Here is my description of the part of my research that has been misrepresented by the Reasons to Believe website. See this post for an explanation.
My paper concerns the regulation of a human gene by DNA derived from an endogenous retrovirus (ERV). An ERV is a viral sequence that has become part of the infected animal's genome. Upon entering a cell, a retrovirus copies its RNA genome into DNA, and inserts the DNA copy into one of the host cell's chromosomes. Different retroviruses target different species and types of host cells; the retrovirus only becomes endogenous if it inserts into a cell whose chromosomes will be inherited by the next generation, i.e. an ovum or sperm cell. The offspring of the infected individual will have a copy of the ERV in the same place in the same chromosome in every single one of their cells.
This happens more often than you might think; 8% of the modern human genome is derived from ERVs. Repeated sequences of this kind were formerly considered to be non-functional, or "junk" DNA. However, we're gradually finding more and more examples of viral sequences that appear to have some kind of function in human cells. For example, many ERV sequences play a role in human gene regulation. ERVs contain viral genes, and also sequences - known as promoters - that dictate when those genes should be switched on. When an ERV inserts into the host's chromosome, its promoter can start to interfere with the regulation of any nearby human genes. In the example that I researched, the ERV promoter has become responsible for most of the expression of a particular human gene in the large intestine.
Creationists and intelligent design advocates like to think that because some ERVs have useful functions in the human genome, they must have been deliberately put there by a creator / designer with that particular purpose in mind. Of course, no-one can explicitly prove that that is incorrect - it's not a falsifiable hypothesis, and therefore it's not science. What we can show is that ERVs provide evidence in support of the theory of evolution.
Let's imagine how ERVs would behave within a model of evolution by common descent. An ancient creature, let's call it the common ancestor of all modern mammals, is infected by a retrovirus that becomes endogenous. All of the animal's descendants (i.e. all mammals) would be expected to carry the same ERV insertion (ERV1) in the same chromosomal location.
Fast forward in evolutionary time. Different lineages have evolved and diverged from the original common ancestor and there are now many different types of mammal in existence, all carrying ERV1. A small rodent, let's call it the common ancestor of mice and rats, is again infected by a species-specific retrovirus that becomes endogenous. This is ERV2. In a parallel event in a different lineage, the common ancestor of all great apes acquires a third insertion, ERV3.
Moving forward again, a fourth ERV appears in some of these new-fangled human thingies that are running around in Africa, but not in their hairier relatives who will eventually evolve into modern chimpanzees. The early humans spread out, and a fifth and (don't worry) final ERV arises in a population that is isolated in a discrete geographical location. The infection does not spread to other human populations.
So what would we expect? Humans, chimps, mice and rats should all possess ERV1. The mouse and rat genomes will also contain ERV2, the virus that infected their common ancestor, but not the primate-specific ERV3, 4 or 5 insertions. All great apes will share an identical ERV3 insertion; all humans will also possess an ERV4 insertion that is not found in chimps or other apes. In addition, some, but not all, humans will carry an insertion of ERV5. The rodent-specific ERV2 insertion will not be found in any primate species.
Now that several genomes have been sequenced, we have begun to test these predictions. The patterns of ERV insertions observed in modern species exactly match the predictions made by the model described above. Some insertions are shared between humans and mice and represent truly ancient viral infections. Others are found only in primates, and not in other species, obviously derived from an infection of the ancestral primate species after its divergence from other lineages. More modern insertions are found only in humans, while the youngest ERVs of all are found in some humans, but not in all. We do not find any examples of ERV insertions shared by, say, humans and mice, but not by chimps. Insertions are always shared by all species, and only by those species, that have a common ancestor. ERV insertions therefore provide excellent support for the theory of evolution by common descent.
My particular favourite ERV is found in various primate species, and therefore must be at least 25 - 30 million years old. I compared the sequences and activities of the same ERV promoter in the human, chimp, gorilla, and baboon genomes. Despite some minor "single-letter" point mutations caused by DNA copying errors, the promoter had essentially the same function in all four species. I struggle to understand why any kind of designer would decide to use different codes to perform the same function in different species, but there it is. I hypothesised that the ERV was only allowed to persist (that is, its meddling in gene regulation didn't kill the first organism in which it inserted, which was therefore able to pass the insertion on to its offspring) because the incoming ERV promoter behaved in a very similar way to the original host cell's gene promoter. I wasn't able to do the experiments I wanted in order to investigate this point, but another group subsequently did, and their findings supported my hypothesis. That's what happens when you make and test falsifiable predictions.
I could go on and on about the role of ERVs in genome evolution, but this post is too long already. I would encourage anyone who's interested to search for "endogenous retrovirus" AND evolution in the PubMed database of peer-reviewed research papers. You won't find much in there about creationism or intelligent design. ERVs are also the subject of their own blog, a decent novel (although the sequel was disappointing) and a post on This Week in Evolution!
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Thanks for that post. It's nice to read a scientist carefully and clearly debunk this creationist nonsense.
ReplyDelete... You have a first-author PNAS paper?
ReplyDelete*blink*
IM NOT WORTHY! IM NOT WORTHY! IM NOT WORTHY! {/Waynes World}
AHH!
It's nice to hear a scientist lay out such clear evidence for evolution.
ReplyDeleteDon't worry too much about the creationists. Calling someone a creationist is tantamount to calling them stupid.
There's a correlation between IQ and secularism that can't be denied, so if it's science against the morons in a battle for the country, who do you think is going to win?
Andrew
www.thegreathive.com
Thanks for this thorough debunking of their nonsense. I have personal experience with RTB, and I'm preparing to write a review of their latest book. I'll definitely be citing your post on my blog sometime.
ReplyDeleteThanks all for your comments - I'm a little overwhelmed by my Pharyngula / Reddit-based traffic spike at the moment and your feedback is very gratifying!
ReplyDeleteERV - my PNAS paper is the pinnacle of my achievement! I still think that my later paper on the same gene (linked later in this post) is the better paper though, despite not being in as prestigious a journal.
Andrew - you are right about that correlation, but unfortunately there are just so many of them!
IM - I look forward to reading your review! Please let me know when it's ready...
*LAUGH!*
ReplyDeletePZ links rock! Youre minding your own business, when WHAM! Site hits increase by 500%
hehehe!
Im really glad you brought this up, because Creationist and HIV Denier Pirating needs to be talked about more. Its happened to a LOT of people, and they probably dont even know it. The ones who do know it cant do anything. Its not right.
I think it is obvious that many functional sequences in the human genome COULD have been inserted by ERVs, but I am skeptical of the 8% number. What are the assumptions? And could the ERV have actually taken the DNA out of the human in the first place, and so the common RNA might have originated in the human? Just asking.
