'Junk DNA' News

New genes come from junk DNA?

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Further to “Linc RNA–once believed useless–plays a role in the genome, here is some interesting research on fruit flies:

From ScienceDaily:

Geneticists have long puzzled about how completely new genes appear. In a well-known model proposed by Nobel laureate Susumu Ohno, new functions appear when existing genes are duplicated and then diverge in function. Begun’s laboratory discovered a few years ago that new genes could also appear from previously non-coding stretches of DNA, and similar effects have since been discovered in other animals and plants.

“This is the first example of totally new genes still spreading through a species,” said Li Zhao, a postdoctoral researcher at UC Davis and first author on the paper.

from The Scientist:

“Until recently, de novo origin of genes was considered to be so unlikely as to be impossible,” comparative genomicist Aoife McLysaght of the Smurfit Institute of Genetics at Trinity College in Dublin, Ireland, who was not involved in the study, told The Scientist in an e-mail. “[T]his population level analysis is important because it gives a new insight into the very early stages of the origin and establishment of genes de novo.”

“To show [the formation of de novo genes] at the population genetics level is really a nice story,” agreed evolutionary biologist Diethard Tautz of the Max Planck Institute for Evolutionary Biology in Plön, Germany, who also did not participate in the research. “It shows the power of generating from nothing, so to speak.”

First, it’s junk. Now it’s “nothing.”

See also:What? Darwin’s followers did not use junk DNA as an argument for their position? Of course they did. It would have been a slam dunk, if their position were correct.

43 Replies to “New genes come from junk DNA?

  1. 1
    tjguy says:

    “Until recently, de novo origin of genes was considered to be so unlikely as to be impossible,” comparative genomicist Aoife McLysaght of the Smurfit Institute of Genetics at Trinity College in Dublin, Ireland, who was not involved in the study, told The Scientist in an e-mail.

    Is that right? How come we only find out about these problems when they are “solved”? Now that they think they have an answer they are willing to admit that they didn’t know the answer up until now. But that’s not what they taught us in school!

    Does anyone remember being told by scientists that the Darwinian evolutionary de novo origin of genes was thought to be virtually impossible up until now?

    This is the kind of honesty that IDers and creationists want to see in the science books!!!

    And, not only when they think they have an answer, even before they have the answer. But I guess this kind of brutal honesty is just not possible for them. They fear the mileage that their opponents will get from it so instead of being honest, they make bold claims and state that evolution is a fact.

    Anyone smell a rat here?

    I don’t know enough about this claim to evaluate it properly, but my guess is that it still doesn’t solve their problem.

  2. 2
    Mapou says:

    ScienceDaily:

    In a well-known model proposed by Nobel laureate Susumu Ohno, new functions appear when existing genes are duplicated and then diverge in function.

    How does anybody conclude from this that new genes are created?
    Copying an existing gene and mutating it is not the same as creating a new gene with a novel functionality. Sorry. It’s just a variant of an old gene.

    Besides, how did this gene creation capability evolve? How does an organism know what kind of new gene is needed? This has DESIGN written all over it.

  3. 3
    wd400 says:

    Anytime someone told you gene duplication was thought to be the major driver of new gene function they were also implying that the de novo origin of genes from junk DNA was unlikely.

    I’m not sure it’s good news for your side that new genes can arise from junk sequences, though…

  4. 4
    wd400 says:

    Mapou,

    You should read Ohno, or perhaps read up about neofunctionalization which is the model of gene evolution that Ohno proposed.

