Home » Intelligent Design » Jumping Genes the Key to Evolution?

Jumping Genes the Key to Evolution?

Here’s a link to a PhysOrg.com article talking about ERV’s (“jumping genes” per Barbara McClintock) and the newly discoverd role they seem to have played in primate evolution. Here’s a quote from the link: “Now it appears that another level of evolution occurs that is not driven by point mutations. Instead, retroviruses insert DNA sequences and rearrange the genome, which leads to changes in gene regulation and expression.”

Excuse me if I’m wrong, but this, it seems to me, is the kind of thing that would be helpful to discuss here at UD.

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26 Responses to Jumping Genes the Key to Evolution?

  1. It’s been discussed for years by panspermia advocates.
    For a nice overview see here

  2. If this has been discussed for years, then why is what they’re reporting considered a new discovery? Have you read the article?

    They talk about the involvement of ERV’s in the development of gene control networks; hardly the stuff of lateral gene transfer—which I think you’re confusing this with.

  3. Yes, I read it.
    They appear to have discovered something about what some of the retrovirally transferred genes do. The fact of transfer is not new.
    I expect there will be more of this type of discovery in the future as more is learned about gene regulation.
    Certainly this is not to suggest it shouldn’t be discussed. It is an interesting and pertinent topic. Pro-Darwinists sometimes point (erroneously) to ERVs as evidence for their side, and against ID.
    Isn’t it interesting that like so many discoveries, these results were somewhat of a surpise to their orthodox discoverers:

    Surprisingly, the infected hosts and their primate descendants also appear to have benefited from this genetic invasion…

    I expect that future discoveries will be no less surprising to those steeped in Darwinian dogma.
    There should be no big surprise here for those sympathetic with panspermia, or ID either.

  4. dacook:

    Thanks for your response. The aspect of all of this that I find intriguing is that the ERV’s seem to occur at just certain sites along the DNA length. My intuition is that this might point to special spots (“hotspots” of a sort) where the genomic program, so to speak, can direct the movement of such regulatory elements. My suspicion, likewise, is that the ERV’s are found at these “hotspots” because it guarantees their reproduction since the “gene regulatory” elements must be expressed themselves for the genome to function properly. So, IOW, the ERV’s, in a parasitic-type manner, either (1) “know” where to attach themselves and so attack at these particular sites, or (2) are found only at these sites since if they are inserted elsewhere, the normal DNA-error correction system would cut them out.

    But, bottom line, my sense is that these so-called ERV’s might point out a ‘non-random’ way in which the genome interacts with itself, and that the kind of shuffling seen might get scientists leaning more and more in the direction of viewing the genome as an overall computer-like program.

  5. dacook:

    The authors wrote:
    “Using the tools of computational genomics, the UCSC team gathered compelling evidence that retroviruses helped out. ERVs jumped into new positions throughout the human genome and spread numerous copies of repetitive DNA sequences that allowed p53 to regulate many other genes, the team contends.”

    Notice the quote ends with the words, “the team contends.” They contend that the ERV jumped around and fixed these numerous copies of repetitive DNA sequences, and thus allowing p53, the “guardian” gene, to control various sections of DNA. But, per my view, these repetitive DNA sequences already existed, and the ERV’s simply attached themselves to them. The idea is that the repetitive sections are a normal part of the genome that provides an “address” for the genomic program and the insertion of “subroutine”, something like the p53 gene, or that have been themselves directed to an already existing “address”.

    What’s important here, I think, is to demonstrate the big difference in viewpoint towards what is happening in the genome, depending upon whether one takes the ID viewpoint (as I, of course, do), or if one is a Darwinian—as are the authors, who then go onto to admit that this new evidence forces them to take a different “view” of evolution.

  6. It’s certainly looking more and more like the genetic code was written with foresight.
    Your “hotspots” look like a preplanned mechanism for making future changes easier.
    Which is not a surprise for ID, and does not require an alteration in “view” as it does the Darwinists.

  7. As to the “hotspots”, it will be interesting to see if the Darwinists got the “cart before the horse”, or not. Which means: they’re assuming the repetitive sections come from the virus, yet it may turn out that the viruses attack whereever the “hotspots” are generated through directed mechanisms. It’s just a way of gauging how much firmer the ID hypothesis is versus the Darwinian. I think I know on which to bet! :)

  8. PaV, Be careful, you are dangerously close to making a prediction!!! IDers don’t do that, right? And, word of advice, don’t design and run any experiments either. You wouldn’t want to show them Darwinists up by doing the lab work they won’t.