ReplyDeleteCreationists and intelligent design advocates like to think that because some ERVs have useful functions in the human genome, they must have been deliberately put there by a creator / designer with that particular purpose in mind.
Again, you are working on the assumption that similarity means relatedness. I mean, what if those promoters evolved independently? That's as likely as any other parallel evolutionary path, maybe even more likely than the parallel evolution of an entire organ.
And while some creationists may believe what you said, what they are really saying is that the ERV did not create any novel information resulting in a new functional protein - it merely inserted existing information. That's not evolution, that's just mutation or insertion, in their minds.
Seeker,
ReplyDeleteGood to hear from you. I hope you don't mind if I answer your questions point by point, and I apologise in advance for length!
1) "I am skeptical of the 8% number. What are the assumptions?"
We now have the whole human genome sequence available to us. We also know a lot about what retroviral sequences look like. They have common features such as the genes that code for the viral coat protein and for the reverse transcriptase that copies the viral RNA genome into DNA. The gene sequences are flanked by a pair of repeats. It's a very easy task to search for viral sequences in the human genome as the pattern is so clear. The answer comes out as 8%.
2)"could the ERV have actually taken the DNA out of the human in the first place, and so the common RNA might have originated in the human? Just asking."
It's an interesting idea, but I'm afraid it's vanishingly unlikely. ERV sequences are clearly viral in origin. They are very similar to some modern infectious viruses, even some that infect species that were around long before mammals.
Retroviral genes produce proteins that have specific roles in the viral life cycle (see above for examples) but that would have very limited usefulness for the human genome. In fact most ERVs do not produce any functional protein - there's no selective pressure on the genes once they're integrated into the host genome and don't need to produce infectious viruses any more, so they are allowed to degrade. You can still see the similarity to viral genes that encode functional proteins, but the ERV proteins are truncated and useless.
It comes down to a question of which is more likely - that a piece of human DNA got copied by a virus and happened to encode for an extremely effective infectious agent, or that viruses (that are known to insert themselves into host cell DNA - we can actually see this happen) managed to get into the human genome. The fact that some humans have ERV sequences that are not present in all members of the species is very strong evidence that ERVs originate from outside the human genome.
3) "Again, you are working on the assumption that similarity means relatedness. I mean, what if those promoters evolved independently? That's as likely as any other parallel evolutionary path, maybe even more likely than the parallel evolution of an entire organ."
It's true that some very complex structures evolved twice independently (e.g. wings in insects and in birds). Those pathways involve multiple genes and haven't been completely worked out yet. But we're looking at the actual DNA sequence here, which is much easier. I guess you're speculating that the thousands upon thousands of ERVs in the human genome all evolved from unrelated parts of the genome and ended up with extremely similar sequences. This is not impossible (we can't prove a negative), but it is statistically extremely unlikely, and there is no evidence in support of this hypothesis. The alternative - multiple independent insertions by the same kind of retrovirus - has plenty of supporting evidence. You could look at modern mouse retroviruses that are still becoming endogenous. You could look at a modern infectious retrovirus such as HIV (not an ERV, but it is responsible for multiple independent insertions into host blood cell DNA). All of these observable examples produce the same patterns of sequences that we see in human ERVs. The evidence is truly overwhelming in favour of multiple insertions into the human genome.
4) "the ERV did not create any novel information resulting in a new functional protein - it merely inserted existing information. That's not evolution, that's just mutation or insertion, in their minds".
First of all, inserting existing new information into a new location where it didn't previously exist does create new information. Context is everything. Second, you don't have to create a "new functional protein" for evolution to take place. Changing the expression patterns of an existing gene can be just as, if not more, powerful. As an example, think of the protein that makes hair in humans and chimps. The proteins themselves are extremely similar, but they're expressed in different areas of the body. The result - hairy chimps, and humans with hair only in a few specific places. Or imagine that a protein that promotes brain growth during development is switched on slightly earlier or switched off slightly later in some individuals than others. The result - some animals are born with larger brains. The evolution of protein expression is an extremely important subject. And there is abundant evidence that ERVs have contributed to it.
You've raised some interesting questions, and I hope I've gone some way towards answering them. There is plenty of other information out there if you're interested in learning more. I'd be happy to recommend some articles if you have any trouble finding something that appeals.
Thanks for reading!
Thanks for the helpful reply. As a former biochemist who did genetic research into lymphoma and leukemia, I understand most of these issues, even though I've been out of the lab since 1993 (I did a lot of southerns and PCR work looking for recombination events in humans).
ReplyDeleteFirst of all, inserting existing new information into a new location where it didn't previously exist does create new information. Context is everything.
Well, I guess in one sense you are creating new data, but I would say that if you insert nonsense DNA into a working protein, that's not really creating information in the sense that it becomes a useful thing. What I mean is, not every random change can be considered an increase in information, if you define information as something that creates or modifies functionality.
And while some modifications might alter funcationality (like reducing the effectiveness of a protein, or changins its specificity, etc.), I would still say that this could be viewed as a change, but not an increase in information, but rather, a corruption of information that led to altered or crippled functionality.
But this is one of the differences between an evolutionary and creationist viewpoint. Creationists start with the assumption that a relatively perfect genome was created, and all changes since then are actually crippling or corrupting the original message - and that even if such "corruptions" have a short term beneficial aspect (e.g. sickle cell), that mutation still has a significant harmful effect in that it's intended functionality is damaged and damaging to the organism.
The evolutionist, however, does not look at existing functionality as good and complete, so all non-lethal changes are viewed as possible improvements, and therefore, increases in information. However, the benefits of such mutations seem to only appear in the hypothetical long-term picture of evolution, and in the near term, they are almost universally harmful.
I think I like the creationist model for this reason - they assume a perfect originating point from which we have diverged, and which we can perhaps piece together again - I see the research into the aging gene as a search for something that was LOST, not something yet to evolve. Evolution, by contrast, has a hard time judging what is helpful except in the immediate context of disease, and the "perfect" genome, of course, does not really exist, though we think of the perfect genome when we talk about living longer, living free from disease, or being stronger, smarter, etc.
But I am digressing. My point is that, while I think context is important because insertions/deletions can alter functionality, I don't think I would agree that this is really a creation of new useful information, but perhaps a corruption. In this case, I would say that your original assumptions (evolution or creation) color how you look at that.
Second, you don't have to create a "new functional protein" for evolution to take place.
I agree that affecting the expression of existing genes is a change, but I doubt that it is evoluion, but again, merely moving existing information around. I understand that putting a functional protein in a new context produces differing results, but again, changing the context is, in my mind, not really creating information but rearranging it. Perhaps we need more exact language for each of these scenarios. But the change you mentioned with apes and humans is, of course, not evolution unless that change was inherited. Again, we are assuming inheritance, but we can't really prove it, though we may propose and test various mechanisms.