  5. 5
    bornagain77 says:

    Funny how all these comparative genomic studies, (i.e. seeing faces in the clouds studies 🙂 , which are always done by Darwinists with Darwinian assumptions of course, the studies always seem to support Darwinian evolution, but when push comes to shove in actually demonstrating in the lab that Darwinian evolution is feasible, then their stories always falls completely apart. For instance in fruit flies, the species they considered in their comparative analysis, we find such examples against Darwinism as the following,,,

    Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) – October 2010
    Excerpt: “Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, “This research really upends the dominant paradigm about how species evolve,” said ecology and evolutionary biology professor Anthony Long, the primary investigator.
    http://eebweb.arizona.edu/nach.....l_2010.pdf

    Darwin’s Theory – Fruit Flies and Morphology – video
    http://www.youtube.com/watch?v=hZJTIwRY0bs

    Response to John Wise – October 2010
    Excerpt: But there are solid empirical grounds for arguing that changes in DNA alone cannot produce new organs or body plans. A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism.
    http://www.evolutionnews.org/2.....38811.html

    …Advantageous anatomical mutations are never observed. The four-winged fruit fly is a case in point: The second set of wings lacks flight muscles, so the useless appendages interfere with flying and mating, and the mutant fly cannot survive long outside the laboratory. Similar mutations in other genes also produce various anatomical deformations, but they are harmful, too. In 1963, Harvard evolutionary biologist Ernst Mayr wrote that the resulting mutants “are such evident freaks that these monsters can be designated only as ‘hopeless.’ They are so utterly unbalanced that they would not have the slightest chance of escaping elimination through natural selection.” –
    Jonathan Wells

    Fruit fly with the wings of beauty – July 2012
    Excerpt: But a closer examination of the transparent wings of Goniurellia tridens reveals a piece of evolutionary(?) art. Each wing carries a precisely detailed image of an ant-like insect, complete with six legs, two antennae, a head, thorax and tapered abdomen.
    http://www.thenational.ae/news.....-of-beauty

    ‘No matter what we do to a fruit fly embryo there are only three possible outcomes, a normal fruit fly, a defective fruit fly, or a dead fruit fly. What we never see is primary speciation much less macro-evolution’ –
    Jonathan Wells

    50 million year old Fruit Fly fossil compared to modern Fruit Fly – picture
    http://en.harunyahya.net/fruit.....on-museum/

    Seeing the Natural World With a Physicist’s Lens – November 2010
    Excerpt: Scientists have identified and mathematically anatomized an array of cases where optimization has left its fastidious mark, among them;,, the precision response in a fruit fly embryo to contouring molecules that help distinguish tail from head;,,, In each instance, biophysicists have calculated, the system couldn’t get faster, more sensitive or more efficient without first relocating to an alternate universe with alternate physical constants.
    per NY Times

    Development of a fly embryo in real time – video
    http://www.youtube.com/watch?v=OQ86d9sTeaQ

    Criticality in morphogenesis – September 17, 2013
    Excerpt: In many regards, a brief time-lapse video can teach more about embryonic development than any amount of reading. It is hard not to be impressed how a repeatable form reliably emerges despite considerable variation in both genes and environment. While it had been hoped that concepts borrowed from statistical mechanics or the ideas of self-organized criticality could help to create some kind of physics-based theory of development, much of what has been done lies only at the level of metaphor. In a paper just released to ArXiv, William Bialek and his colleagues from Princeton University, have taken their search for the signature of criticality in a more specific direction. They looked at a particular set of transcription factors in Drosophila embryos which control spatiotemporal development. By analyzing fluctuations in the expression levels of these so-called gap genes, they found evidence for critical (fine) tuning in this particular network.
    http://phys.org/news/2013-09-c.....nesis.html

    “The brain of a small fruit fly uses energy in the micro-watts for complex flight control and visual information processing to find and fly to food. I don’t think a supercomputer could yet simulate what the fruit fly brain does even while using megawatts of energy. The difference of over ten orders of magnitude and the level of energy used is an indication of just how incredible biological systems are.
    Professor Keiichi Namba, Osaka University
    http://www.youtube.com/watch?f.....48#t=1645s

    TEDx Video: Flight of the Fruit Fly – October 8, 2013
    Excerpt: “Dickinson is a very intense guy himself, and gives a remarkable discussion of what makes the engineering that goes into fruit fly flight so amazing.” (4:50 minute mark of video lists several fascinating high tech ‘accessories’ of the fruit fly, such as a gyroscope)
    http://www.evolutionnews.org/2.....77641.html

  6. 6
    Moose Dr says:

    The vehicle of a friend of mine broke down on a lonely road in Alaska. The hose going to his cabin heater broke, destroying the integrity of his car’s cooling system. He left his car, and began walking up the road to pray. There, laying on the side of the road was the correct hose, cut to the correct length, with the needed hose clamps. He, an air conditioning engineer, was able to permanently repair his vehicle.