  9. Just to put some history on this – the general view that transposons could shuffle bits of DNA around has been around for at least 20 years – it’s something we were taught in undergrad genetics. Since then, the importance of these sorts of changes in the genome has become better appreciated, thanks to more sequence information, so at the general level my react was “ho hum, nothing really new here”. Mike Lynch has a book exploring how this sort of shuffling of the genome affects evolution:

    Lynch, M. 2007. The Origins of Genome Architecture. Sinauer Assocs., Inc., Sunderland, MA.

    PaV –

    The aspect of all of this that I find intriguing is that the ERV’s seem to occur at just certain sites along the DNA length.

    I don’t see any comment about this, where are you getting this idea?

    Bob

  10. Bob O’H: Thanks for the book citation. I’m going to take a look at Amazon. Seems like a book I’d be very interested in reading, especially since its recently published.

    As to the ERV’s occurring at certain specified locations, this is something that I picked up on as we had a discussion of ERV’s some time back. It was never made clear really, but there has been some recent work suggesting that the histone locations along the DNA are very regular and associated with long repeat sections (IIRC). That’s kind of the connection I’m presuming here. (Maybe even more of an intuition of sorts) But, again, the book you cite might provide a clearer view of what is known and what remains unknown regarding these genomic structures.

    ellazimm:

    Yes, ERV’s have been used to tout common descent, and that’s where the idea of their occurring at specified locations come from. We see certain primates having the same ERV’s at the same locations within the human genome and nowhere else among mammals. But this news item talks about a newly found link between ERV’s and regulatory networks–something unexpected from, you know, “junk DNA”.

    As to common descent, I think there is a common ancestry among life-forms, but I’m not 100% behind what is usually understood as common descent. I believe we see bifurcations along the way of life forms where form A becomes form A and form B, with form B getting its entire inheritance, principally, from form A. I just don’t think it’s logically precise to talk about common descent in this way; but, in the end, it’s a minor point.

  11. Neat stuff but how can we test the premise?

    IOW can we insert a retro virus and then see what changes occur?

    To me it seems like some people are “grasping for straws”. That is they “know” humans “evolved” from primates so they are trying anything and everything to force the data into that scenario.

  12. I have read, although rather quickly, the original paper (it is freely available on the PNAS site).
    It seems to me that the basic finding (in a sense, the only finding in this paper) is that many ERVs in the human genome (1509 out of 319000) have a binding site for p53 DNA. So, they represent >30% of the known p53 binding sites in the genome. That’s rather interesting.

    Besides, the authors argue from that that these ERVs are involved in p53 cell regulatory processes (a very complex and important regulatory network indeed). They give also some preliminary evidence for that.

    I think all that is very interesting. The “surprise” of the researchers is rather understandable, if we consider that ERVs are usually considered “parasites” or just “nonsense markers” in the genome. These data, anyway, fit very well with ID’s general idea (which I completely endorse) that non coding DNA has probably very complex, and up to now completely non understood, functions, even in its most peplexing parts, like ERVs and transposons.

    Does the fact that ERVs are probably involved in very high regulatory functions (like the p53 network) support ID? Absolutely. It very much supports ID. We must remember that regulatory networks are, in essence, very, very irreducibly complex. Regulation is a meta-level function, it is a function about functions. It is very intelligent and complex. The idea that ERVs and transposons, randomly shuffling DNA or attaching themselves here and there, may create higher regulation patterns, is a new, unprecedented “fairy tales” level in the darwinian tradition. In comparison, point random mutation appears almost as a likely source for CSI!

    So, it is really highly surprising and exciting that the most “accidental” parts of our genome (ERVs) are perhaps actively involved in the most organized forms of regulation. If that is true, it is really a paradigm shift. And a very designed one.

    But, obviously, all the clever darwinists who for decades have told us that junk DNA, and ERVs in particular, are evidence of the random nature of the genome, will suddenly change their mind, and declare that the new data clearly fit with darwinian concepts, and that darwinian theory, indeed, had always anticipated that.

  13. I have two comments:

    First, maybe someone could do a detailed discussion of just what p53 does and how is it affected by the ERV’s.

    Second, this would be an example of one of Allen MacNeill’s 47 mechanisms of genome change in action. It looks like it is still micro evolution but it does more than a SNP. Anyone have any comments on this.

  14. gpuccio:

    It’s good to see you posting again. I’m going to look for that paper now.

    jerry: here’s the wikipedia page on p53:
    http://en.wikipedia.org/wiki/P53

  15. Thank you gpuccio,

    I’ve had that ERV insertion presented as evidence for evolution many times in the past at least now I can reply to their claims..