As you can tell, I am a creationist sympathizer (some would call me a creationist, but I reserve the right to change my mind, as I have once from my previous strong evolutionary beliefs). But I raise these questions, at least, so that we clarify and examine our assumptions, and try to make conclusions based on the data and not beyond it.
Thanks for your explanations, they are helpful.
Respectfully,
Seeker
Hi again Seeker
ReplyDeleteDon't worry, I hadn't forgotten you - real life just intruded for a while. Also, giving your last post the time it needed almost made me late for work last week, so I have to be careful!
Tonight I'm trying to make my weekly poker game on time, so I'll try to keep this brief... a lot of your points involved the definition of "an increase in information". I would argue that any mutation increases information, in that you suddenly have a different DNA sequence in one individual than in others. The amount of information in the population thus increases. And while individuals can not evolve within their life time, populations of individuals can.
But this is one of the differences between an evolutionary and creationist viewpoint. Creationists start with the assumption that a relatively perfect genome was created, and all changes since then are actually crippling or corrupting the original message - and that even if such "corruptions" have a short term beneficial aspect (e.g. sickle cell), that mutation still has a significant harmful effect in that it's intended functionality is damaged and damaging to the organism.
The evolutionist, however, does not look at existing functionality as good and complete, so all non-lethal changes are viewed as possible improvements, and therefore, increases in information. However, the benefits of such mutations seem to only appear in the hypothetical long-term picture of evolution, and in the near term, they are almost universally harmful.
Here is the link to a paper I think you should read. http://www.pnas.org/cgi/content/full/101/6/1626 I covered it for a journal club before I left the lab and it's a really nice study. There's free access at PNAS, and with your biochemical background it should be very readable! They found a transposon insertion (similar to an ERV) that increased the expression of a fly protein that's involved in insecticide resistance. In populations that have had a lot of exposure to insecticide, the transposon was present in almost all flies. Insertion of the transposon had been so benefical that the mutation was positively selected and spread rapidly in the population. In other populations of the same species that had not been exposed to the chemical, the transposon was much less common. There just wasn't the selective pressure there to make the transposon as beneficial in these areas.
I think you have to agree that this insertion is a beneficial mutation.
The evolutionary model actually predicts that most mutations will disrupt normal function and be harmful. That's why the most important genes - e.g. the ones that control embryonic development - are so similar in all species: there's very very little wiggle room for them to change. They're conserved by negative selection. But every once in a while a beneficial change takes place - like an insertion that makes flies resistant to insecticides. These mutations are much less common, but if you consider all possible mutations in all the billions of flies out there over thousands of gnerations, they're gonna happen sooner or later. I just don't buy that all mutations have to be harmful and a "corruption" of a "perfect" ancestral genome.
As for long vs. short term effects - evolution doesn't "see" the long term. The only thing that matters is whether a given mutation is likely to increase or decrease the average number of the mutated individual's offspring in the next generation. Mutations that disrupt some essential gene will decrease the number of offspring in the next generation. Mutations that increase resistance to toxins tend to increase the number of offspring. The same is true for the descendants of the original mutated individual. The usefulness or harmfulness of the mutation will change over time as the environment changes, which may or may not mean that a once-beneficial mutation becomes harmful, or vice versa. e.g. having one copy of the sickle cell gene is a helpful barrier to malarial infection when you live in the tropics, but is nothing other than a devastating disease waiting to happen in an immigrant or descendant of immigrants to a country with no malarial mosquitoes.
I agree that affecting the expression of existing genes is a change, but I doubt that it is evoluion, but again, merely moving existing information around. I understand that putting a functional protein in a new context produces differing results, but again, changing the context is, in my mind, not really creating information but rearranging it. Perhaps we need more exact language for each of these scenarios. But the change you mentioned with apes and humans is, of course, not evolution unless that change was inherited. Again, we are assuming inheritance, but we can't really prove it, though we may propose and test various mechanisms.
I have to disagree. We can quibble all you like about the definition of information, but I think it should be self-evident that changing the pattern of protein expression is a change. Can you really give me a definition of evolution that does not contain the word change? Altered patterns of protein expression are acknowledged to be extremely important in evolution. Here are 2 recent examples, both open access (doncha just love open access?):
http://genomebiology.com/2007/8/6/R98
http://genomebiology.com/2007/8/6/R118
And there are many, many known examples of heritable variations in gene promoter regions that influence the level and pattern of gene expression. I've been to conferences where every 3rd or 4th poster seemed to be about promoter variation.
As you can tell, I am a creationist sympathizer (some would call me a creationist, but I reserve the right to change my mind, as I have once from my previous strong evolutionary beliefs). But I raise these questions, at least, so that we clarify and examine our assumptions, and try to make conclusions based on the data and not beyond it.
Thanks for your explanations, they are helpful.
I hope these new points are helpful to you too! I think we've proved that it is actually possible to have a proper debate without resorting to name-calling. If you'd like more information about ERVs and evolution, ERV's blog now contains an excellent section on this very topic. See http://endogenousretrovirus.blogspot.com/2007/07/index-to-common-creationist-claims.html - enjoy!
p.s. I promise to figure out how to embed links in comments at some point...
I would argue that any mutation increases information, in that you suddenly have a different DNA sequence in one individual than in others. The amount of information in the population thus increases.
ReplyDeleteI guess we have a simple definition of terms issue here. I think of information as intelligently created data, not just randomly created data. I mean, a random sequence of numbers is not information, it's just data.
Now, when you are inserting one piece of functional "information" into another, you MIGHT create new useful information, but in almost all cases, you damage the initial message and create a new nonsense message.
I mean, how many times have we actually seen a new functional protein created from non-coding DNA? That would be information creation to me.
that increased the expression of a fly protein that's involved in insecticide resistance.
But did it create a new protein or did it change the expression of an existing one? The former MAY be considered an increase in information, but the latter, probably not. I'll go read the article.
changing the pattern of protein expression is a change. Can you really give me a definition of evolution that does not contain the word change?
I would say that evolution has many definitions. But I would say that random mutations, natural selection, nor re-arrangements to DNA are evolution. They are all proposed mechanisms, which also fit into a creationist model. To me, what is uniquely evolutionary is the idea that new, positive DNA changes are made that are then passed on to progeny, and that this "micro" evolution leads to a "macro" evolution, known as common descent.
Interestingly, even Creationists believe in a type of adaptation with descent, that is, from the original Noahic "kinds." So while they would exist that all canines may have descended from a common ancestor, they would deny that such descent with modification could ever produce a cat, or any other order/family/ (a rough approximation of "kind").
And there are many, many known examples of heritable variations in gene promoter regions that influence the level and pattern of gene expression.
