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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.

Comments
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.gpuccio
January 25, 2014
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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.bornagain77
January 24, 2014
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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.gpuccio
January 24, 2014
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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. -QQuerius
January 24, 2014
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as well gpuccio, are you agreed that the new gene degraded the maize?bornagain77
January 24, 2014
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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?bornagain77
January 24, 2014
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Thank you- that clears it up very nicely.Joe
January 24, 2014
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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.gpuccio
January 24, 2014
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of footnote to post 21,, https://uncommondescent.com/junk-dna/new-genes-come-from-junk-dna/#comment-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/scripts/viewDB/filesDB-download.php?command=download&id=7751bornagain77
January 24, 2014
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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/~cbcs/articles/CBCS_2_1_7.pdfbornagain77
January 24, 2014
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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.Joe
January 24, 2014
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Mapou, I yield to your superior descriptor.Joe
January 24, 2014
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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/2013/08/hopeless_matzke075631.htmlbornagain77
January 24, 2014
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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.,,," https://uncommondescent.com/intelligent-design/on-the-non-evolution-of-irreducible-complexity-how-arthur-hunt-fails-to-refute-behe/#comment-373178bornagain77
January 24, 2014
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Joe @28, I would not say that the concept is imperfect. I would call it what it is: pure unmitigated BS.Mapou
January 24, 2014
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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? :)Joe
January 24, 2014
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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).gpuccio
January 24, 2014
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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.Joe
January 24, 2014
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If Darwinian evolution necessitates the duplication and modification of existing genes, how did this ability evolve before it existed? Talk about voodoo science.Mapou
January 24, 2014
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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. https://uncommondescent.com/intelligent-design/on-the-non-evolution-of-irreducible-complexity-how-arthur-hunt-fails-to-refute-behe/comment-page-3/#comment-373178 How Arthur Hunt Fails To Refute Behe (T-URF13)- Jonathan M - February 2011 https://uncommondescent.com/intelligent-design/on-the-non-evolution-of-irreducible-complexity-how-arthur-hunt-fails-to-refute-behe/#comment-373010bornagain77
January 24, 2014
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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)Joe
January 24, 2014
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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...Joe
January 24, 2014
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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/2009/05/a_primer_on_the_tree_of_life_p_3.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/content/330/6011/1682.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/2012/02/a_piece_from_th055921.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/2013/12/a_listeners_gui079811.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!bornagain77
January 24, 2014
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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?Eric Anderson
January 24, 2014
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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.gpuccio
January 24, 2014
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@Bornagain: That's exactly what I was thinking when I read this. Thanks for confirming.sixthbook
January 24, 2014
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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.gpuccio
January 24, 2014
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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?gpuccio
January 24, 2014
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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.phoodoo
January 24, 2014
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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.gpuccio
January 24, 2014
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