    Darwinists say, “accidents happen”. He calls it a miracle.

  7. 7
    gpuccio says:

    wd400:

    I’m not sure it’s good news for your side that new genes can arise from junk sequences, though…

    It is extremely good news for our side.

    This is exactly what I have always stated here. New genes are intelligently engineered as non coding sequences, and when they are functional they are released as coding sequences.

    That simply means that NS has no role in engineering new genes (it can simply act in fixing them once they are ready).

    That simply means that new genes are either generated by a merely random search (which is practically impossible) or that they are designed.

    That simply means that “our side” is right. 🙂

  8. 8
    nightlight says:

    #7 “This is exactly what I have always stated here. New genes are intelligently engineered as non coding sequences, and when they are functional they are released as coding sequences.”

    That’s what James Shapiro calls “natural genetic engineering.” Unfortunately, the present ID is being derailed and mislead by the consciousness-talk and super-naturalism (heavenly interventions overriding natural laws), micro vs macro evolution, natural vs ???, the absurd part-time intelligent agency helping out when the “nature” can’t do it… from Discovery Institute and their choir.

    As result, thanks chiefly to DI, this whole field of cellular intelligence, natural genetic engineering, cellular biochemical networks as self-programming distributed computers which are the intelligence behind the design of evolutionary novelty, etc, has been and will continue to be claimed by neo-Darwinists as what they were always saying, as they gradually phase out the “random mutation” from their story and morph it into whatever the latest findings come out in these fields.

  9. 9
    Joe says:

    New genes can arise from non-coding sequences by design. THat is exactly what I was trying to tell wd400 earlier, in another thread. The alleged junk DNA is there for future considerations, sort of like a stock room with parts ready for assembly and use.

    Also, as Dr Spetner pointed out, there is no reason to say that gene duplications are a Darwinian mechanism. IOW if Darwinism/ neo-darwinism wants to call on point mutations for the source of variation, they are welcome to it. All other genetic changes have to first be demonstrated to be happenstance/ accidents as opposed to just baldly declaring them to be.

  10. 10
    bornagain77 says:

    Hate to burst you guys bubble, but they have not actually demonstrated that a functional protein/gene can arise from non-coding sequences, they merely hypothesize that the similar sequences they found in non-coding regions,,,

    “gives a new insight into the very early stages of the origin and establishment of genes de novo.”

    Personally, I certainly would not put any stock whatsoever into this since they merely believe that the similar sequences they found ‘gives insight’ into how evolution happene9d because of course, in their Darwinian worldview, IT MUST have evolved. There is no other option for them! In other words, There is no actual empirical evidence that sequences that not currently code for proteins will magically start coding for proteins in the future. In fact, This study is another example of how Darwinian presupposition constantly mislead science down rabbit trails!

  11. 11
    Joe says:

    An aha moment- thanks bornagain77…

  12. 12

    This isn’t that new, see On the origin of new genes in Drosophila by Zhou Q et al Genome Res. 2008;18:1446–1455 etc etc ad nauseum. This work has been going on for years. Still quite funny how the claims about “junk DNA” raise their head again. Does anyone use that term other than ID theorists and creationists when discussing genetics ?

    In the end it isn’t very good for ID. The only argument ID have is it can’t be done with a random search of all the space.

    But stored and forwarded copies with changes means that there exists mechanistic (spontaneous i.e. no ID) mechanisms for copying genes and there exists mechanistic (spontaneous i.e. no ID) mechanisms for mutations and there exists a mechanistic (spontaneous i.e. no ID) mechanisms for selection (i.e. natural selection).