Again, I see where you are coming from, but I think it's a huge jump from modifying and controlling genes to creating novel proteins from arranging random sequences.
I think we've proved that it is actually possible to have a proper debate without resorting to name-calling.
Thank you, I really appreciate your respectful demeanor.
BTW, the way to insert hyperlinks is to use this format: [a href="insert URL here"]Insert text for link[/a]
The only thing you have to change is use the greater and less than signs instead of the square brackets used above. It's a little cumbersome, but that's how. But posting the url like you are doing works fine.
You dismiss arguments from design with an 'it's not a falsifiable hypothesis, and therefore it's not science.' If you will permit me to say it however, your just so story is also not falsifiable. You assert: Some insertions are shared between humans and mice and represent truly ancient viral infections. But you actually have no evidence that there ever was such an infection as you suppose. It is an inference - it may be a valid inference - from the appearance of similar sequences in the two genomes, but it is not the only valid inference that can be taken. Your assertion and your inference are not falsifiable and are therefore, on your own terms, no more science than you claim the ID inference is.
ReplyDeleteI would have expected better from you than this.
The presence of similar sequences in a variety of genomes, which can be identified with sequences found in viruses is not in itself evidence that a virus placed any of those sequences there. Likewise the similarity of function from one organism to another is not in itself evidence of, speaking very broadly, common descent. You claimed to have made and had tested a falsifiable prediction, but all that was demonstrated was that one sequence which did a particular job was a good as a different sequence which did a similar or the same job. The test did not demonstrate that the sequence had been inserted by a virus. If you wish to demostrate that a virus inserted the sequence, then you really do need to start of with a viable genome without the sequence, watch a virus insert the sequence and then observe the growth of a viable organism afterwards. Even that however will only show that the particular insertion you saw actually took place. It does nothing to support any assertion that any other insertions have taken place.
Secondly to my mind, there is no good reason not to understand why any kind of designer would not decide to use different codes to perform the same function in different species. I understand the economy of design, but even with our own limited understanding, we can see that there are always trade offs to be made between efficiency, economy and security, by which I mean all of those mechanism which prevent errors arising, eg in copying, in production, in function. We know about this in every day life; when you buy a car you must take these things into consideration. In the context of different organisms different considerations must apply. Perhaps in a short lived organism security is less important (perhaps it is more important!) and in a long lived one more important, as the long lived organism must survive through many more reduplications of the code within. The designer would choose the code that is most apporpriate for each organism. Perhaps it is sometimes only in the single letter points that the distinction is necessary, but unless we understand fully the implications of the single letter changes, we really should be careful not to pronounce on them as minor mutations caused by copying errors. In the particular oganism concerned they may be vital to its development or continued existence, and in another organism be entirely detrimental.
Think again, carefully, please, and try to recognise when you step over the mark from science, our knowledge of the world as it is, and into the realm of philosophy, our ideas about where we would like to think we came from.
Hi CAD, another Pharyngulite here (though I linked from Skeptics' Circle #64). Well done for the detailed but clear explanation of ERVs and their likely origins. Kudos to seeker too - but don't you two know you're supposed to be SHOUTING AT EACH OTHER? ;-)
ReplyDeleteRichard, I suspect CAD will reply to you herself, but in the meantime I'm a little puzzled. Science is only interested in the evidence, and doesn't care "where we would like to think we came from" (except maybe in psychology). There is plenty of evidence pointing to ancient retroviral infections, and CAD has not only outlined it, but replied to good questions by seeker, and linked to the original research. Where's the philosophical musing?
Wow, there's been some action on this, my most-linked post, recently!
ReplyDelete-----------------------------------
Seeker: I'd be very interested to hear what you think of the PNAS paper on insecticide resistance. Did you get a chance to read it? From what you've written so far, I gather that you have no problem accepting some kind of theistic microevolution (I may not have chosen the most appropriate term here!), but not macroevolution. You say:
"To me, what is uniquely evolutionary is the idea that new, positive DNA changes are made that are then passed on to progeny, and that this "micro" evolution leads to a "macro" evolution, known as common descent".
I think the PNAS paper I cited is evidence for everything in your statement except, obviously, macroevolution.
You've probably gathered that I'm a microevolution kinda gal. That's what all my research has always involved. I don't pretend to be an expert in the field of macroevolution, so I'm going to direct you to Talk Origins (thanks for the linking lesson!). I know that as a creationist who posts on evolutionary blogs you've probably been sent there a lot, but that's because it really is very good. It's an excellent resource for subjects outside any scientist's area of expertise, and I refer to it a lot myself.
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Stuart arcs:
Welcome! I'm glad you've realised that I'm happy to (rationally) debate other points of view.
The main counter argument to your POV is that it makes things so much more complicated. Given that we can observe modern day retroviruses inserting with patterns that are identical to those of ancient ERVs (see this blog for the example of the mouse mammary tumour virus), and given that we have a very good understanding of the mechanisms that generate point mutations, I really don't see the need to bring in a designer who inserts sequences that look like retroviruses and in some cases produce retroviral proteins, and who comes up with ever so slightly different sequences for them that perform the same function in different species.
I know that in some complex cases a designer can seem to make things easier to understand, but when the underlying mechanisms are so well understood, why create a scenario where you suddenly have to answer so many new questions? e.g. what is the nature of the designer? Who/what designed the designer? Who/what designed the designer's designer? And so on.
You say:
"You claimed to have made and had tested a falsifiable prediction, but all that was demonstrated was that one sequence which did a particular job was a good as a different sequence which did a similar or the same job."
I know I wrote a very long post initially - if brevity is the soul of wit, then I am a half-wit. But I think you've mixed up two different parts of it. My falsifiable hypothesis did not refer to the different sequences of the ERV promoter in different primates. Here's my original statement:
"I hypothesised that the ERV was only allowed to persist (that is, its meddling in gene regulation didn't kill the first organism in which it inserted, which was therefore able to pass the insertion on to its offspring) because the incoming ERV promoter behaved in a very similar way to the original host cell's gene promoter."
The falsifiable hypothesis was that the original host cell's gene promoter behaved in a similar way to the incoming ERV promoter. I wasn't able to identify the original promoter (looking in the wrong tissue - d'oh!) but another group did. It had the same patterns of activity, and bound the same regulatory proteins, as the ERV promoter. That is specifically what I was referring to.
Elsewhere in my original post I said: "What we can show is that ERVs provide evidence in support of the theory of evolution".
Please note that I did not say evidence of evolution, I said evidence in support of the theory of evolution. There is lots of it. In contrast, I have never seen any evidence in support of the theory of intelligent design. As I said, you can not prove a negative. But if I had to gamble every single thing I own, I would bet that there is no designer and that modern day species evolved from a common ancestor. And my poker buddies consider me to be a conservative gambler, easily intimidated by a $2 bet...
