applies to these) it’s the onset of expression that marks the “birth” of the gene (…)

    Unresponsive. Maybe I wasn’t clear here also … My question about regulation was: How do we get to a regulatory system given that a novel gene arises from junk-DNA. How do you envision the steps towards a (novel) regulatory system?

    1. We have a novel gene.
    2. …
    3. …
    …..
    … now we also have a regulatory system.

  69. 69
    wd400 says:

    Seems to me that this shows that in fact a staggering amount of biological function has been found in sequence space .

    Why? I honestly can’t work out why someone would think this. I mean, that 99% of species are dead tells you that there are lots of ways to be alive, it doesn’t tell you anything about how many ways there are to not be alive, does it?

    My question about regulation was: How do we get to a regulatory system given that a novel gene arises from junk-DNA. How do you envision the steps towards a (novel) regulatory system?

    I explained one way — an element with it’s own cis-regulatroy sequences integrates alongside. That way you get expression down stream. Because expression also depends on DNA accessibility and methylation state you end up with tissue-specific expression too.

  70. 70
    Upright BiPed says:

    Describe a formal test that intelligent design in biology.

    Rec, it is not difficult to give you such a test, the question is: “Why are you asking?”

    It is certainly the case that you will never accept the test, nor the results. You will make pointless objections here and lodge irrelevant complaints there – but hell will freeze over before you accept the outcome of a purely empirical test of design in biology.

    So why even ask? What do you gain by the charade?

  71. 71
    Box says:

    WD400:

    Box: Seems to me that this [99.9% of all species that have ever lived on Earth are now extinct] shows that in fact a staggering amount of biological function has been found in sequence space.

    Why? I honestly can’t work out why someone would think this.

    Do you really ask “why?”? You amaze me.

    WD400: I mean, that 99% of species are dead tells you that there are lots of ways to be alive, (…)

    More precisely, it tells us that “a lot of biological function has been found in sequence space”, exactly what I said. Just think of all the intermediate forms — that have never been found …

    WD400: (…) it doesn’t tell you anything about how many ways there are to not be alive, does it?

    No, but did I or anyone else even hint at the possibility that it does? And how is this relevant? I sincerely hope that you are not suggesting that there are not many ways of being dead so that therefor the amount of biological function that has been found cannot be said to be “staggering”. Suggesting that would be utter madness.

    Again, lots of biological function has been found in sequence space, now my question is: how does that square with your belief that it is so difficult to find?

  72. 72
    wd400 says:

    I really don’t see what any of that has to do with extinct species.

    My comment simply meant that if do novo genes are common then in suggests that biological function is so dense in the sequence space that random streches of intergenic DNA might fall in to them. I don’t think biological function is quite that easy to come by (or at least no the funcions we generally asociated with proteins). Instead I think biologically functional sequences don’t arise from one-of random sampling sequence space but by natural selection (and gene duplication and exon shuffling and all that).

  73. 73
    bFast says:

    wd400, “The meme that ENCODE proved 80% of the genome has function is, I’m afraid, just rubbish.”

    You got the meme from me? I said, “encode project suggests”. They certainly did make that suggestion. They did not provide proof.

  74. 74
    bornagain77 says:

    DNA far outclasses anything man has ever created in terms of its ability to store information.

    DNA: The Ultimate Hard Drive – Science Magazine, August-16-2012
    Excerpt: “When it comes to storing information, hard drives don’t hold a candle to DNA. Our genetic code packs billions of gigabytes into a single gram. A mere milligram of the molecule could encode the complete text of every book in the Library of Congress and have plenty of room to spare.”
    http://news.sciencemag.org/sci.....-code.html

    Information Storage in DNA by Wyss Institute – video
    https://vimeo.com/47615970
    Quote from preceding video:
    “The theoretical (information) density of DNA is you could store the total world information, which is 1.8 zetabytes, at least in 2011, in about 4 grams of DNA.”
    Sriram Kosuri PhD. – Wyss Institute

    Moreover, from just barely starting to scratch the surface of the encoding that is written on DNA, it is discovered that there are multiple layers of overlapping coding on DNA that far, far, outclasses anything man has ever programmed.

    Second, third, fourth… genetic codes – One spectacular case of code crowding – Edward N. Trifonov – video
    https://www.youtube.com/watch?v=fDB3fMCfk0E

    In the preceding video, Trifonov elucidates codes that are, simultaneously, in the same sequence, coding for DNA curvature, Chromatin Code, Amphipathic helices, and NF kappaB. In fact, at the 58:00 minute mark he states, “Reading only one message, one gets three more, practically GRATIS!”. And please note that this was just an introductory lecture in which Trifinov just covered the very basics and left many of the other codes out of the lecture. Codes which code for completely different, yet still biologically important, functions. In fact, at the 7:55 mark of the video, there are 13 codes that are listed on a powerpoint, although the writing was too small for me to read.

    Concluding powerpoint of the lecture (at the 1 hour mark):
    “Not only are there many different codes in the sequences, but they overlap, so that the same letters in a sequence may take part simultaneously in several different messages.”
    Edward N. Trifonov – 2010

    ‘It’s becoming extremely problematic to explain how the genome could arise and how these multiple levels of overlapping information could arise, since our best computer programmers can’t even conceive of overlapping codes. The genome dwarfs all of the computer information technology that man has developed. So I think that it is very problematic to imagine how you can achieve that through random changes in the code.,,, and there is no Junk DNA in these codes. More and more the genome looks likes a super-super set of programs.,, More and more it looks like top down design and not just bottom up chance discovery of making complex systems.’ –
    Dr. John Sanford – Inventor of the ‘Gene Gun’ – 31 second mark – video
    http://www.youtube.com/watch?f.....dM_s#t=31s

    Jeffrey Tomkins, Ph.D., Duons: Parallel Gene Code Defies Evolution, January 6, 2014
    Excerpt: The human mind struggles to comprehend the overall complexity of the genetic code—especially the emerging evidence showing that some genes have sections that can be read both forward and backward.3 Some genes overlap parts of other gene in the genome, and now it has been revealed that many genes have areas that contain dual codes within the very same sequence.
    Even the most advanced computer programmers can’t come close to matching the genetic code’s incredible information density and bewildering complexity.
    http://www.icr.org/article/7870/

    Moreover, the 3-D fractal global architecture present in DNA operation and repair processes would make any computer engineer drool with envy.

