Another Day, Another Bad Day for Darwinism

_{June 23, 2010

Evolutionary biology, Intelligent Design

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Evolutionary biology
Intelligent Design}

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In the latest issue of Nature, a definitive role for pseudogenes is established. In the last sentence of the Abstract the authors conclude:

These findings attribute a novel biological role to expressed pseudogenes, as they can regulate coding gene expression, and reveal a non-coding function for mRNAs.

Haven’t read the full article* (no time at present), but there’s a related link at PhysOrg.com that gives an overview.

Yes, “junk” DNA now “communicates” with itself. A new “language”, an RNA language, is discovered. Another 30,000 pieces of functional information (over and above proteins) are part of cell architecture. And even more for Darwinists to explain per RM+NS. And the old standard explanation, of gene duplication and pseudogenes ‘evolving’ new function, takes a hit. You’ve got to feel bad for these Darwinists. What’s tomorrow going to bring!?!

*BTW, somehow I gained access to the pdf version of the article.

Comments

Art:
And, as I have stated before, and as countless ID proponents have insisted every time they are asked about gene duplication as it relates to the origins of new proteins, the ID party line is that this is not a change in information.
If you have one dictionary and I give you a copy of the same dictionary, do you have more information or just two dictioaries with the same information? Also you need to read "Not By Chance"- it explains gene duplications. you seem to miss the simple point that the duplicate gene will automatically be “finely tuned” to co-express with the original gene. Not without all the regulatory stuff that goes along with the expressing part. And even then all you are going to get is another polypeptide that can clog things up.
We know that all of these processes involve well-understood chemical rules, and that no “hand of God” (with all apologies to football fans, and especially those aggrieved by the alluded-to event) need be invoked to understand the past, present, or future when it comes to gene duplication.
Don't need a programmer present to run my computer and perform spell-checks. You should read "Not By Chance". That way you may understand the argument you are trying to "refute".Joseph_{July 10, 2010
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PaV (101), "You’re quite right. Now, tell me, just what exactly DOES Darwinism predict?" It predicts common ancestry for life on Earth. "It predicts that we will find lots of fossil remains prior to the Cambrian. But, of course, there are none." Actually, Darwinism didn't predict that there would be lots of fossils prior to the Cambrian - at the time of Darwin it was thought that there weren't any fossils before the Cambrian because they weren't known. But Darwinism predicted that there would have been life before the Cambrian, based on the fact that fossils of multicellular organisms were found in the Cambrian so there would have been life before then even if it hadn't been left in the fossil record. In fact since then multicellular fossils have been found in Ediacaran strata, stromatolite fossile have been found in 3.5 billion year strata (and recently multicellualr fossils from 2 billion years BP appear to have been found). "It predicts that the earth is quasi-eternal, with an extremely long geological history. But, we know that instead it is of finite duration." Is it even possible for something to be "quasi-eternal"? But in any case, Darwinism certainly doesn't predict an eternal earth, just an age of earth long enough for life to evolve.Gaz_{July 3, 2010
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Jo (aozinho) hn, Honestly I find you astoundingly hypocritical. You come to this blog under false and deceptive pretenses and have the gall to call others not credible? And I'm supposed to believe that you're just "seeking" the truth in your Darwinism? People like you, that I've encountered since I began questioning Darwinism, have again and again confirmed that I am dealing with people defending a worldview by any means possible. I used to think that scientists were completely honest and impartial, but that was when I was a naive child, I know better now, I became a man and put childish things away. If the theory cannot actually be sustained by physical evidence, any tactic will work for its defenders, including dishonesty. It's people like you that affirm that I have correctly rejected the naive assumption of the complete objectivity and honesty of scientists, and that I have correctly rejected Darwinism which needs to rely on such dishonesty as its defenders are ready to give.Clive Hayden_{June 30, 2010
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Jo (aozinho) hn,
Clive, “It’s the same as yours as far as pointing to what others say.” But what about as far as pointing out what is or isn’t known, Clive?
What about it? Do you really want to talk about pointing some more? You have two options when you claim that credibility is lost by virtue of pointing to what others say. Either you lose credibility given that you also point to what others say, or you lose credibility by lying about who are and who this "friend" is to which you point. Which do you want? I know very well who you are. You are not a religious studies major, and you have no "friend" that you've continually made reference to. Thus you've lost credibility here. Would you like me to "out" you on this blog? What religious studies are you studying at Stanford? Why not stay in Montana for that?