Pete seems to have taken care of the final paragraph of your comment already, so I'll let that one be. But not this one...
"I would have expected better from you than this".
I'm sorry, do I know you? It's possible that you are the one Stuart that I know, but I'd be very surprised if you are.
I suspect this debate will be continued!
-----------------------------------
Pete: thanks mate! I'll click through to your link once I'm done here and find out more about you. Please stick around, I think this one could keep on going...
Seeker, I just re-read one of your earlier comments and clued into the fact that you used to be in the cancer research field. I'd love to hear your feedback on this post. (Now you've taught me how to link, there'll be no stopping me!).
ReplyDeleteI was thinking more of solid tumours but I'm sure some of it also applies to hematopoietic malignancies.
Thanks in advance!
CAD taking your points in turn, I am not trying to make things seem any less or more complex than they are. The genome is a hugely complex code even before we take into account all of the hardware surrounding it, but comparisons between silicon based and carbon based intelligent systems are really hardly satisfactory. Whether we have a designer or not it does not make it any easier to understand. We can look at parts of it and say, this bit encodes for that protein, and that bit for that and so on. We may even be able to describe the functions of the proteins and some of the circumstances in which production is turned on and off, but how much do we really know? How much do we really understand? I submit that we will only really understand when we can look at an genome from an unknown organism then from its elements and structure describe what it does and what form of organism it produces.
ReplyDeleteIt is rather like reading computer code. I am now a programmer. I work in higher level languages than some of my colleagues, whose ability to read code that they have never previously looked at astonishes me. they can describe what it does, but they are looking at very small stretches of code in a very large system. There are very few who have a grasp of the whole thing and how a change in one small area might affect many others, on the other hand some small changes have nothing more than a cosmetic effect. When I write code I take into account the three things I mentioned earlier - economy, efficiency and security. Sometimes, if the code is for one off use by me then it will be efficient, and complete disregard security. At the other extreme if it will be used mutliple times under automated control then security will be high on the agenda, and economy may well be very low. The code in both cases may do exactly the same thing, ie have the same function, but it will look very different. Sometimes we will write code that is highly redundant, sometimes even write code that will never run, or at least ought never to run, but we write it because something may change when we do not expect it to do so, eg if the are only two outcomes I could write: if 1 do A else do B. But I may prefer to write: if 1 do A else if 2 do B else do C. C will never happen, as we said there are only two outcomes, or at least we think that there are only two outcomes. C may be an instruction to try to ascertain whether we should have had a 1 or a 2 and try again, or it may be an instruction to halt the system aka MS blue screen of death: The system has been halted to prevent data loss.
Where am I going, well, I read about the genome and it is a very poor comparison with our human programming, but there are illustrations that may be helpful. Seekers reference to the sickle cell variation is a point. In human code it is possible to replace code for code, but sometimes doing that can be an accident waiting to happen, like sickle cell and perhaps even toxin resistance in certain flies. We need to understand the parts in the context of the whole before we truly understand the genome. That is why I think we must now be hasty in the conclusions we draw today. They are literally ephemeral. Tomorrow's conclusions may well be quite different.
As for asking questions about the designer, well that is rather like a computer asking questions about the one who made it, is it not? The computer must be taught. It is not for the designed to question the designer. It is for the designed to get on with the job for which it was designed. If the designer chooses to teach the designed about himself then the designed may have some hope of understanding a little bit about him. But it is the height of folly for the designed to think that he can grasp the being of the person who designed him!
I accept what you say concerning your falsifiable hypothesis, but it is a long way to go from there to say that this insertion took place at some distant time in the past. That is not a justifiable inference from the demonstration that a particular ERV did a similar job as the sequence it replaced.
What I do find uncanny is the suggestion that it has been possible to identify the piece of code that was replaced by the ERV. If the ERV replaced the code, then the original code is no longer there. How then can we know what it was? It may be suggested that we know what it is because we find the original code in a different genome. If the two genomes had a common ancestor then you may be able to make that inference. However, if they did not have a common ancestor, then you can make no such inference.
You said: "What we can show is that ERVs provide evidence in support of the theory of evolution". As may be seen,. ERVs only provide evidence in support of evolution if there is a common ancestor, ie if evolution is 'true'. If evolution is not 'true' then they only provide evidence for themselves.
Given your prediliction for gambling you must know of Pascal's wager? if I may restate it to your case: if I bet $2 that there is no god, and there is no god, I lose my $2. If I bet $2 that there is a god, and there is no god, I lose my $2. If I bet $2 that there is a god, and there is a god, I lose my $2 but I might keep my soul. If I bet $2 that there is no god, and there is a god, I lose my $2 and I lose my soul. Pascal looked at the odds. I leave you to work out on which side they are stacked.
Hi again stuart
ReplyDeleteAnother long post, so I'll take a point-by-point approach again, starting with the scientific details:
"What I do find uncanny is the suggestion that it has been possible to identify the piece of code that was replaced by the ERV. If the ERV replaced the code, then the original code is no longer there. How then can we know what it was? It may be suggested that we know what it is because we find the original code in a different genome. If the two genomes had a common ancestor then you may be able to make that inference. However, if they did not have a common ancestor, then you can make no such inference."
The ERV didn't actually replace anything. When a retrovirus inserts, it interrupts the existing DNA sequence, but doesn't remove any of it. It's as if the sequence AACGGGTTCA now reads AACGERVGGTTCA. So the original gene promoter is still there. The ERV promoter has replaced a large part of the function of the original promoter, but both promoters are present and active. The two sequences are actually quite different to each other, but both bind the same regulatory proteins and activate gene expression in very similar tissues.
"As may be seen,. ERVs only provide evidence in support of evolution if there is a common ancestor, ie if evolution is 'true'. If evolution is not 'true' then they only provide evidence for themselves".
My orignal post provided an example prediction of how an ERV would behave in a model of evolution by descent from a common ancestor. When you then look at ERVs' actual behaviour, they fulfill all predictions. Therefore they provide evidence in support of the theory of evolution by descent from a common ancestor. If evolution was not "true" then we would not expect ERVs to meet the predictions made by the evolutionary model. If ERVs ever did not meet predictions, you would indeed need to come up with a better model. But that hasn't happened yet.
Moving on to your more philosophical points:
You say a couple of times that
"comparisons between silicon based and carbon based intelligent systems are really hardly satisfactory"
However, you then go on to explicitly compare the human genome to a code run by a computer:
"As for asking questions about the designer, well that is rather like a computer asking questions about the one who made it, is it not? The computer must be taught. It is not for the designed to question the designer. It is for the designed to get on with the job for which it was designed. If the designer chooses to teach the designed about himself then the designed may have some hope of understanding a little bit about him. But it is the height of folly for the designed to think that he can grasp the being of the person who designed him!"