    3-D Structure Of Human Genome: Fractal Globule Architecture Packs Two Meters Of DNA Into Each Cell – Oct. 2009
    Excerpt: the information density in the nucleus is trillions of times higher than on a computer chip — while avoiding the knots and tangles that might interfere with the cell’s ability to read its own genome. Moreover, the DNA can easily unfold and refold during gene activation, gene repression, and cell replication.
    http://www.sciencedaily.com/re.....142957.htm

    Quantum Dots Spotlight DNA-Repair Proteins in Motion – March 2010
    Excerpt: “How this system works is an important unanswered question in this field,” he said. “It has to be able to identify very small mistakes in a 3-dimensional morass of gene strands. It’s akin to spotting potholes on every street all over the country and getting them fixed before the next rush hour.” Dr. Bennett Van Houten – of note: A bacterium has about 40 team members on its pothole crew. That allows its entire genome to be scanned for errors in 20 minutes, the typical doubling time.,, These smart machines can apparently also interact with other damage control teams if they cannot fix the problem on the spot.
    per Science Daily

    Moreover, bacteria have been shown to reconstruct their own genome after it has been blown to pieces by radiation.

    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/

    Imagine your computer breaking its hard drive into a quarter million pieces and then putting it back together again. That would be roughly similar to what is happening here.

    Needless to say, no computer in the world is even close to reconstructing its own hard drive.

    And yet, despite all this unfathomed complexity being discovered in DNA that our best engineers have not even come close to imitating, wd400 has the sheer audacity to claim, not only that unguided material processes put that unfathomed complexity together, but that the vast majority of information on DNA must be junk. 🙂

    For wd400 to state such a thing would be absolutely hilarious for me, instead of just mildly humorous, if it were not for the dire consequences implicit for wd400 in wd400 resolutely setting himself against God as he has apparently chosen to do,,, even to the point of making himself look completely ridiculous by stating such obvious, and over the top, lies about the actual state of the evidence for obvious widespread DNA multi-functionality.

    Verse:

    Romans 1:25
    for that they exchanged the truth of God for a lie,,,,

  75. 75
    Mapou says:

    The average size of the nucleotide search space for a single human gene is:

    4^23000 !!!!!

    I claim that this kills Darwinism dead, period. Can any Darwinist here gather enough gonads to refute this claim? Or are you all a bunch of wussies? And BTW, materialist abiogenesis never even made it to the gates.

    ahahaha…

  76. 76
    Mapou says:

    @75

    My challenge still stands. Anybody?

    It all comes down to whether you got gonads or not. And if you don’t, can you grow a pair? Wussies.

    ahahaha…

  77. 77
    Box says:

    WD400: I think biologically functional sequences don’t arise from one-of random sampling sequence space but by natural selection (…).

    How? A la Dawkins Weasel?
    Natural selection needs biologically functional sequences in order to have something to select on. It doesn’t make sense to say that natural selection produces biologically functional sequences.
    Natural selection produces zero information — instead it subtracts massive amounts of information.

  78. 78
    EugeneS says:

    WD400,

    “Why? I honestly can’t work out why someone would think this. I mean, that 99% of species are dead tells you that there are lots of ways to be alive, it doesn’t tell you anything about how many ways there are to not be alive, does it?”

    Another example of quasi-scientific equivocation. “Many”, “a lot”, “lots of”.

    Any living system is a functional hierarchically organized whole. The fact that living organisms die out is irrelevant to the question of biological function.

    You guys need to show how biological functionality, which is in its essence decision making, arises without recourse to decision making.

    Random shuffling, gene duplication etc are biological functions themselves. I.e. all this is used in a context of decision making. The cell decides to do something. The simple yet profound intuition behind this is that the cell is doing it for a reason. BTW, this kind of intuition is traditional in science.

    All this glaringly intelligent behaviour cannot just emerge simply by virtue of replication errors and a coarse grained filter of natural selection. On the contrary, it must be loaded. Natural selection cannot decide, nor can random variation, nor can their combination. Law and Chance are not up to the task of explaining the presence of Logic that uses Law and Chance in order to achieve utility.

    The biggest challenge for you guys is to explain naturalistically the emergence of decision making in the living organisms. There is no such explanation available so far, only question begging.

  79. 79
    Silver Asiatic says:

    The idea is “things happened, therefore evolution caused them”.

    We see a huge space for random search, but this is supposedly not a problem because “it must be easier to find function than we thought”. Proof? “Obviously, evolution already found lots of function”.

    If there were a a hundred billion different species, this would mean “it’s even easier for evolution find function”.

    Then we have the theory itself, which “predicts what happened in history by adjusting itself to new observations”.

    My New Ultimate Theory (NUT) is that the entire cosmos is made from blue plastic. Proof? Here’s some blue plastic. See? The NUT is validated! Look, the sky is blue – it’s probably plastic. The NUT wins again!

    Wait, this thing is yellow. No problem! The NUT accommodates that. Yellow is a color and so is blue. Hey, this other thing is not plastic. Well, now we have the neo-NUT. Same theory, of course. It states: “The entire cosmos is made from something with some kind of color or not, which might or not be plastic.”

    The Root core of the New Ultimate Theory always stands, everybody accepts it: “The entire cosmos is.” Only an Idiot would deny that.

    Everything else is just incidental detail, subject to change. That’s just the way science works. 🙂

  80. 80
    Box says:

    Silver: The idea is “things happened, therefore evolution caused them”.

    We see a huge space for random search, but this is supposedly not a problem because “it must be easier to find function than we thought”. Proof? “Obviously, evolution already found lots of function”.