I’m pointing to what they did.
What they did, but not what they said? Are you pointing to actions or to a manuscript? I thought you said it was a manuscript, which is words on a page? Didn't you begrudge gpuccio's credibility by claiming that he points to what others say? Does the manuscript actually show actions, like a movie, with no words? They didn't say anything? That would be an interesting manuscript indeed.
I’ll go with evidence. When I do go with what someone says (and we all have to do that in many cases), it’ll be based on how much evidence is offered with the rhetoric.
Wonderful, then let's quit this absurd red-herring argument about credibility by virtue of pointing to manuscripts. Do you know what red herring means in relation to an argument?
Wouldn’t looking at the Biologic Institute’s IRS Form 990 to see what they’ve purchased give us a general idea?
It would give you series of assumptions, such as claiming that the wine I used to marinate my steak meant I was an alcoholic. You're welcome to "know" this, it's better name is ignorance.Clive Hayden_{June 29, 2010
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Second Opinion:
As far as I know the ToE does not predict that pseudogenes can’t have a function or generally that “junk DNA” can’t be found to have a function.
You're quite right. Now, tell me, just what exactly DOES Darwinism predict? It predicts that we will find lots of fossil remains prior to the Cambrian. But, of course, there are none. It predicts that the earth is quasi-eternal, with an extremely long geological history. But, we know that instead it is of finite duration. So, its only predictions turn out to be wrong, and, after the wrong predictions it has made, it makes no further predictions. You're free to give us one.PaV_{June 29, 2010
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Joaozinho: From the cheekiness of your comments on this thread, I rather suspect that you have misrepresented yourself here. I find it hard to believe that you're a religion studies major. I think you're simply a Darwnist in sheep's clothing. If this is true, you should admit to it. Now, you say:
I’m still trying to understand how the particular mechanism described in the Nature paper is thought to be more likely to have been produced by ID than by evolution.
Two things: (1) ID doesn't "produce" anything. ID provides an explanation for known and discovered biological complexity, and (2) "evolution" doesn't produce anything either. Evolution is a fact. That is, looking at the fossil record, it is obvious that life forms have changed and grown in complexity over time. Darwinism seeks to provide a mechanism for this change and growth in complexity (i.e., the "appearance of design"). ID posits that only "agency" (a Designer) can explain the observed historical changes of form and sophisticated complexity.
Can you explain that to me? . . . no one here AFAIK has attempted a step by step interpretation of the data from the paper. This seems odd given that you are clearly claiming to understand the data better than the authors do.
What's to explain? They found a functional role for parts of a transcribed psuedogene. And the pseudogene's miRNA is involved in regulatory behavior. This is perfectly consistent with what IDists have been PREDICTING; likewise, it is in contradiction to neo-Darwinist claims that pseudogenes are no more than duplicated genes that have, through neutral drift, moved along towards the eventual goal of fulfilling some other function. (IOW, a broken down former gene, on its way to becoming a new gene---and no more.) To have pseudogenes involved in RNA regulation undermines that claim. You see, it's the Darwinists who need to 'explain' these results. As I stated in the original post, they cannot explain the development of the genetic code, and now, lo and behold, an RNA code is rising up alongside the DNA code. Another day, another bad day for Darwinism!!!
I’m just not seeing how the demonstration that ~20 of ~2 billion bases of DNA has a function represents a bad day for Darwinism.
You don't seem to understand what the authors are implying. They're not saying we found a functional role for 20 bp out of the cell's 2 billion. They're saying that when it comes to this one gene they've found a 23 bp portion of the transcribed RNA that has a function. But the implication is that there is a whole slew of these psuedogene miRNA's, and further, that this then implies the presence of a regulatory RNA language, with RNA "speaking" to itself. All of that remains to be discovered down the road. But this new added layer of complexity only further strains the credulity of proposing that these highly regulated networks/languages all arose simply through chance modifications. Another day, another bad day for Darwinism . . . .PaV_{June 29, 2010
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scordova: You say that darwinists argue that: “unconserved regions” = “non-functional DNA” but that's not always true. We have the important example of HARs, to see that, even to darwinists, that is not an universal principle. So, that would appears as: "unconserved conserved regions" = "super-functional DNA"gpuccio_{June 29, 2010
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Joaozinho: Of all people, you are not the one I am most interested to discuss with. That, just to be frank. But you can always look at my ongoing discussion with Arthur Hunt and, if you like, comment on that. Or just ask your friend to do that.gpuccio_{June 29, 2010
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gpuccio: Can you understand what “a low bound estimate” means?