    ID theorists claim that random searches are impossible (and that’s a fact which also brutal for a “designer” unless it is outside of our spacetime) but the copy and mutate with natural selection is a biased random walk. Whilst biased random walks have no guarantee of success (and neither does the random search that is so loved by ID theorists when constructing their arguments about how nature doesn’t work) the time is vastly reduced from brute force.

    What people forget is that we’re not looking for an EXACT match but a just-good-enough. This is a significant point that dramatically changes the problem landscape.

    If you are brute forcing a software key then you need an EXACT match but given isoforms exist then clearly an exact match is not a requirement for nature. How good is good-enough ? NO one knows. ID theorists don’t know though they seem to be demanding exact matches.

    A biased random walk must have “islands” of fitness. Why ? Well for a sequence to be naturally selected it must be fitter in some way that other combinations.If the distance between islands of fitness is too great (the worse case is to have only ONE fit solution), then the time complexity of O(c^n) is a brutal barrier to success. In effect the near impossibility of a solution becomes a natural selector in that nature randomly discovers the advantages of dynamic programming.

  13. 13
    phoodoo says:

    Lincoln,

    Are you seriously going to claim that evolutionists have not been saying for years (including many of the leading figures in American culture)that junk DNA is a prediction of Darwinian evolution, and that if the there really is no junk DNA than then this is a big problem for the theory?

    Let me make sure you want to stand firmly behind that statement, and don’t go running off and claim you are not saying that when you are proven wrong.

  14. 14
    gpuccio says:

    nightlight:

    “Natural genetic engineering” has two problems:

    1) How can it generate a completely new complex functional protein sequence, if it does not already know it? We cannot do that today, with all our knowledge of biochemical laws, and all our computing power. How do you believe that natural algorithms do that acting on some non coding sequence, that cannot even be tested by NS?

    2) If complex algorithms embedded in the cell could really do that (which I absolutely don’t believe they can do), you should still explain the origin of those immensely complex algorithms, whose purpose seems to be to compute new functional protein sequences.

  15. 15
    phoodoo says:

    Nightlight,

    I agree with you to a great extent, but when you say:

    “(heavenly interventions overriding natural laws), micro vs macro evolution, natural vs ???, the absurd part-time intelligent agency helping out when the “nature” can’t do it… from Discovery Institute and their choir”

    I am not so sure this is an accurate representation of anything DI says about ID. Who says “part-time intelligent agent helping out when nature can’t?”

    But again, I do agree the evolutionists have tried to completely shift their claims in the middle of the discussion, and suddenly claim this is perfectly compatible with Darwinian processes. I find Shapiro to be completely disingenuous when he tries to give up random mutations but still claim its fits the theory fine. Anything fits the theory if that’s the case.

    Why does he think no one would notice the contradiction? I guess he is just afraid of what Coyne would say if he jumps ship completely.

  16. 16
    gpuccio says:

    Lincoln Phipps:

    Useless probably, but let’s try:

    But stored and forwarded copies with changes means that there exists mechanistic (spontaneous i.e. no ID) mechanisms for copying genes and there exists mechanistic (spontaneous i.e. no ID) mechanisms for mutations and there exists a mechanistic (spontaneous i.e. no ID) mechanisms for selection (i.e. natural selection).

    OK, and so please explain:

    How do those mechanistic mechanisms generate by mechanistic mutations exactly the functional sequence in a non coding gene, which by definition cannot be selected by NS? Violating all the probabilistic barriers for a merely random system?

  17. 17
    gpuccio says:

    BA and Joe:

    I could not read the original paper (it is not free), but it seems that they found about 100 new protein genes that are specific to Drosophila Melanogaster, and not present in other Drosophila species.

    But, in those other species, non coding sequences which presented significant homology to the Melanogaster new genes were present.