    If there were a a hundred billion different species, this would mean “it’s even easier for evolution find function”.

    Indeed. If there were so staggeringly many different species — 99.9% went extinct (the countless posited “intermediate forms”) and a multitude of viable organisms that were never allowed to prosper because NS eliminated them for whatever reason — it has to be rather easy to find new biological function.
    Hence my question to WD400. How can his position allow for the belief that it would be difficult to find biological function in sequence space? IMO he — as a true Darwinian — is compelled to hold the belief that finding biological function is a walk in the park. Which is, needless to say, absurd.

  81. 81
    Silver Asiatic says:

    Box – True. In the end, the challenge to explain function got more difficult, not easier.

  82. 82
    ppolish says:

    Innovate or Die. Nature is innovative in tooth & claw & feather & thumb.

    How does the innovation emerge? It’s either a random walk in the park, or a guided one. The park sure looks designed though. Mountains of evidence on that design.

  83. 83
    wd400 says:

    Wow, you guys have really lost it…

    Box, yes, I forgot about your peculiar misunderstanding about natural selection. Leaving that aside, it is true that selection only works on a sequence once it exists. But if de novo genes are not common then then the origin of new functiona sequences from junk DNA can be an exceedingly rare event and still provide us will all the superfamalies we know about.

    EugeneS,

    There is no reason to think cells make decisions in the way you describe. If you drop an engineered gene into a genome with the right promoter sequence to express in , say, kidney epithelial cells, it will express that gene in kidney epithelial cell. It’s just biochemistry.

    SA,

    Nope. I literally can’t see anything in there that relate s to anything I’ve said.

  84. 84
    Mapou says:

    Darwinists are not just mentally ill, they’re cowards to boot. Yellow fruitcakes. 😀

  85. 85
    Silver Asiatic says:

    wd400

    Nope. I literally can’t see anything in there that relate s to anything I’ve said.

    Ok, I thought I made at least a few points that were quite clear, but I guess not. I’ll try again on your comment following.

    But if de novo genes are not common then then the origin of new functiona sequences from junk DNA can be an exceedingly rare event and still provide us will all the superfamalies we know about.

    If de novo genes are not common, then they’re an exceedingly rare event, but you’re using a statistical approach to explain their origin. You already said this, that where there is more junk (complexity) there will be more opportunity for the emergence of de novo genes. But you’ve said nothing about how the junk produces specified order. From the article …

    Yet creating a gene from a random DNA sequence appears as likely as dumping a jar of Scrabble tiles onto the floor and expecting the letters to spell out a coherent sentence.

    This is pretty simple and I think every IDist here understands it. Unfortunately, you haven’t understood it at all. You’re claiming that by merely adding more junk (more scrabble letters) this increases the likelihood of spelling out a coherent sentence. Try it with scrabble some time.

    Beyond that, you’re looking at the pile of letters and noticing a sentence (a de novo gene). Now you calculate the odds based on the presence of one sentence appearing in a pile of letters. This you’re considering “an exceedingly rare event”. However, if there were several paragraphs of complete, coherent sentences, you say “It’s a lot easier to create function this way than we thought”.

    Again, if there’s any IDist on this site that doesn’t understand the problem you have stumbled into, I’d really like to hear it. Amazingly, you simply can’t understand this at all.

    You’re dealing with an entirely stochastic process. Selection is not going to help you.

    For de novo genes, their origin remains as difficult to explain if they appear rarely or if they’re extremely common (although more remarkable if common).

    You’re fond of modelling evolutionary scenarios. All you have to do is start with random junk and show us the specified order that arises out of it, and then explain why it has done that.

    So far, you’re willing to accept that fully-formed coherent sentences can simply arise from a pile of scrabble letters (which is a vastly simpler task than what we’re talking about).

    After that, you’ve basically said nothing. I’ll add that you did admit there was a surprise here, but you seem to think that any wildly conflicting data from observations can be imported into your theory without negative consequences.

    To make it simple:

    1. You assume evolutionary theory is correct and will absorb conflicting observations into the theory without admitting that the theory has been falsified.
    2. Your assumption that “things evolved that way” is used as an explanation for every observation.

    Again, I mentioned that I was concerned for you because anybody can see what you’ve been doing. You’re totally blind to the issues. I don’t think you even realize what you’ve been saying and it’s pretty clear you don’t know what ID is, even after the many hours you spend here. Again, I find that very sad.

    You need to come to grips with this — at the very least — for the sake of whatever personal integrity you want to have for yourself.

  86. 86
    Box says:

    WD400: I think biologically functional sequences don’t arise from one-of random sampling sequence space but by natural selection (…).

    Box: Natural selection needs biologically functional sequences in order to have something to select on. It doesn’t make sense to say that natural selection produces biologically functional sequences.

    WD400: (…) it is true that selection only works on a sequence once it exists.

    Thank you for acknowledging my point. So functional sequences arise by chance (random sampling sequence space) — given unguided evolution.

    WD400: But if de novo genes are not common then then the origin of new functiona sequences from junk DNA can be an exceedingly rare event and still provide us will all the superfamalies we know about.

    I’m not sure I get your point. Starting with LUCA I see an obvious problem: the finding of biological function cannot always have been an exceedingly rare event in the evolutionary narrative.
    Right?

  87. 87
    wd400 says:

    SA,

    Leaving out the childish concern trolling

    You’re claiming that by merely adding more junk (more scrabble letters) this increases the likelihood of spelling out a coherent sentence.

    Right. Are you seriously claiming that’s not true?

    The question though is what is the equivalent of a “coherent sentence” in sequence space.

    If you’d read what I said to start with, it’s hard to see an ID explanation for what we know about existing de novo genes. As I said, it’s hard to imagine that humans are carrying around a sequence homologous to Poldi because it was designed to later become a gene in mice! i.e. A sequence that is very close to the functional poldi gene exist in your intergenic DNA.