Yes, and I understand what "MAY be a low bound estimate" and "that's ABSOLUTELY not known" mean as well. I'm still trying to understand how the particular mechanism described in the Nature paper is thought to be more likely to have been produced by ID than by evolution. Can you explain that to me? Because it's clear that the authors of the paper don't agree with your interpretation of their data, and no one here AFAIK has attempted a step by step interpretation of the data from the paper. This seems odd given that you are clearly claiming to understand the data better than the authors do. I'm just not seeing how the demonstration that ~20 of ~2 billion bases of DNA has a function represents a bad day for Darwinism.Joaozinho_{June 29, 2010
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TYPO:
“NON-conserved regions” = “functional differently”
Sorry!scordova_{June 29, 2010
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The ENCODE project found "conserved" regions in pseudogenes. The idea is that:
"conserved regions" = "functional DNA"
The unstated implication of such a Darwinist view is that
"unconserved regions" = "non-functional DNA"
But I disagree with that. In contrast to the Darwinist view, let me offer my speculation inspired by Dembski's Steganography hypothesis:
"conserved regions" = "functional the same way"
and
"conserved regions" = "functional differently"
Thus the ENCODE methods could understate functionality. It should be noted that the "conserved" regions are hierarchically organized. This represents a problem. Say a feature is only "conserved" among primates in one way, and "conserved" among birds another way. Does that mean the primate conservation is non-functional or the avian conservation is non functional since relative to each other these regions are "non-conserved". No, it suggests they function differently. And species specific "conservation' (intra species "conservation", or monomorphism) may indicate unique functionality to a species. The hierchical structure of "conserved" regions screams "steganography" optimized for scientific discovery. Single Nucleotide polymorphism may signify permitted variation or dysfunction. There is too much we don't know. The point is the ENCODE methodology is reasonable to identify lots of common functions, but may understate the level of functionality since it may exclude uncommon function.scordova_{June 29, 2010
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second opinion: Is it thus just a bad day for “Darwinism” because it is a god day for ID? I don't know: darwinists seem to rejoy so much for our troubles, maybe they can suffer a bit for our joys :)gpuccio_{June 29, 2010
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What is not clear to me why this is a bad day for “Darwinism”. As far as I know the ToE does not predict that pseudogenes can't have a function or generally that “junk DNA” can't be found to have a function. Is it thus just a bad day for “Darwinism” because it is a god day for ID?second opinion_{June 29, 2010
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Joaozinho: Can you understand what "a low bound estimate" means?gpuccio_{June 29, 2010
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me: "He laughed at it and said that only a tiny bit of junk dna is pseudogenes, only a minority of pseudogenes are expressed as rna…
gpuccio: That’s absolutely not known.
Emphasis mine. 19% is a minority, is it not?Joaozinho_{June 29, 2010
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joazihno: (2007) Genome Res 17: 839-51 Pseudogenes in the ENCODE Regions: Consensus Annotation, Analysis of Transcription and Evolution: "We believe that the data obtained by RACE experiments or by sequencing analyses (CAGE, PET, EST, and mRNA) provide unambiguous evidence for pseudogene transcription. Altogether, these data indicate that 38 (19% of 201, 20 non-processed and 18 processed) pseudogenes are the sources of novel RNA transcripts. This may well represent a low-bound estimate and does not include the ambiguous and possibly inconclusive cases supported only by transfrags." Emphasis mine.gpuccio_{June 29, 2010
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Arthur Hunt (#57): I think it needs to be pointed out that the sort of duplication event that yields pseudogenes such as PTENP1 does not involve merely the protein-coding sequence; all of the gene, including promoter, 3’ UTR, and miRNA target site (the decoy site in the pseudogene-encoded RNA) come from the original gene, and they are all duplicated. To be more precise, according to the paper: "PTENP1 is a processed pseudogene located at 9p13.3; it is highly homologous to PTEN, with only 18 mismatches throughout the coding sequence. A missense mutation of the initiator methionine codon prevents translation12. PTENP1 possesses a 39 UTR that is 1 kilobase shorter than that of PTEN (Fig. 1b). It can be divided into two regions relative to its homology with the PTEN 39 UTR: a high homology (95%) 5' region and a low homology (50%) 3' region (Fig. 1b and Supplementary Fig. 1). Within the high homology region, we found perfectly conserved seed matches for the PTEN targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families" That's not exactly the picture of a complete passive duplication, but of duplication with many specific variations. you seem to miss the simple point that the duplicate gene will automatically be “finely tuned” to co-express with the original gene. It’s unavoidable, and a natural consequence of the random duplication event. I don't agree. The key point here is that the duplicated gene is not only "co-expressing" with the original gene. It is regulating its expression. That's a completely different