I guess I'm a little confused as this is such a foreign concept to me. Are you really saying that you think humans are running a code introduced by a designer, and not only can we not hope to understand the nature of the designer, but we shouldn't even try? I would say that modern man has failed at that last instruction throughout its entire history...
"Given your prediliction for gambling you must know of Pascal's wager? if I may restate it to your case: if I bet $2 that there is no god, and there is no god, I lose my $2. If I bet $2 that there is a god, and there is no god, I lose my $2. If I bet $2 that there is a god, and there is a god, I lose my $2 but I might keep my soul. If I bet $2 that there is no god, and there is a god, I lose my $2 and I lose my soul. Pascal looked at the odds. I leave you to work out on which side they are stacked."
As I understand it, Pascal's wager says much more about the value of the stake than it does about the odds of winning the bet. I know that Pascal would have calculated the odds differently than I would -a lot has happened since the 17th century and he was living in a society where a creator deity would have seemed like the only possible explanation for life on Earth. Different people living at different times will calculate the odds using different information and end up with different answers. You are right, there is a chance that I'm wrong and will spend an eternity in hell. But, looking at the evidence, the chance is so tiny that it is still logical to make the gamble. It's like betting your house on the outcome of tomorrow's sunrise. The stakes are huge, there's a lot to lose, but the odds are awesome.
By the way, the Genomicron blog has a challenge for proponents of the theory that repetitive DNA is a designed component of the genome. ERVs and other transposable elements are only one component of repetitive DNA, but you might be interested anyway. I'd be interested to hear what you think.
Sorry, my stupidity about ERVs inserting, but I do not think it changes my position.
ReplyDeleteI did say that comparison of the biological code and man written code is hardly satisfactory, but an analogy, if we recognise its limits, can sometime be helpful, hence why I went on.
I did not intend to say that we are running a code introduced by a designer, what I intended is that we run with that code, or perhaps it should be in that code or by reason of that code. We are the products of the running of the genetic code. If the genetic code had ceased to run correctly at our beginning, we would not be here today, would we?
That said, we are more than the simple product of the code. We know that. Often when we see the sunlight playing in the rain and at many other times we know that. But we also know that because the designer has told us so. He told us that we are made of the dust of the ground - the combinations of chemical elements and their chemistry - and that he breathed life into us so that we became a living soul, made in his image.
I really did mean it when I said we cannot grasp the being of the one who made us. That does not mean we cannot understand the chemistry within, though it will take a lot of hard work, and even then we may never quite get to the bottom of it; it seems that the more we understand about something the more questions flood up to our minds. But to understand him, well that is a different matter. Of course we can begin to do so, and he has not left us ignorant of himself, but the finite cannot comprehend the infinite.
Turning to the web page to which you pointed me I found the following points, and have added a few comments, all of which could be better thought out and expressed, but here is a start:
1) Specify the basis for assuming that all non-coding DNA must be functional.
I dealt with this point in the bit of my previous post which you confessed not to understand - it 'is ..foreign .. to me'. Of course this could be simply turned around and put positively: Specify the basis for assuming that not all DNA is functional. There is no challenge here.
2) Specify how one would go about demonstrating evidence of functions for non-coding DNA in the absence of a framework based on common descent.
Search for the evidence? Experiment, experiment, experiment! It may only be a happy accident that opens up a new avenue of research for us; like a discarded petri dish, or an apple from a tree (sic!). A recent article on the fly's body plan and Bicoid levels suggest very clearly that we do not know what is going on! But oh how much we would like to!
3) Make specific predictions about what function(s) all non-coding DNA is likely to be fulfilling, and propose ways to test those predictions.
It is pretty difficult to make specific predictions about what something will do if you do not even undersatand the code in which it is written. I dealt with this point too in my previous post. Perhaps it could be likened to predicting what a computer prgramme will do from its name or the shape of the icon. Even when we do know what a programme does in general terms, it then becomes like opening up Excel, refusing to read the help file, then trying to code some actuarial calculations. A lot of guess work will be required as to precisely what arguments the functions required, even if you managed to guess correctly the names of the functions.
4) Propose functions for transposable elements that take into account their parasitic characteristics (e.g., as disease-causing mutagens) but do not invoke the notion of co-option.
Surely we do not propose functions, we identify the function of something by looking to see what it does.
5) Provide a specific explanation for how the great majority of transposable elements in the human genome can be functional while showing clear signs of being inactive.
As in man written code, there are many inactive parts, as I sought to suggest in my earlier post. Just because they appear to be inactive now, it does not mean that they have always been inactive in the life of the organism, nor that they always will be. Perhaps much of the code is now inactive because it has fulfilled its purpose which was to build the organism from single cell. See the article about flies to which I referred above.
6) Provide an explanation for why the DNA sequences of non-coding regions in different species appear to correspond to degree of relatedness.
Species share common characteristics, and would therefore share code to produce those characteristics, just as in man written code there is shared code. Code which in the earlier days would have had to be written into every programme is now contained in in shared files, eg common controls for printers. In the biological world that code must reside in the organism which wishes to use it not in an external repository.
It is not necessary to postulate a common ancestor to explain similar code.
7) Propose a testable explanation for why similar species may have widely different quantities of non-coding DNA in their genomes.
It has yet to be shown that there is any non-coding DNA in any organism. Something may appear to have no function, but that does not mean that it has no function. It would be folly - and it has been folly - to delete the boot sector of your hard drive just because whenever you used the computer you never saw anything happen there. It may appear to be completely nonfunctional in use, but we all know that it is vital. But then we do know that, we do not understand the DNA code, so how can we say it is non-coding or not functional?
8) If one does accept common descent, propose a testable explanation for how there can be significant reductions in DNA content in some lineages.
I need make no comment to this.
In short, the answer to all of these, is simply get on with the work. Understand how every mechanism in the body of an organism works and what controls it. Understand how the adult body is constructed from the single cell, what the mechanisms are and what controls them - what switches are used. Succinctly, understand the code, find out what it means and what it does. This is nothing to do with evolutionary hypotheses or ID hypotheses, this is basic chemistry. If we can't get our chemistry right, what then?
So, only then, when we have identified every function of every part will we be able to say of the bits that have not been used, they are not functional. But then, what if those bits that we have never seen used are only ever brought into use when something goes wrong. Perhaps there is code in drosophila which sits there simply watching as other code controls the mechanisms which drive the distribution of Bicoid, and only ever becomes active if the distribution does not match the expected pattern. We may conclude that that code was inactive, because we never saw it watching. We would be wrong.
Sorry, my stupidity about ERVs inserting, but I do not think it changes my position.