    Box,

    Without selection lineages would not be able to explore sequence nearly as efficiently, so I think it does makes sense to say selection creates functional sequences. If you’d like some sophmoric philosophical debate about the meaning fo teh word create you’ll have to find someone else.

    The rest of your post is the classic retreat to the origin of life tactic. All I can say is that we know that function is much denser is the space of short RNAs than typical proteins. There are many unanswered questions about the origin of life, but, again, selection and recombination (and, in fact HGT!) mean that even rare events can be amplified and shared across species.

  88. 88
    wd400 says:

    I should add, SA, the idea that sequence space will have more function than previously thought if de novo genes are common is also a prediction of evolutionary biology. If they are really performing biological functions, there is good reason to think they will be less biochemically specific functions, and use shorter amino acids sequences to get them done.

  89. 89
    EugeneS says:

    wd400: It’s just biochemistry.

    Nope. You are not seeing the wood for the trees. Gene expression employs rules as well as the laws of nature. So when you appeal to gene expression and other sophisticated functionality in the cell, be careful to distinguish rules from the laws of nature.

    There is logic implemented using biochemistry on all levels of biological organization. Biochemistry alone cannot explain the presence of if-then-else rules. The same laws of nature act upon a switch in either position ON or OFF. Biochemistry is about constraints, not rules. Rules can apply where biochemistry is indeterminate. The same biochemistry will apply in any of the biochemically indeterminate states. Biochemistry cannot account for the existence of logic circuitry. Likewise, electromagnetism alone cannot account for the existence of television or sound waves cannot account for the existence of speech.

    Logic is irreducible to the laws of nature. Logic traces back to choice contingent causation and, ultimately, to agency (which manifests itself in decision making in the context of planning with forethought) because naturalistic means are limited to chance and necessity and consequently are not capable of explaining the existence of logic.

    It is clear that you have a few major flaws in your current understanding of biology. Removing those flaws is dependent on you understanding the following:

    (i) logic is not the same as the laws of nature;
    (ii) biological organization is replete with built-in decision making;
    (iii) the decision making capability can plausibly only be a result of prior decision making, planning and forethought (intelligent causation);
    (iv) intelligent causation is irreducible to the limited naturalistic causation;
    (v) naturalistic causation is incapable of explaining the origin of life.

  90. 90
    wd400 says:

    That may be the strangest ID argument I’ve ever seen. Best of luck with it, I guess.

  91. 91
    Mung says:

    wd400: Wow, you guys have really lost it…

    Some of us never had it in the first place!

  92. 92
    bornagain77 says:

    wd400:

    “the idea that sequence space will have more function than previously thought if de novo genes are common is also a prediction of evolutionary biology.”

    And there you have it folks. No need for experimentation to establish just how common functionality is in sequence space. (Behe, Axe, Gauger, etc..). If functional ORFans are common then evolution must have predicted it. Save for the fact that, of course, evolution predicted no such thing at all and in fact ‘predicted’ quite the opposite.

    Similar species share similar genes – Cornelius Hunter
    The only figure in Darwin’s book, The Origin of Species, showed how he envisioned species branching off of one another. Similar species have a relatively recent common ancestor and have had limited time to diverge from each other. This means that their genes should be similar. Entirely new genes, for instance, would not have enough time to evolve. As François Jacob explained in an influential paper from 1977, “The probability that a functional protein would appear de novo by random association of amino acids is practically zero.” (Jacob) Any newly created gene would have to arise from a duplication and modification of a pre-existing gene. (Zhou et. al.; Ohno) But such a new gene would retain significant similarity to its progenitor gene. Indeed, for decades evolutionists have cited minor genetic differences between similar species as a confirmation of this important prediction. (Berra, 20; Futuyma, 50; Johnson and Raven, 287; Jukes, 120; Mayr, 35)
    But this prediction has been falsified as many unexpected genetic differences have been discovered amongst a wide range of allied species. (Pilcher) 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

    For wd400 to try to turn around and say that widespread ORFans are a successful prediction of evolution, is yet another shining example of the non-falsifiable, pseudo-scientific, nature of the religion of neo-Darwinism, which wd400 apparently believes in with all his heart, mind and soul.

  93. 93
    Box says:

    #92 bull’s eye, BA77!

    WD400: “the idea that sequence space will have more function than previously thought if de novo genes are common is also a prediction of evolutionary biology.”

    Translation:

    We now think that there is not much function in sequence space, but we predict that IF de novo genes are found to be common we will adjust our belief accordingly.
    Yes folks, yet another dashing prediction of evolutionary biology!

  94. 94
    wd400 says:

    The rest of my comment appears just up there Box, anyone can read it.

  95. 95
    bornagain77 says:

    EugeneS succinctly lays out the vast difference between agent causality and the chance/necessity causality of atheists.

    To which wd400 responds with dumb founded surprise that there could be such a sharp dividing point:

    “That may be the strangest ID argument I’ve ever seen. Best of luck with it, I guess.”

    Here are a few references that have been cited several times over the past few years which wd400 apparently has never seen before:

    Is Life Unique? David L. Abel – January 2012
    Concluding Statement: The scientific method itself cannot be reduced to mass and energy. Neither can language, translation, coding and decoding, mathematics, logic theory, programming, symbol systems, the integration of circuits, computation, categorizations, results tabulation, the drawing and discussion of conclusions. The prevailing Kuhnian paradigm rut of philosophic physicalism is obstructing scientific progress, biology in particular. There is more to life than chemistry. All known life is cybernetic. Control is choice-contingent and formal, not physicodynamic.
    http://www.mdpi.com/2075-1729/2/1/106/