    This is a very good argument, IMO. The best explanation for that is that the new genes were engineered in the other species, and expressed in Melanogaster for some new function.

    Exactly like a human protein engineer would do. And exactly like a computer software engineer can do, when he gradually writes new part in an existing software, but only activates them in the end, when they are necessary for the final outcome to be tested.

  18. 18
    sixthbook says:

    @Bornagain:
    That’s exactly what I was thinking when I read this. Thanks for confirming.

  19. 19
    gpuccio says:

    phoodoo:

    But again, I do agree the evolutionists have tried to completely shift their claims in the middle of the discussion, and suddenly claim this is perfectly compatible with Darwinian processes. I find Shapiro to be completely disingenuous when he tries to give up random mutations but still claim its fits the theory fine. Anything fits the theory if that’s the case.

    Why does he think no one would notice the contradiction? I guess he is just afraid of what Coyne would say if he jumps ship completely.

    I perfectly agree with you.

    That’s the problem with these neo-neo-darwinists. They are good at seeing the problems in neo-darwinism. But they are much less credible than neo-darwinists when they try some alternative explanation, always, obviously, leaving out design.

  20. 20

    Technical question:

    . . . new genes could also appear from previously non-coding stretches of DNA . . .

    Does this mean (i) that the relevant DNA strand was re-written so that it now became “coding” DNA, or (ii) that the strand stayed the same, but the cell treated it differently, transcribing, translating and then producing a protein product from the string?

    Just wondering if anyone knows?

  21. 21
    bornagain77 says:

    gpuccio you state:

    “This is a very good argument, IMO.”

    But alas ‘a very good argument’ does not empirical evidence make! If I wanted ‘a very good argument’ instead of actual empirical evidence to form my basis for making a valid scientific inference, I would have stopped at “Origin of Species” like Darwinists did:

    “As this whole volume is one long argument, it may be convenient to the reader to have the leading facts and inferences briefly recapitulated . . .”
    Charles Darwin, “On The Origin of Species”

    A note of interest is that genetic similarity is overrated:

    A Primer on the Tree of Life (Part 4)
    Excerpt: “In sharks, for example, the gut develops from cells in the roof of the embryonic cavity. In lampreys, the gut develops from cells on the floor of the cavity. And in frogs, the gut develops from cells from both the roof and the floor of the embryonic cavity. This discovery—that homologous structures can be produced by different developmental pathways—contradicts what we would expect to find if all vertebrates share a common ancestor. – Explore Evolution
    http://www.evolutionnews.org/2......html#more

    Neo-Darwinism’s Gene Homology Problem – video
    http://www.youtube.com/watch?v=_6P6bXA50c0

    as well New ORFan gene are often found to be deeply embedded in embryonic development:

    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

    Yet mutations expressed early in embryonic development are the most likely to be catastrophic and therefore are the least likely to be tolerated:

    Darwin or Design? – Paul Nelson at Saddleback Church – Nov. 2012 – ontogenetic depth (excellent update) – video
    Text from one of the Saddleback slides:
    1. Animal body plans are built in each generation by a stepwise process, from the fertilized egg to the many cells of the adult. The earliest stages in this process determine what follows.
    2. Thus, to change — that is, to evolve — any body plan, mutations expressed early in development must occur, be viable, and be stably transmitted to offspring.
    3. But such early-acting mutations of global effect are those least likely to be tolerated by the embryo.
    Losses of structures are the only exception to this otherwise universal generalization about animal development and evolution. Many species will tolerate phenotypic losses if their local (environmental) circumstances are favorable. Hence island or cave fauna often lose (for instance) wings or eyes.
    http://www.saddleback.com/mc/m/7ece8/

    A Piece from the Developmental Symphony – February 2012
    Excerpt: Embryonic development is an astounding process that seems to happen “automatically.”,,, The timing of each step is too precise and the complexity is too intricate to assume that these processes are the mere accumulation by happenstance of changes to regulatory genes. Each gene plays its role at a certain time, and like a symphony, each is activated and silenced in turn such that the final result is a grand performance of orchestrated effort that could only have occurred through design.
    http://www.evolutionnews.org/2.....55921.html