concept. IOW, simple random co-expression of an already regulated gene cna probably only interfere with the fuin ction of that gene system. Here, instead, what we observe is that the regulatory function of the duplicated gene is essential to the function of the existing gene, so much so that, according to the authors, it has a tumour suppressive role. That's what I mean with "fine tuning". A mere duplication with co-expression, with or without translation, is not fine-tuned at all. Fine tuning implies that the whole system (gene + duplicated gene) exhibits a perfect functional equilibrium. I don’t believe you have any data to support the ID position that such events are so impossibly rare as to be beyond the bounds of normal evolutionary processes. Indeed, the deep sequencing that is being done in humans reveals just the opposite – that all manner of genetic alterations, such as deletions and duplications, are not impossibly rare. Again, I think you misunderstand. The ID position is certainly not that deletions and duplications and all other kinds of genetic alterations are rare. The ID position is that, if they are truly random, it is not credible that they can generate complex functional results. Again, it's completely different. This ID point is clearly not correct. I don't understand. Again, you are not demonstrating in any way that the molecular events you are pointing to could generate function through a random search. I will go back to the essential: single point mutations. Not because they are the only mechanism, but because what is true for them is true for all random variations. I am not saying that single point mutations don't happen (that would be very silly). I am just saying that purely random single point mutations cannoy build a new protein domain. But designed mutations certainly can. The same is true for all kinds of genetic variation. RV cannot generate complex function, while designed variation certainly can. This is the ID point. To show that it is wrong, you don't have to just say that variation happens in different ways, and that different types of variation can be responsible of the origin of different types of genes. I agree on that. You have to credibly demonstrate that those variations are in the reach of random events, even with the help of NS, if and where that help can be credibly incorporated in the model. The problem is that, in the case under discussion here, all of this fine tuning is an unavoidable consequence of a single random event. As I have argued above, that's not true. A single random event of duplication would only bring non functional, or probably harmful, competition. Fine tuned regulation is all another thing. We know that all of these processes involve well-understood chemical rules, and that no “hand of God” (with all apologies to football fans, and especially those aggrieved by the alluded-to event) need be invoked to understand the past, present, or future when it comes to gene duplication. The argument about chemical rules is really old and poor. There is no reason to break chemical rules to design a protein. Protein engineering is all about designing proteins, and I don't thing protein engineering breaks any chemical rule. And still it is a designed process. Information is intelligently guiding the process, without violating any chemical rule. How is it possible that darwininsts miss so easily the difference between deterministic laws at low level, and the supervening informational order at higher level? And yet it is not a complex concept. Do you really believe that software is not designed, because processors and hard disks and RAM do not break any physical law? I would definitely say that, to have complex functional software, a "hand-of-designer" is badly needed. If you have positive, repeatable and controlled experimental data that suggests otherwise, please discuss it. Until then, the suggestion that something other than chemistry is behind gene duplication must be considered as idle fancy. Again, the suggestion is that something other than chemistry is behind functional, tweaked and finely tuned gene duplication which implements a very successful regulation. The pseudogenes of interest here have nothing to do with transposons (which are not guided in any ways, other than the substrate preferences, as determined by chemistry, of the enzymes that catalyze transposon duplication and movement). From the paper: "Pseudogenes exist as either processed or non-processed genetic elements. Although non-processed pseudogenes arose from genetic duplications, processed pseudogenes were generated through retrotransposition" and: "PTENP1 is a processed pseudogene" Did I miss something? And is your certainty that the activity of retrotransposons is determined only by chemistry, and cannot be guided by design, on the same level as the certainty that the assemblage of software is determined only by the electromagnetic force? Will protein engineers always be denied the chance to use transposons in their procedures, only because you don't like the idea? To reiterate, we are talking about something here that is at best information-neutral, and at worst involves a loss of information. And it is the result of a common and random process. You are only reiterating a false reasoning.gpuccio_{June 28, 2010
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Even if, right now, the amount of pseudogenes that have function is small (per A Hunt’s calculation), neo-Darwinian theory is nevertheless under duress since even a 23 bp miRNA doesn’t just happen by chance—which is exactly the neo-Darwinian understanding of how gene duplication + RM(=neutral drift) + NS = a new, “coding” gene. Did the 23 bp regulatory function come about by chance?