  16. Jerry you stated:
    Second, this would be an example of one of Allen MacNeill’s 47 mechanisms of genome change in action. It looks like it is still micro evolution but it does more than a SNP. Anyone have any comments on this.

    No!, as gpuccio clearly pointed out, it is part of a multi-tiered Irreducibly complex system which in effect means that the system itself is poly-constrained to any type of random mutations.

    Just like in a car engine, you do not just add key functional parts to the car engine. You carefully design any modification you make to the car engine.
    ERV’s being proven to be poly-functional is very bad news for Prof. Macneil if he was hoping this was one of the “engines” for change.

  17. Let me try to understand what is going on here. At numerous places on the genome these ERVs have inserted themselves near genes that are regulated by the p53 protein.

    The ERV enables the p53 protein to bind on it and then when p53 protein is bound to the ERV, it regulates the expression of the other nearby genes that produce the proteins that are used in protecting DNA and ensuring good cell division.

    These are not the only binding spots for the p53 protein but represent 30% of the total binding spots. The others I assume are just other regulatory regions of the genome.

    I do not see how these various ERVs are coordinated but are just independent binding sites that produce a good effect, namely the expression of these beneficial proteins. The term network is used frequently but do they work as a system or just are a large number of sites all doing something similar and independent of each other?

  18. jerry:

    1) p53 is a transcription factor: it is a 393 aminoacids protein, which binds to a great number of genes and regulates their transcription. As it is the case for many transcription factors, it probably interacts with a lot of other proteins, modulating many fundamental activities of the cell, especially those related to the control of cell cycle and of DNA duplication.
    p53 was discovered as a broad-band anti-tumoral factor, which is a consequence of its many fundamentakl roles.

    On a specific web site, I have found a list of about 2500 human genes which are supposed to bind p53, in 14 different cellular pathways, such as apoptosis, cell cycle, membrane receptors, intermediate signaling, cell ahesion, etc. According to the paper we are discussing, a significant percentage of these binding sites would be located inside specific ERVs, which is the rational to infer an important role of ERVs in the p53 regulatory pathways.

    The paper does not give any clue regarding specific roles of these ERV sites, only some evidence that a few of them can really interact with p53 and in some way functionally respond to it. In other words, it seems that many p53 binding sites in the human genome, many of which were already known, are indeed located inside ERVs.

    It must be said that the network of transcription factors is probably the most important regulatory level in the cell, and certainly the least understood. It’s the transcription factors network which determines, in each moment, what part of the genome is transcripted in each single cell, and how much: in other words, determines the individual transcriptome of each cell, the transcription pattern which makes a fibroblast a fibroblats, a lymphocyte a lymphocyte, a stem cell a stem cell, and specifies also the specific functional state of each cell, including cell cycle status, apoptosis, and so on.

    In the transcription factors network, p53 is certainly a major actor, but the complexity of the whole network is utterly unimaginable, and almost totally unknown.

    2) Given what I have said at point one, it should be obvious that the involvement of so many (about 1500) ERV sites as p53 binding sites can in no way be considered a minor fact, and certainly not the result of microevolution. Instead, it is a clearly designed pattern, although certainly a very mysterious one. If confirmed, it is certain evidence that ERVs are not random parasites of the genome, but rather a very intelligent and complex part of it.

    The 1500 ERVs containing p53 binding sites are only the top of the iceberg. More than 300000 ERVs can be found in the human genome, for a total of about 5% of the whole genome (3-5 times the total coding DNA). If the evidence about p53 is confirmed, it is perfectly natural to anticipate that also the remaining 300000 ERVs may have an important role in cell regulation. To think that such a complex system, involving so many apparently exogenous DNA components, may be the product of random insertion or reshuffling of DNA is simple folly.

    MacNeill has only listed mechanisms of variance, all of them supposedly random. None of them can do anything more than single point mutations can. All random mechanisms can perform just the same way in creating new complex information: practically nil.

    At the level of transcription factors network, perhaps even more than at any other cellular level, we witness utter complexity and specificity, a wonderful and mysterious product of intelligence, indeed of genius. All the miracles in the life of the single cell, as well as in multicellular organization, must necessarily find their explanation, at least in some part, at the level of transcription regulation.

    Therefore, if ERVs have really an important role in transcription regulation, they must necessarily be a very fundamental piece of the whole design of life.

  19. gpuccio,

    Thank you and Wow!! Don’t go away too long. We miss your input.