    Indeed as Dr. Meyer pointed out in ‘Darwin’s Doubt’ (and took Marshall to school on), the flexibility of developmental gene regulatory networks (dGRNs) in minimal:

    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
    http://www.evolutionnews.org/2.....79811.html

    Thus it is not just a matter of expressing a new protein from junk DNA, of from wherever, it is a matter a rewriting an entire developmental Gene Regulatory Network so as to incorporate the new hypothetical gene/protein into the developmental process that is not catastrophic. A much harder proposition for ‘bottom up’ neo-Darwinian mechanisms than most people realize!

    i.e. ‘Top Down’ not ‘Bottom up’ construction is required!

  22. 22
    Joe says:

    FYI- Art Hunt’s favorite is TURF-13- a new gene that produced a new protein in maize- due to a recombination of previously non-coding DNA.

    I’m surprised he hasn’t shown up or perhaps he is just shaking his head…

  23. 23
    Joe says:

    Eric Anderson (aka Mr Anderson, aka Neo) 🙂 :

    Does this mean (i) that the relevant DNA strand was re-written so that it now became “coding” DNA, or (ii) that the strand stayed the same, but the cell treated it differently, transcribing, translating and then producing a protein product from the string?

    (i)

  24. 24
    bornagain77 says:

    as to TURF-13,,

    On the non-evolution of Irreducible Complexity – How Arthur Hunt Fails To Refute Behe
    Excerpt: furthermore, T-urf 13 involves a kind of degradation of maize. In the case of the Texas maize–hence the T—the T-urf 13 was located by researchers because it was there that the toxin that decimated the corn grown in Texas in the late 60?s attached itself. So the “manufacturing” of this “de novo” gene proved to make the maize less fit. This is in keeping with Behe’s latest findings.
    http://www.uncommondescent.com.....ent-373178

    How Arthur Hunt Fails To Refute Behe (T-URF13)- Jonathan M – February 2011
    http://www.uncommondescent.com.....ent-373010

  25. 25
    Mapou says:

    If Darwinian evolution necessitates the duplication and modification of existing genes, how did this ability evolve before it existed? Talk about voodoo science.

  26. 26
    Joe says:

    bornagain77- That is why I refrained from going further than what I posted. It is still a new gene that codes for a new protein. And it came from non-coding DNA via recombination.

    Art is full of it wrt his claims about it and ID/ IC.

  27. 27
    gpuccio says:

    Eric:

    It’s definitely the second option.

    Again, I could not read the whole paper, but from the abstract I would say that they found important homologies between the new genes in Melanogaster and non coding sequences in the other species. That means that non coding DNA in the other species of Drosophila already has a significant part of the functional sequence, but in those other species it is not translated into a protein, and therefore it is not used and has no real function.

    In Melanogaster, further variation transforms the non coding sequence into an ORF, which is both transcripted and translated, but keeps the information that was already present in the non coding sequences. So, the protein appears.

    The important point here is that NS can have no role in finding the correct sequence when the protein is still non expressed. IOWs, the protein is expressed only when it is “ready”. Then NS can act fixing it ansd expanding it to the whole population (of Melanogaster).

  28. 28
    Joe says:

    Mapou:

    If Darwinian evolution necessitates the duplication and modification of existing genes, how did this ability evolve before it existed?

    They bypass that part and start with imperfect replicators that already have genes ready for modification. What do you expect from an imperfect concept? 🙂

  29. 29
    Mapou says:

    Joe @28,

    I would not say that the concept is imperfect. I would call it what it is: pure unmitigated BS.