ReplyDeleteDon't worry, it wasn't stupidity at all! If I was any good at graphics I would have included diagrams in my original post that would have made things a lot clearer. But you really don't want to see any of my illustrations, I'm notoriously useless.
I did say that comparison of the biological code and man written code is hardly satisfactory, but an analogy, if we recognise its limits, can sometime be helpful, hence why I went on.
I did not intend to say that we are running a code introduced by a designer, what I intended is that we run with that code, or perhaps it should be in that code or by reason of that code. We are the products of the running of the genetic code. If the genetic code had ceased to run correctly at our beginning, we would not be here today, would we?
Sorry, I guess I misunderstood you. It was really your assertion that we shouldn't ask questions about the nature of the Designer that threw me off. Pretty much every theistic culture in recorded history has claimed to know the nature of its creator, and I thought it was a strange thing for a religious person (which you clearly are) to say...
Your answers to the Genomicron challenge are interesting (did you post any of them on the other thread? I haven't looked in a while), but I think there are obviously some basic differences between programming and the testing of scientific hypotheses that cause you some problems.
2) Specify how one would go about demonstrating evidence of functions for non-coding DNA in the absence of a framework based on common descent.
Search for the evidence? Experiment, experiment, experiment!
Yes, but how? It would be helpful if an ID supporter could come up with an alternative framework that makes certain testable predictions that are different to those made under the common descent framework. Then we could get started on the experiments. Experimenting without a starting hypothesis is unlikely to get you anywhere - yes, you could get lucky and accidentally discover penicillin, but those stories are rare.
4) Propose functions for transposable elements that take into account their parasitic characteristics (e.g., as disease-causing mutagens) but do not invoke the notion of co-option.
Surely we do not propose functions, we identify the function of something by looking to see what it does.
But how do you know how to test for function without having at least a vague prediction of what something does? For example, imagine you cut the brake fluid line in a car. If all you do next is run the engine with the bonnet (hood) up, you won't figure out what that part usually does. However, if you infer from the destination of the fluid line that it has something to do with the wheels, then you might consider driving the car to determine the effect of cutting the line.
Similarly, you have to design the right exeriments to determine genetic function. And to do that you need a prediction of function to test. For example, if you think that an ERV is involved in gene regulation, you alter the ERV and look for effects on gene expression. Measuring something else, e.g. cell division rate, won't necessarily be informative, although again you might get lucky. Just blindly altering non-coding DNA to see what happens is unlikely to tell you much.
7) Propose a testable explanation for why similar species may have widely different quantities of non-coding DNA in their genomes.
It has yet to be shown that there is any non-coding DNA in any organism.
Non-coding DNA refers to DNA that does not code for protein, not for DNA that has no function. The vast majority of human DNA does not correspond to any protein that has ever been found in any part of the body under any circumstances. You're right though if you meant that it has yet to be shown that there's any non-functional DNA - although there's an awful lot of DNA that has shown no signs of function in any test that's been thrown at it so far. Yet again, you can't prove a negative.
In short, the answer to all of these, is simply get on with the work. Understand how every mechanism in the body of an organism works and what controls it. Understand how the adult body is constructed from the single cell, what the mechanisms are and what controls them - what switches are used. Succinctly, understand the code, find out what it means and what it does.
Now there's something we can both agree on!
As ever, it's very enjoyable to debate science with you and to hear some of your more philosophical points. I tend not to respond to them much as you will get much better quality answers elsewhere, but keep 'em coming if you like, it's interesting reading for me. I may not agree with a lot of them, and I'm sure you don't agree with a lot of what I say, but dialogue is good, right?!
I'm obviously a bit late on this one (why didn't you tell me about your blog earlier? you knew I'd like it), but I have to comment on the two creationists' remarks.
ReplyDeleteDon't you love how creationists of the seeker kind demand that evolution must require "new information", but then go on to define "new information" as everything that evolution isn't? By their definition of "new information", evolution at the genetic level neither involves nor requires "new information".
And the sophistry of stuart arcs is astounding. How the creationist tries to downplay what we do know, and inflate what we don't, beyond all proportion - the mind boggles!
I had fun debating these two! You know what it's like when you're in a lab environment, you rarely meet anyone who disagrees with you and when they do it's usually on something small and nitpicky. It's exceptionally rare that I meet someone who doesn't believe in evolution at all, and when I do I get to debate the big juicy stuff and back it all up with lots of evidence and publications. I also don't have to worry about offending someone, as the only creationist I've met in Vancouver is a friend's mum and I wasn't about to try and take her down in her own house!
ReplyDeleteIf they come back I'll let you know and you can join in the fun!
You said:
ReplyDeleteNow that several genomes have been sequenced, we have begun to test these predictions. The patterns of ERV insertions observed in modern species exactly match the predictions made by the model described above.
Is there a public data that shows which ERVs are in which genomes that I can use to validate this assertion?
Hi IDer, and welcome!
ReplyDeleteThe genome sequences are all publicly available. The best tool is at the University of Santa Cruz's website. You can expand the repeat masker track to see all the ERVs and other classes of repetitive DNA. This link should take you to the gene I described in this post, but you can look in other species and other genes too.
Or you can read the original genome sequencing papers, which all have sections on ERVs and other repeats. Here are some links to the human, mouse, chimpanzee and macaque genomes to get you started. There are many more out there now - try PubMed. Off the top of my head, the cat, dog, cow, pig, chicken, puffer fish, C elegans nematode, and several species of Drosophila flies are all done, but there are probably many more by now. All genome sequences are publicly available, the details will be in the papers.
Have fun!
I don't have access to Nature. When I have more time to read it I'll fork over the $198 to get an individual subscription.
ReplyDeleteThe genome database link looked interesting but as far as I could tell it wasn't organized in the way I was hoping in my original question. I thought that perhaps someone had collected the known retrovirus sequences and put them in an access file or some other relational database in such a way that one could see which genomes they appeared in by executing some simple SQL statements.
I like your blog. I was going to answer your survey but I didn't see the option I was looking for. Maybe something like "I'm an IDiot and I still don't believe in Junk DNA"
Hi again
ReplyDeleteSorry about that - I thought the genome papers were all public access. The human paper definitely was at the time of publication, but maybe the policy has changed. I still think those papers are an excellent source of information, especially the post-human genome papers that compare all repetitive DNA to that found in humans. If you're comfortable with this, you can email me and I'll send the PDFs directly to you.
I don't think anyone's put together a database like the one you describe, but I could be wrong. It would be a huge job to assemble something that contains all ERVs in all species. I'll do some digging. There are definitely some papers out there that compare a few ERVs at a time across multiple species - would you be interested in those if I can find some open access examples? They even managed to analyse the repeats in DNA extracted from a frozen woolly mammoth and found shared insertions with living species, which is pretty damn cool.