    The Law of Physicodynamic Incompleteness – David L. Abel – 2011
    Excerpt: “If decision-node programming selections are made randomly or by law rather than with purposeful intent, no non-trivial (sophisticated) function will spontaneously arise.”
    If only one exception to this null hypothesis were published, the hypothesis would be falsified. Falsification would require an experiment devoid of behind-the-scenes steering. Any artificial selection hidden in the experimental design would disqualify the experimental falsification. After ten years of continual republication of the null hypothesis with appeals for falsification, no falsification has been provided.
    The time has come to extend this null hypothesis into a formal scientific prediction:
    “No non trivial algorithmic/computational utility will ever arise from chance and/or necessity alone.”
    https://www.academia.edu/11759341/Physicodynamic_Incompleteness_-_Scirus_Sci-Topic_Page

    The Formalism > Physicality (F > P) Principle – * David L. Abel – 2011
    ABSTRACT:
    The F > P Principle states that “Formalism not only describes, but preceded, prescribed, organized, and continues to govern and predict Physicality.” The F > P Principle is an axiom that defines the ontological primacy of formalism in a presumed objective reality that transcends both human epistemology, our sensation of physicality, and physicality itself. The F > P Principle works hand in hand with the Law of Physicodynamic Incompleteness, which states that physicochemical interactions are inadequate to explain the mathematical and formal nature of physical law relationships. Physicodynamics cannot generate formal processes and procedures leading to nontrivial function. Chance, necessity and mere constraints cannot steer, program or optimize algorithmic/computational success to provide desired nontrivial utility. As a major corollary, physicodynamics cannot explain or generate life. Life is invariably cybernetic. The F > P Principle denies the notion of unity of Prescriptive Information (PI) with mass/energy. The F > P Principle distinguishes instantiation of formal choices into physicality from physicality itself. The arbitrary setting of configurable switches and the selection of symbols in any Material Symbol System (MSS) is physicodynamically indeterminate—decoupled from physicochemical determinism.
    https://www.academia.edu/12952944/The_F_P_Principle_The_Formalism_Physicality_Principle_

  96. 96
    bornagain77 says:

    wd400 @ 94, and just what part of the rest of your evidence free ‘just so story’ do you think helps you with ORFans?

    You live in a pseudo-scientific fantasy land sir in which no matter how contradictory the finding, evolution morphs into what ever theoretical posture it needs to in order to explain the contradictory evidence away!

    As I have heard said before, the only evidence for the unlimited plasticity predicted Darwinism is within the theory itself. It can explain anything and be falsified by nothing.

  97. 97
    Silver Asiatic says:

    wd400 – ok, wow. There’s clearly nothing anyone can say at this point.

    Box and BA77 – you saw exactly what he did right there. I’m very glad about that because nobody would believe it if it was just me.

    Talk about losing it. Mapou is going to have a melt-down.

    If de novo genes are more common, then that means there is more function, and evolution predicted that. ???? My head is going to fall off.

    Ok, you win WD. I mean, nobody can beat that argument.

    More seriously, it’s pretty clear you don’t understand what we’re saying. It’s probably best just for me to leave it at that (I was not trolling previously but I also will not continue that line of discussion).

  98. 98
    wd400 says:

    It’s certainly clear that one of us doesn’t understand what I’m saying… The prediction is if de novos really are performing biological functions, then those functions will not be as biochemically-specific as those usually performed by older proteins and they will use shorter a/a sequences to perform them.

    Again, I really don’t know how that can be explained more simply. You seem to want to read some other meaning into it

  99. 99
    bornagain77 says:

    wd400 goes fishing for a just so story to save his blind faith in his Darwinian religion,,,

    i.e. Evolutionists have never demonstrated the origin of a single gene in the laboratory, and Darwinian evolution certainly never predicted ORFan genes in the first place.
    In fact, as pointed out previously, ORFans falsify a major prediction of evolution (see Cornelius Hunter post 92), but in case evolution ever did predict ORFans then I guess wd400 is hoping it would have predicted this following pattern,,,

    “The prediction is if de novos really are performing biological functions, then those functions will not be as biochemically-specific as those usually performed by older proteins and they will use shorter a/a sequences to perform them.”

    And yet ‘new’ ORFan genes are found to be just as essential as ‘older’ genes:

    Genes from nowhere: Orphans with a surprising story – 16 January 2013 – Helen Pilcher
    Excerpt: When biologists began sequencing genomes they discovered up to a third of genes in each species seemed to have no parents or family of any kind. Nevertheless, some of these “orphan genes” are high achievers (are just as essential as ‘old’ genes),,,
    http://ccsb.dfci.harvard.edu/w.....n_2013.pdf

    Can new genes arise from junk DNA? – August 2015
    Excerpt: Researchers are beginning to understand that de novo genes seem to make up a significant part of the genome, yet scientists have little idea of how many there are or what they do. What’s more, mutations in these genes can trigger catastrophic failures. “It seems like these novel genes are often the most important ones,” said Erich Bornberg-Bauer, a bioinformatician at the University of Münster in Germany.,,,
    “How does novel gene become functional? How does it get incorporated into actual cellular processes?” McLysaght said. “To me, that’s the most important question at the moment.”
    http://www.uncommondescent.com.....-junk-dna/

    New genes in Drosophila quickly become essential. – December 2010
    Excerpt: The proportion of genes that are essential is similar in every evolutionary age group that we examined. Under constitutive silencing of these young essential genes, lethality was high in the pupal (later) stage and (but was) also found in the larval (early) stages.
    http://www.sciencemag.org/cont.....2.abstract

    Dr. Giem has a lecture video on the subject:

    New Genes Are Essential 6-13-2015 by Paul Giem – video
    https://www.youtube.com/watch?v=6qgGPV1AO1E

    As to ORFan length, the following study is relevant:

    The following researchers removed 1,177 “orphan” DNA sequences, which were long stretches of 300 or more nucleotides, from the human gene catalogs simply because they did not fit the Darwinian story line:

    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

    In fact it turns out that the authors of the preceding ‘kick the ORFans out in the street’ paper actually did know that there was unbiased evidence strongly indicating the ORFan genes encoded proteins but chose to ignore it in favor of their preconceived evolutionary bias:
    http://www.uncommondescent.com.....ent-358547

    As should be needless to say, ‘adjusting evidence’ to fit a theory is NOT how science is done!