PaV, you may have missed the back-and-forth with gpuccio, so I'll repeat the bottom line - the probability that the expressed pseudogenes will have the microRNA target is exactly 1. This is because the same microRNA target that is in the progenitor gene gets duplicated, along with everything else. That having been said, your estimates of the "probability" of origination of microRNA targets is quite wrong. I explain why here. One aside - a comment Wells made directly to me several years ago on another board:
[Art] seems to have missed my main point, which I will re-state: whatever is controlling development and morphology (and is thus the key to evolution), it is NOT the genes (Hox or any others). Here's why: 1) The cells in a multicellular animal are radically different from each other in structure and function, yet virtually all of them contain the same DNA; therefore, whatever is making them different must be something other than their DNA. 2) The animal phyla are radically different from each other in body plans, adaptations and life histories, yet they all contain similar homeobox genes (of which Hox genes are one kind); therefore, whatever is making them different from each other must be something other than their homeobox genes.
Substitute "hox genes" with "DNA" and you can see where I get my (accurate) estimations of the assertions of IDists.Arthur Hunt_{June 28, 2010
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Contrary to Art's misrepresentation of Wells, here is an example that shows that Wells accepts that there is a genetic basis for form:
Hox genes, which affect the character of body segments during embryo development. For example, a mutation in one Hox gene can cause a fruit fly to sprout a leg from its head in place of an antenna. Remarkably, vertebrates possess Hox genes that are very similar to a fruit fly's, so similar that a mouse Hox gene can enable normal development in a fly embryo that lacks its corresponding Hox gene Uncommon Descent: Jonathan Wells on the contemporary state of Evo-Devo
I think a retraction of this misrepresentation by Art is in order:
the claims of Wells et al., the nuclear DNA does indeed determine form. It’s entirely consistent with, oh, a hundred years or more of genetic and molecular analysis that shows that form and function in all living organisms has a genetic basis.
scordova_{June 28, 2010
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scordova, When you asked Art for a reference for someone alluding to a "ethereal" force in body formation,,,,,, actually I, though many of my opinions are certainly not highly regarded nor shared by others, have argued for a more direct role for God in "conducting" the formation of humans: Primarily because of this: Jeremiah 1:5 Before I formed you in the womb I knew you, before you were born I set you apart; https://uncommondescent.com/intelligent-design/central-dogma-revisited/#comment-338098 basically I tried to defend that position from a Quantum Mechanic/4D space-time angle plus from the fact that no one really knows for sure where the complete set of ontogenetic information resides for body formation. I don't think I convinced many people, and empirical validation would seem to only be possible through total elimination of all other possibilities, but none the less, I still am fairly confident that God will be found to have some "orchestrating" role in body formation however long it takes to "prove" it.bornagain77_{June 28, 2010
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Being disingenuous is typically grounds for the loss of credibility. I've never noticed GP being disingenuous, in fact, the opposite is his unsolicited trademark.Upright BiPed_{June 28, 2010
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Clive, "It’s the same as yours as far as pointing to what others say." But what about as far as pointing out what is or isn't known, Clive? "Having a manuscript doesn’t mean that you’re not pointing to something someone else said." I'm pointing to what they did. "Anyone can point to a manuscript. You just did, and gpuccio certainly can. But it should be remembered that the mere pointing to others is what loses one credibility, according to you. Did you write that manuscript, or are you pointing to what another person said?" What they did, more specifically, what is known about pseudogenes. "If you are pointing to what another said, you lose credibility in the same way you claim others do." I'm pointing to what they did. "Are you going to argue the merits of the argument at hand …" I'm not sure what that means. I'll go with evidence. When I do go with what someone says (and we all have to do that in many cases), it'll be based on how much evidence is offered with the rhetoric. "Neither one of them actually know what the Biologic Institute is or isn’t looking at as a research project." Wouldn't looking at the Biologic Institute's IRS Form 990 to see what they've purchased give us a general idea?Joaozinho_{June 28, 2010
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1. One report (of hundreds or thousands) that describe the regeneration of normal plants from isolated somatic cells.