  30. 30
    bornagain77 says:

    Joe, actually even your restrained claim is overstating the case:

    Per PaV
    Excerpt,,,,”(5) In a recent paper, a “de novo” gene was being touted. Guess what? It turns out that a portion of a “non-coding” gene and its flanking element was involved in the manufacturing of this “de novo” gene. This is exactly what we find in T-urf 13. Hence, when I used the term “machinery” in (3) above, indeed, this seems to be a maneuver that living cells have at their disposal, thus warranting a search for this new mechanism and not the false claim of truly “de novo” genes. As in the case with T-urf-13, the “new” gene is nothing more than the demolishing of another gene: i.e., the critical portion of the “de novo” gene represented no more than a portion of another gene. (The transcribed portion of T-urf 13 that provides this ‘amazing’ gated ion-channel, is only a very small part of the “de novo” gene.) Again, this is consistent with Behe’s latest article.

    (6) There are two “nuclear restorers” that can restore the plant to ‘male fertility’ from the sterile condition found in the Texas maize from which T-urf 13 is derived. Interestingly, and provocatively, when the “nuclear restorers” work their magic, guess what? T-urf 13 is no longer found: evidence, again, that a “mechanism”, and “machinery” is at play.

    Getting back to the original post here, Jonathan quite correctly demonstrates that Darwinian mechanisms are being assumed to be at work with the manufacture of URF-13 protein, and, yet, from all indications, whatever is happening to the maize, has very little to do with true Darwinian mechanisms. I would hope Arthur Hunt might acknowledge this.

    Let’s just finish here by pointing out again that T-urf 13 involves a kind of degradation of maize. In the case of the Texas maize–hence the T—the T-urf 13 was located by researchers because it was there that the toxin that decimated the corn grown in Texas in the late 60?s attached itself. So the “manufacturing” of this “de novo” gene proved to make the maize less fit. This is in keeping with Behe’s latest findings.,,,”
    http://www.uncommondescent.com.....ent-373178

  31. 31
    bornagain77 says:

    Of related note, other popular examples of supposed de-novo gene evolution are debunked here:

    Hopeless Matzke -David Berlinski & Tyler Hampton August 18, 2013
    http://www.evolutionnews.org/2.....75631.html

  32. 32
    Joe says:

    Mapou, I yield to your superior descriptor.

  33. 33
    Joe says:

    bornagain77- Apologies but I think we are talking past each other.

    Are you saying there wasn’t a new gene formed or that the new gene degraded the maize or that the new gene did not arise via darwinian mechanisms?

    TURF-13- de novo gene from non-coding DNA, yes or no? Or part was from non-coding and part was from an existing gene?

    I understand that the protein isn’t helping the maize. That is not the point.

  34. 34
    bornagain77 says:

    Joe hopefully this brings clarity, from what I can tell from this following paper, TURF-13 is a constitutively transcribed mitochondrial gene that is derived from two already existing genes.

    Genetic and molecular basis of cytoplasmic male sterility in maize – 2007
    Excerpt page 51:The specific virulence of B. maydis towards CMS-T maize was found to be due to mitochondrial gene Turf 13, which is also responsible for the CMS phenotype in CMS-T. It is a constitutively transcribed gene which produces a 13 kd polypetide (Williams et al., 1992). Such a polypeptide is not found in CMS -S, CMS -C or normal maize cytoplasm. Turf 13 is a chimeric region gene which is a recombination product of 5’ region of the atp 6 gene and 3’ region of the 265 ribosomal gene (rrn 26). Its transcription is presumably under the control of the atp 6 promoter (Stamper et al., 1987). It is located in 3547-nucleotide mt DNA sequence that contains two open reading frames, one coding for urf 13 and the other for orf 221, which codes for a 25 kd polypeptide consisting of 221 amino acids and is 77 nucleotides downstream of urf 13 (Levings, 1990). The orf 221 encodes a membrane bound protein that has been identified as ATP4 (Heazlewood et al., 2003).
    http://agrobiol.sggw.waw.pl/~c....._2_1_7.pdf