  20. Thank You gpuccio,

    I hope you don’t mind if I quote you if I’m confronted with the “ERV is proof of evolution” thing again.

  21. As to the ERV’s occurring at certain specified locations, this is something that I picked up on as we had a discussion of ERV’s some time back. It was never made clear really, but there has been some recent work suggesting that the histone locations along the DNA are very regular and associated with long repeat sections (IIRC).

    Ah, yes. I went to a seminar about this last year. Grrr, I can’t remember the name of the guy (he’s on the advisory board for our centre of excellence, so I should be able to!).

    I might have to check this up.

    Bob

  22. The whole story is another Darwinian mixup. Darwinians tend to always misinterpret biological data. What the researchers discovered is easily explained. First of all we have to realize ERVs (retrotransposons) are not derived from integrated RNA viruses. IT IS THE OTHER WAY AROUND: The elements known as ERVs are in fact variation inducing genetic elements (VIGEs). (Barbara McClintoc couls have told you so.) RNA viruses emerge from VIGEs, which normally already carry two genes typically found in retroviruses and which are required for replication and transposition. These VIGEs do the fine-tuning of impliciet morphogenetic programs, such as beaksizes, in order to adapt rapidly to novel environments.
    What the researchers porpose is rediculous. p53 is the main switch for cells to divide or to go into apoptosis. Without the p53 control system there wouldn’t even be organsims possible. All life would have demised as bulky tumours. So, what really happened in the human genome is a read-through of polymerase II in a VIGE that was next to a gene that contained already a binding site for p53. Or it was excised improperly taking a bit of a nabouring gene containing the p53 binding site. Next the modified VIGE amplified, transposed, amplified, etc. That explains this family of transposons.

  23. peter borger:

    First of all we have to realize ERVs (retrotransposons) are not derived from integrated RNA viruses. IT IS THE OTHER WAY AROUND: The elements known as ERVs are in fact variation inducing genetic elements (VIGEs). (Barbara McClintoc couls have told you so.)

    Thanks for the post. In post #7 I was suggesting that the Darwinists may have the “cart before the horse”. Is there some good reference you could recommend on this, some review article perhaps?

  24. Here’s an abstract I just looked at. I’ll highlight the phrases that support my thesis on this thread:

    There is no logical or theoretical barrier to the proposition that organismal and cell signaling could transduce environmental signals into specific, beneficial changes in primary structure of noncoding DNA via repetitive element movement or mutation. Repetitive DNA elements, including transposons and microsatellites, are known to influence the structure and expression of protein-coding genes, and to be responsive to environmental signals in some cases. These effects may create fodder for adaptive evolution, at rates exceeding those observed for point mutations. In many cases, the changes are no doubt random, and fitness is increased through simple natural selection. However, some transposons insert at specific sites, and certain regions of the genome exhibit selectively and beneficially high mutation rates in a range of organisms. In multicellular organisms, this could benefit individuals in situations with significant potential for clonal expansion: early life stages or regenerative tissues in animals, and most plant tissues. Transmission of the change to the next generation could occur in plants and, under some circumstances, in animals.

    I believe that this is just another instance wherein scientific knowledge is misinterpreted by Darwinists because the possibility of “design” is ‘verbotin’ to them. How many other instances are there?

  25. ellazimm,

    Next time you leave your house look for a rock. In order to completely describe that rock you will need a lot of information. It might take more information than any computer could handle to place each molecule of the rock in its proper place.

    Take some chewing gum and slap it on the rock. Now the rock and chewing gum are even more complex and the information to accurately describe it would be greater. So by slapping the gum on the rock you have increased the information necessary to reproduce the rock/chewing gum exactly.

    Neither the information in the rock or the chewing gum are very useful and neither is the combination. So the concept of adding information is not a useful one per se.

    Take a computer and add some liquid to it. The information increased but the functionality has decreased. The new information does not get you anywhere. Instead add another disk drive to the computer and you get increased information and increased functionality.

    It was thought the added ERV added nothing to the genome in terms of functionality. They did add information but now we learn they added functionality. The long term implications are at best speculative now.

    I personally don’t know what to think and I am certainly not an expert on this and can somewhat follow the arguments. The insertions of the ERV can happen naturalistically with no problem. That they then as a whole are so useful is what is interesting. There may be a reasonable naturalistic explanation and we will have to wait and see was comes of this.

  26. All life would have demised as bulky tumours.-Peter B

    There was a tumor guy on the X-Files. Now Scully has a scientific explanation. ;)

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