I think it inappropriate to generalize the development of plants to animals and humans and things like Dolly the Sheep. :-) I don't know many embryologists who would think what you see happen in tobacco will happen in a live human being or even a clonable sheep. The experiment you cited discussed tobacco cells put in agar and then growing. I'd expect you wouldn't want to be arguing that such a thing will happen for humans, but that is exactly your inference. It is unwarranted extrapolation. Wells focuses on animal embryology, not plant embryology. Thus your supposed counter examples are suspect. Epigenetic Developmental plasticity is in Mary Jane West Ebberhard's book. Her work lists counter examples to your generalization that what happens in certain nuclear DNA of plants must necessarily be generalized to animals!
2. The cybrid example is one that shows that, contrary to the claims of Wells et al., the nuclear DNA does indeed determine form. It’s entirely consistent with, oh, a hundred years or more of genetic and molecular analysis that shows that form and function in all living organisms has a genetic basis.
Wells never said there is no genetic basis, that is your misrepresentation. You're welcome of course to provide citations where Wells said: "there is no genetic basis for form". I recall some of us have requested citations to support your other misrepresentations of ID proponents, like "ethereal force" that ID proponents somehow invoke to explain development. So the request remains: 1. citation for "ethereal force" that is involved in animal development 2. citation where Wells says there is no genetic basis for form PS Wells cites hox genes in the Icons Video invovled in form, so Wells does claim genetic involvement in form. Art's misrepresentation is just that, a misrepresentation. I appreciate Art's valor and determination to oppose us, and I appreciate his visits and participation. But if attributes arguments to ID proponents which they've never made, I feel a bit compelled to speak up. Art may think that's what he heard them say. He may think that's what they mean. But let's clarify what they really said versus what he thinks they said.scordova_{June 28, 2010
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bornagain77 (77) and Clive Hayden (79), Okay - are they doing the work or not? If not, maybe they should be.Gaz_{June 28, 2010
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Jo(aozinho)hn,
And then what absolutely happens to gpuccio’s credibility?
It's the same as yours as far as pointing to what others say. Having a manuscript doesn't mean that you're not pointing to something someone else said. Anyone can point to a manuscript. You just did, and gpuccio certainly can. But it should be remembered that the mere pointing to others is what loses one credibility, according to you. Did you write that manuscript, or are you pointing to what another person said? If you are pointing to what another said, you lose credibility in the same way you claim others do. Are you going to argue the merits of the argument at hand or keep making red herring arguments about credibility that are self-referentially damaging?Clive Hayden_{June 28, 2010
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Clive: "And you don’t point to what your “friend” says about the evidence?" Yes, but I also get actual evidence. For example, gpuccio says, "That’s [what proportion of genes are transcribed is] absolutely not known." Then I get this manuscript and others: http://papers.gersteinlab.org/e-print/chr22-pgene-exp/preprint.pdf And then what absolutely happens to gpuccio's credibility?Joaozinho_{June 28, 2010
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bornagain77,
Where have I heard that question several times before??? My My,,, I think Nakashima has a twin.
Neither one of them actually know what the Biologic Institute is or isn't looking at as a research project.Clive Hayden_{June 28, 2010
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Joaozinho,
This has been a real education for me…gpuccio admitted that PaV’s post wasn’t accurate, but when I contrast what my friend says with what the rest of you are saying, my friend has a lot more credibility. He points me to evidence, while you point me to what people say about the evidence.
And you don't point to what your "friend" says about the evidence? The only way that your statement above doesn't also lose credibility for you in the same way that you begrudge others, is if there is no "friend", in which case you would lose credibility too. It looks like a no-win situation for you Jo(aozinho)hn.Clive Hayden_{June 28, 2010
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why isn’t the Biologic Institute looking at it as a research project? Where have I heard that question several times before??? My My,,, I think Nakashima has a twin.bornagain77_{June 28, 2010
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PaV (75), I think it was George Bernard Shaw. The thing that gets me about this junk DNA business is: if there's a view that it isn't junk then why isn't the Biologic Institute looking at it as a research project? It should be a fertile research area if it isn;t really junk.Gaz_{June 28, 2010
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