  100. 100
    Mung says:

    wd400: The prediction is if de novos really are performing biological functions, then those functions will not be as biochemically-specific as those usually performed by older proteins and they will use shorter a/a sequences to perform them.

    The claim then is that genes get longer over time and gain in specificity over time. Is this testable?

    A question about length. So the cell starts reading a stretch of DNA not previously transcribed. How likely is it that a stop codon will be encountered after some number of codons? Is this scenario even realistic any more given the findings of the ENCODE project?

  101. 101
    wd400 says:

    The test is pretty easy: are the functional de novos shorter.

    If we assume codons are sampled uniformally then the probability of getting a stop is 3/64. It would be different if you wanted to include nucleotide composition,but that differs among species any way. The probability of getting a string n codons long without a stop is (1-3/64)^n.

    So, there’s a 0.8% of a 100 codon run having no stops, should be plenty of those in a 3 billion bp genome.

    I’ve no idea what ENCODE has to do with such a scenario.

  102. 102
    Box says:

    WD400: But if de novo genes are not common then then the origin of new functiona sequences from junk DNA can be an exceedingly rare event and still provide us will all the superfamalies we know about.

    Box: I’m not sure I get your point. Starting with LUCA I see an obvious problem: the finding of biological function cannot always have been an exceedingly rare event in the evolutionary narrative.
    Right?

    WD400: (…) your post is the classic retreat to the origin of life tactic.

    My “starting with LUCA” isn’t an attempt to bring abiogenesis into the discussion. I did no such thing. I merely pointed out that your story doesn’t hold when we start with LUCA.
    If new functional sequences from LUCA’s junk DNA and her descendants are “an exceedingly rare event”, then it’s hard to see how this process can “still provide us will all the superfamilies we know about”.

    WD400: Without selection lineages would not be able to explore sequence nearly as efficiently (…)

    Interesting point. So this adds to the problem: starting with LUCA, in the absence of large selection lineages, exploring sequence space is inefficient.

  103. 103
    bornagain77 says:

    wd400 claims that evolution predicts that

    “genes get longer over time”

    except, or course, for when evolution predicts that genes will stay exactly the same size over time.

    Like, for instance, when Graur and company supposedly refuted ENCODE’s finding of widespread functionality in the genome by appealing to “how much of our genome has avoided accumulating changes over 100 million years”

    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 evolution predicts that genes will both grow longer and that genes will avoid accumulating change over time?

    How can that be? And exactly where is the mathematical equation, and empirical evidence, that predicts these two different results?

    Of course there is no mathematical equation, nor empirical evidence, that makes such contradictory predictions. The exact ‘prediction’ that Darwinists choose to invoke, i.e. staying the same or growing larger, depends entirely upon which data set the evolutionist is trying to avoid falsification by.

    Of supplemental note: In the following podcast, Dr. Sternberg’s emphasis is on ENCODE research, and how that research overturned the ‘central’ importance of the gene as a unit of inheritance. As well he reflects on how that loss of the term ‘gene’ as an accurate description in biology completely undermines the modern synthesis, (i.e. central dogma), of neo-Darwinism as a rational explanation for biology.

    Podcast – Richard Sternberg PhD – On Human Origins: Is Our Genome Full of Junk DNA? Part 5
    http://www.discovery.org/multi.....-dna-pt-5/

    Here is the rest of Dr. Sternberg’s lecture for those who may be interested in listening to it:

    Podcast: Richard Sternberg PhD – ” On Human Origins: Is Our Genome Full of Junk DNA? part 1
    http://www.discovery.org/multi.....-junk-dna/

    Podcast – Richard Sternberg PhD – On Human Origins: Is Our Genome Full of Junk DNA? Part 2 (Major Differences in higher level chromosome spatial organization)
    http://www.discovery.org/multi.....-dna-pt-2/

    Podcast: Richard Sternberg PhD – ” On Human Origins: Is Our Genome Full of Junk DNA? Part 3
    http://intelligentdesign.podom.....4_33-08_00

    Podcast – Richard Sternberg PhD – On Human Origins: Is Our Genome Full of Junk DNA? Part 4
    http://www.discovery.org/multi.....-dna-pt-4/

  104. 104
    Dr JDD says:

    Wd400 – you must also consider the frame the stop codon is in relative to the probability of a start codon (met) with appropriate transcriptional control sites up and downstream of the met start.

    This will significantly reduce the 0.8% probability figure.

  105. 105
    Box says:

    WD400,

    Box: How do we get to a regulatory system given that a novel gene arises from junk-DNA. How do you envision the steps towards a (novel) regulatory system?

    WD400: I explained one way — an element with it’s own cis-regulatroy sequences integrates alongside. That way you get expression down stream.

    Ok, so the novel gene is expressed by CREs. Let’s assume we are talking about a new protein. How do we get to regulation of the proper amount? And how does it reach its proper location?
    Simply producing a new protein without regulation, as you suggest, must be a threat to the organism.

    WD400: Because expression also depends on DNA accessibility and methylation state you end up with tissue-specific expression too.

    Sure …. If the new protein is only functional in the context of tissue-specific expression (due to epigenetic modifications such as DNA methylation) — IOW the protein has a very specific function — the problem of “how to get to regulation” increases.
    How can the new protein be tolerated by the organism, when it takes many generations to “install” regulation? How can the new gene be selected for if without regulation it has no function?
    And how can a step-by-step coming into existence of regulation be selected for if it is only functional when complete?