  35. 35
    bornagain77 says:

    of footnote to post 21,,
    http://www.uncommondescent.com.....ent-488367

    ,,,is the fact that the development Gene Regulatory Network of fruit flies is shown not to be reducible to the sequential information in DNA but ‘Depends on Pre-existing Spatial Coordinates’

    Gene Regulatory Networks in Embryos Depend on Pre-existing Spatial Coordinates – Jonathan Wells – July 2011
    Excerpt: The development of metazoan embryos requires the precise spatial deployment of specific cellular functions. This deployment depends on gene regulatory networks (GRNs), which operate downstream of initial spatial inputs (E. H. Davidson, Nature 468 [2010]: 911). Those initial inputs depend, in turn, on pre-existing spatial coordinate systems. In Drosophila oocytes, for example, spatial localization of the earliest-acting elements of the maternal GRN depends on the prior establishment of an anteroposterior body axis by antecedent asymmetries in the ovary. Those asymmetries appear to depend on cytoskeletal and membrane patterns rather than on DNA sequences,,,
    http://www.discovery.org/scrip.....38;id=7751

  36. 36
    gpuccio says:

    Joe:

    TURF-13- de novo gene from non-coding DNA, yes or no? Or part was from non-coding and part was from an existing gene?

    Just to understand, I have looked at the pertinent sources.

    The gene is 348 bp long.

    Very simply, most of the gene (about 260 nucleotides) is obviously derived, with some modifications, including mutations, insertions and deletions, from a sequence of non coding mithocondrial DNA (the flanking region of a ribosomal RNA gene). The homology is very high (about 86%), with an expect of 9e-72.

    The following 40 nucleotides (more or less) have no homology with anything.

    The final 49 nucleotides have absolute homology with a small part of a mithocondrial DNA gene coding for ribosomal RNA (49 identities), with an expect of 4e-15.

    These are the facts.

  37. 37
    Joe says:

    Thank you- that clears it up very nicely.

  38. 38
    bornagain77 says:

    Well Joe, I’m sorry for any misdirection I may have given you. gpuccio, if I could trouble you for a reference(s) so that I may adjust my notes to more precisely reflect what is happening with Turf-13?

  39. 39
    bornagain77 says:

    as well gpuccio, are you agreed that the new gene degraded the maize?

  40. 40
    Querius says:

    tjguy noted:

    Is that right? How come we only find out about these problems when they are “solved”? Now that they think they have an answer they are willing to admit that they didn’t know the answer up until now. But that’s not what they taught us in school!

    Exactly! I guess the goal is to jump from the safety of one dogmatic position to another, with a minimum amount of vulnerable exposure to critical thinking and the scientific method.

    -Q

  41. 41
    gpuccio says:

    BA:

    I think you can find most of the information in the original essay by Arthur Hunt, but I have blasted personally the gene to check, and the numbers I have given are from my blast.

    I have not checked about the protein function. Indeed, I believe that not enough is known about the protein.

    I agree that the two main effects seem to be degrading (male sterility and susceptibility to a toxin), but I am not really any expert of maize. I would wait to know more about the protein structure, the sequence structure relationship and its biochemical interactions.

  42. 42
    bornagain77 says:

    Well gpuccio not to knock your blast work, but since my reference post dates Art Hunt’s references, and since I don’t trust Art Hunt as far as I can throw him, (he is up there with Moran and Myers in my book), then I will stick to my reference for now, with more of a emphasis on the degrading and cyclical nature of the adaptation, until more is learned about it. As far as I can tell, from Berlinski’s take down of Matzke’s examples, this is a lone outlier example that deserves to be questioned.

  43. 43
    gpuccio says:

    BA:

    OK, that’s fine.

    I would add that I trust Art Hunt for his technical work, which as far as I can judge is very good, but I absolutely don’t trust him for his conclusions and general reasoning.

    However, I repeated personally the blast work exactly to be certain of what I was saying.

    I think that this particular example is very interesting, and that it deserves further attention. I agree with you that we have not sufficient data, at present, to draw final conclusions. That’s why I limited myself to providing some undeniable facts.

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