T Ryan Gregory at Genomicron
has a great collection of posts about so-called Junk DNA that you might find interesting!
And thanks for your comment!
From time to time I drop by Genomicron's blog. I noticed that he wisely does not endorse the use of the term "junk DNA" even though he embraces the concept. Personally, I would like to see a lot more government money spent investigating genomes. Humankind certainly has a lot more to gain from knowledge about genomes than, say, sending a space probe to Mars or building a missile defense system. If you were a congressman would you be excited about spending money to research junk DNA? The term “non-coding DNA” is certainly more accurate but isn’t going to generate much more spending enthusiasm than “junk DNA”. Perhaps genome research folks should hook up with some marketing types to develop a vocabulary that is both scientifically accurate and more likely to score grant money.
ReplyDeleteTry as I might, I cannot conclude that ERV provide evidence for either evolution or creationism, at least not from this post. The very workings of a virus indicate that they will persist in favorable (for them) host environments, even when their persistence means the death of the host.
ReplyDeleteYou have to come to the data fairly intent that evolution is a given for this to be evidence of it.
This is not to indicate that twisting this information would support creationism. However, voluminous and detailed information regarding viruses and their persistence throughout natural history does not address holes in the fossil record whose persistence leave evolution a theory.
I admit to being a skeptic of evolution; it never answers the pressing question of why there is life. Endless discussions regarding an incomplete theory regarding the workings and processes of life are ample fodder for what passess for higher education, but do nothing to advance human understanding.
Apparently, your faith is stronger than mine; I at least compel God to prove Himself to me; if He did not, I doubt that I could continue to follow Him. Apparently, you take everything God created as proof that He had nothing to with its creation.
Oh well, I guess I'll drag my knuckles to heaven. I imagine you'll present your papers and degress to . . . exactly where do you appear after you go the way of all the earth?
Hello Anon
ReplyDeleteI was going to address your first few points properly, but then you launched a personal attack so I'm not going to bother wasting my time looking up references for you. I'll just say this: evolution has never claimed to explain WHY life is here. I don't think there is a why. Does the Bible ever explain God's motives, or does it just describe how he did it?
And thanks for your dig about my papers. When I die, I'll go into the ground. But my papers will still be there, part of the permanent record of human scientific inquiry. I'm more than happy with that arrangement.
I have found this blog very, very interesting and uniquely engaging. Thank you. I am not a scientist, though I did take biology and physical anthroplogy in college (A in both :). I hope to be able to add a slightly different perspectiive to this conversation.
ReplyDeleteI'm a literature major with an emphasis in classical British and American literature and minors in humanities and liberal arts. I've taught high school for 15 years. These areas of study have opened up various doors leading to studies in philosophy and the general teleology of man in various cultures. Most of the classical writers I have studied were believers in God on some level, and many had a working knowledge of the scientific studies of their day. These were people who dealt in more than just science, but in logic, philosophy, psychology, and certainly theology, all of which are to me valid areas of study.
In today's science maelstrom, it seesm that most scientists have utterly dismissed these other avenues of thought in favor of a much narrower channel of thought ie, that ONLY science as seen through a microscope can serve as any foundation of explanation for life/existance. I fear the short-sightedness of this approach to explanating life.
So now to my concern about the ERV issue at hand. I do not doubt that as scientists peer through their microscopes that they can correctly determine where an erv sits on a genome. That is actually the lowest level of thought -- definition/description. (I'm sorry if that sounds insulting; it isn't meant to be -- it's just an allustion to Bloom's Taxomony, which puts "knowledge" of this sort at the lowest level of the pyramid. The pyramid is set in this way, which knowledge being the lowest or first: knowledge, comprehension, application, analysis, synthesis and finally evaluation being the highest order of thinking.
It seems that no one can question what "knowlege" you have of the erv placement and mechanism of placement (it inserts itself there and the genome allows it to do so). After that, though it seems science is at a loss at this stage. I believe I'm correct in stating that scientists cannot fully "comprehend" what the erv function is in every case, though they may in some. (This is where hte "junk dna" comes in I believe).
Moving on to "application" -- they cannot with any assurance apply the erv to evolution (show it's application to it) or even manage it once it's there. (Hope this makes sense, sorry if it doesn't).
Scientists immediately appear to be jumping to the "analysis" stage where they claim to have rightly analyzed an aspect about this, but I don't see how that is so when the information isn't clearly orgnaized or easily shown to those of us who aren't in the labs. (I would think that if this really is evolution's "smoking gun" that they would have charts and pamphlets galore out there ready to educate those like myself (whom many in the science coats consider too stupid to even join the conversation -- never mind how insulting this is -- I'll let that go for now.)
Moving on to "synthesis" -- I'm sure there are scientists who are attempting this vital process on some level, but I think to date they realize that they are stumped on this one.
And finally, there's "evaluation", which I firmly believe that though they think they are qualified to make such lofty statements as "ervs PROVE evolution", I am left befuddles at how they can say this when they clearly haven't even met the criteria for reaching this level of thought about the ervs because they haven't met the criteria really past the "knowledge" level.
Everything I've read about ervs to day keeps the focus on these aspects of the erv: 1. the germline insertion points 2.the insertion site itself 3. the duplication of this erv and insertion site in next generations 4. the idea that erv insertion sites are random and therefore could not in all probability insert themselves in the same position on the genome
Is that about right?
Ok, if that is correct so far, then answer this for me please.
If evolutionists are perfectly fine with asserting that the improbability of "nature" evolving itself in the way that it did over millions of years is perfectly acceptable, despite the randomness and chance of that possibility, then why are they not willing to concede that the seemingly low probability of the erv inserting itself in the same sequence on different genomes in completely separate species (with no common ancestor) is just as much a possibility?
Again, I really appreciate this blog and your responses throughout. I'm sorry that some on both sides think that calling others "stupid" or "hell-bound" is occuring at all. It realy distracts from the overall point of it all for all of us who want to discuss it, which is the search for truth.
Peace.
How do we know which ERVs are the youngest?
ReplyDeleteThis will be the last comment on this post.
ReplyDeleteThe original post was written almost a year ago, and yet it still takes up more of my time than all my other posts put together. People keep inserting links to this page on internet discussion boards etc, and while I'm flattered that they'd think of me, it's something I have no control over and it makes a huge amount of work for me. I just don't have the time to keep on answering questions from comments that run to several pages, or even from short comments such as the one immediately above, the answer to which would require me to make some diagrams and write a whole new post. Quite frankly, as someone who is just starting out on a freelance writing career, if I'm going to put that amount of work into it, I may as well write an article or even a book and make some money!
So thank you all for your comments and for this conversation. Comments are now disabled on this post.