  106. 106
    bornagain77 says:

    OT: Of semi related note from crevo:

    Fate of a mutation in a fluctuating environment – March 17, 2015
    Excerpt: Evolution in variable environments depends crucially on the fates of new mutations in the face of fluctuating selection pressures. In constant environments, the relationship between the selective effect of a mutation and the probability that it will eventually fix or go extinct is well understood. However, our understanding of fixation probabilities in fluctuating environmental conditions is limited. Here, we show that temporal fluctuations in environmental conditions can have dramatic effects on the fate of each new mutation, reducing the efficiency of natural selection and increasing the fixation probability of all mutations, including those that are strongly deleterious on average. This makes it difficult for a population to maintain specialist adaptations, even if their benefits outweigh their costs.
    Abstract
    Natural environments are never truly constant,,,
    http://www.pnas.org/content/ea.....2.abstract

    More Flaws in Darwin’s Mechanism – August 27, 2015
    http://crev.info/2015/08/more-.....mechanism/

    That is certainly not a good finding if you are a neo-Darwinists, to put it very mildly.

    And that finding is on top of this finding:

    Using Computer Simulation to Understand Mutation Accumulation Dynamics and Genetic Load:
    Excerpt: We apply a biologically realistic forward-time population genetics program to study human mutation accumulation under a wide-range of circumstances.,, Our numerical simulations consistently show that deleterious mutations accumulate linearly across a large portion of the relevant parameter space.
    http://bioinformatics.cau.edu......aproof.pdf

    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

    What motivates many neo-Darwinists to persist in promoting such a failed theory? I think money may play a huge part in their lack of scientific integrity.

    Lynn Margulis Criticizes Neo-Darwinism in Discover Magazine (Updated) – Casey Luskin April 12, 2011
    Excerpt: Population geneticist Richard Lewontin gave a talk here at UMass Amherst about six years ago, and he mathemetized all of it–changes in the population, random mutation, sexual selection, cost and benefit. At the end of his talk he said, “You know, we’ve tried to test these ideas in the field and the lab, and there are really no measurements that match the quantities I’ve told you about.” This just appalled me. So I said, “Richard Lewontin, you are a great lecturer to have the courage to say it’s gotten you nowhere. But then why do you continue to do this work?” And he looked around and said, “It’s the only thing I know how to do, and if I don’t do it I won’t get grant money.”
    Lynn Margulis – biologist
    http://www.evolutionnews.org/2.....45691.html

  107. 107
    Dr JDD says:

    Box:

    We know that gene misregulation is a classic hallmark of disease. This is why there is a buzz in industry around epigenetic control of genes, how it works and is aberrant in disease, and how to modify it to treat disease.

    This is in adults as well. When we consider the regulation of developmental genes we see an even narrower windows for deviation from the tight genetic control – otherwise disaster occurs.

    The EVO narrative would have us believe that initially these genes didn’t need to be so tightly controlled but over time as they play an important role, and as other new genes evolve to be important, the regulation systems evolved and in turn regulation became more important.

    The problem with this is, it is purely a “just so” story with no actual evidence to support it. The only evidence that can be used is less complex species have less complex regulation. But this is a fallacy as it is circular and also does not demonstrate how you can maintain a viable organism while transitioning from one level of complex regulation to the next. It also misses the point that even simple organisms have quite complex regulation control of their genes.

    This is not evidence based science – it is who can come up with the best story science.

  108. 108
    Silver Asiatic says:

    … that creative ” Cosmic Substance,” with its “nebulous potentiality,” and ” indefinable latency,” to which in the end of his days Professor Huxley transferred the sceptre of creation, rudely snatched from the hand of his water-god Bathybius”. — William Bullen Morris

    Bathybius haeckelii was a substance that British biologist Thomas Henry Huxley claimed a source of all organic life.
    In 1868 Huxley studied an old sample of mud from the Atlantic seafloor taken in 1857. When he first examined it, he had found only protozoan cells and placed the sample into a jar of alcohol to preserve it. Now he noticed that the sample contained an albuminous slime that appeared to be criss-crossed with veins.

    Huxley thought he had discovered a new organic substance and named it Bathybius haeckelii, in honor of German biologist Ernst Haeckel. Haeckel had theorized about Urschleim (“primordial slime”), a protoplasm from which all life had originated. Huxley thought Bathybius could be that protoplasm, a missing link (in modern terms) between inorganic matter and organic life.

    Huxley published a description of Bathybius and also wrote to Haeckel to tell him about it. Haeckel was impressed and flattered and procured a sample for himself. In the next edition of his textbook The History of Creation Haeckel suggested that the substance was constantly coming into being at the bottom of the sea. Huxley did not agree but speculated that Bathybius formed a continuous mat of living protoplasm that covered the whole ocean floor.

    In 1872 the Challenger expedition began; it spent three years studying the oceans. The expedition also took soundings at 361 ocean stations. They did not find any sign of Bathybius, regardless of the claim that it was a nearly universal substance.

    In 1875 ship’s chemist John Young Buchanan analyzed a substance that looked like Bathybius from an earlier collected sample. He noticed that it was a precipitate of calcium sulfate from the seawater that had reacted with the preservative liquid (alcohol). Buchanan suspected that all the Bathybius samples had been prepared the same way and notified Thomson, the leader of the expedition. Thomson sent a polite letter to Huxley and told about the discovery.
    Huxley realized that he had been too eager and made a mistake. He published part of the letter in Nature and recanted his previous views. Later, during the 1879 meeting of the British Association for the Advancement of Science, he stated that he was ultimately responsible for spreading the theory and convincing others. Most biologists accepted this acknowledgement of error.

    Haeckel, however, did not want to abandon the idea of Bathybius because it was so close to proof of his own theories about Urschleim. He claimed without foundation that Bathybius “had been observed” in the Atlantic. He continued to support this position until 1883.

    Huxley’s rival George Charles Wallich, in turn, claimed that Huxley had committed deliberate fraud and also accused Haeckel of falsifying data; Haeckel did draw a series of pictures of the evolution of his Urschleim, supposedly based on observations.

  109. 109
    bornagain77 says:

    Dr JDD @ 107, that sounds a lot like Dr. Meyer’s criticism of Dr. Marshall’s attempted peer-reviewed rebuttal of ‘Darwin’s Doubt’:

    When Theory Trumps Observation: Responding to Charles Marshall’s Review of Darwin’s Doubt – Stephen C. Meyer – October 2, 2013
    Excerpt: Of course, Marshall thinks that these networks could have had a different, more flexible, character in the past. Yet, given what dGRNs do, namely, that they enable different cell types to organize themselves, and differentiate themselves from each other, in precise ways at precise times during the development of specific animal forms, it is hard to see how dGRNs could have functioned as regulatory networks and also exhibited the kind of flexibility that Marshall envisions. Developmental gene regulatory networks are control systems. A labile dGRN would generate (uncontrolled) variable outputs, precisely the opposite of what a functional control system does. It is telling that although many evolutionary theorists (like Marshall) have speculated about early labile dGRNs, no one has ever described such a network in any functional detail — and for good reason. No developing animal that biologists have observed exhibits the kind of labile developmental gene regulatory network that the evolution of new body plans requires. Indeed, Eric Davidson, when discussing hypothetical labile dGRNs, acknowledges that we are speculating “where no modern dGRN provides a model” since they “must have differed in fundamental respects from those now being unraveled in our laboratories.”8
    By ignoring this evidence, Marshall and other defenders of evolutionary theory reverse the epistemological priority of the historical scientific method as pioneered by Charles Lyell, Charles Darwin and others.9 Rather than treating our present experimentally based knowledge as the key to evaluating the plausibility of theories about the past, Marshall uses an evolutionary assumption about what must have happened in the past (transmutation) to justify disregarding experimental observations of what does, and does not, occur in biological systems. The requirements of evolutionary doctrine thus trump our observations about how nature and living organisms actually behave. What we know best from observation takes a back seat to prior beliefs about how life must have arisen.
    http://www.evolutionnews.org/2.....77391.html

    Further notes:

    Stephen Meyer Answers Charles Marshall (Peer Reviewed Paper) on Darwin’s Doubt – October 2013 (4 part response)
    http://www.evolutionnews.org/2.....77371.html

    Stephen Meyer vs. hostile reviewer Charles Marshall (audio of debate) – Dec. 1, 2013
    https://www.youtube.com/watch?v=wKqzQwT3JXk

    Response to Critics – Marshall – Part 1
    https://www.youtube.com/watch?v=zqYUoRVswRY

    Response to Critics – Marshall – Part 2
    https://www.youtube.com/watch?v=Cg8Mhn2EKvQ

    Response to Critics – Marshall – Part 3
    https://www.youtube.com/watch?v=fR_Agl41TbE

  110. 110
    wd400 says:

    JDD,

    Sure, I don’t that was what mung was asking. But if you calcualte the probability of start followed by n non-stop codons it’s 1/64 * (1-3/64)^n, which is abut 0.01% for 100 codons.

    The problem with this is, it is purely a “just so” story with no actual evidence to support it

    Nah. There are plenty of ways to test such and idea. The distribution of the age of genes is an obvious one. I presented another test above: we expect de novo genes to have relatively non-specific roles.

    Box,

    I don’t think you understood by point. You would end up with tissue-specific expression of transcripts in one go, because the expression of a gene depends on the local conditions re DNA methylation and accessibility. Those conditions already make tissue-specific expression patterns and they would apply to any newly expressed transcript int a given region too.

    For the rest of your comment you seem to conflate “LUCA” with a lone organism. That’s not the case at all, LUCA would have been the result of evolution itself (and quite likely one of many creatures alive at the time). The “L” is for last, after all.

  111. 111
    Virgil Cain says:

    Evolutionism requires de novo genes- how else did the first life arise if not from de novo genes?

    That is the whole argument- that materialistic processes couldn’t produce those de novo genes.

  112. 112
    bornagain77 says:

    “There are plenty of ways to test such an idea.”

    Caveat: Just be sure not to ask Darwinists for any real time empirical evidence/tests of unguided material processes ever creating new genes. Because there is ZERO evidence in that regards.

    Be sure only to ask for historical genetic evidence that assumes the conclusion of evolution into the premise of its analysis of genetic sequences.

    Then they got plenty of evidence because they’ve already pulled a shell game on you by assuming the de novo sequences evolved in their analysis of the sequences.

    Yet they have never actually experimentally established that it is even remotely possible for unguided material processes to create genes in the first place. i.e. it’s a shell game!

    Three Shell Game
    https://www.youtube.com/watch?v=IFLa_tl4Rk0

  113. 113
    Mung says:

    wd400,

    Thanks. So just looking at basic probabilities any de novo gene is likely to be very short. I think the words I was looking for were promoter and terminator.

    https://en.wikipedia.org/wiki/Promoter_%28genetics%29

    https://en.wikipedia.org/wiki/Terminator_%28genetics%29

    ENCODE may be relevant because it seems to indicate a high probability that the region is already being transcribed.

    Perhaps the while idea of a de novo gene is absurd.

    Your choice of a 100 codon sequence seems pretty arbitrary, and obviously there is a much greater probability of shorter de novo sequences, by your own admission.

    Is there evidence for this?

  114. 114
    wd400 says:

    I’m not quite sure what you are trying to ask. Terminators don’t have anything to do with stop codons which is what you asked about in the first place. Calculating the probability of hitting a transcription terminator is not straightfoward, partly because transcription is pretty sloppy in big eukaryotes.

    In reply to your other comments.

    About 1% of random ORFs will be 100 codons or longer . Of course 100 is arbitrary, you can do the calculation for any length you like (it’s 1 – [ Sum 1 to n [(1-3/64)^(n-1) * 3/64 ] ]).

    So, yes, most randomly generated ORFs will be shorter than 100 codons. But the question for do novo genes is about random ORFs that have a biological function. There might well be more very short random proteins, but if such small proteins are unlikely to have functions they won’t stick around or get fixed by selection. I chose 100 as a middle ground, as I say, it’s easy to calculate for any number.

    You’ll have to ask the people that are making a big deal of do novo genes whether ENCODE undercuts them — thought I still can’t see how it would.

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