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| Mike Gene - Error Correction Runs Deep | Pages: 1 - 2 - 3 - 4 - 5 |
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quote: That will probably take years. Decoding what I call "God's software" will be very difficult indeed. However even that might not give us the complete picture. We need to somehow understand how all the interactions of life work. That seems to me to involve more than just breaking the code. I think this is what IBM is attempting to do with their reverse engineering project: "The list of genes and proteins of an organism, however, constitute only the ground zero in a pyramid of biological complexity, whose top is life itself. This pyramid is a metaphor for the hierarchy of structures out of which biological function (such as metabolism or replication) arises. Elements at each level in this hierarchy interact with each other to produce a higher level of organization, thus climbing up one step in the pyramid of bio-complexity. It follows that the information of all the genome and all the proteome (which is roughly where we stand now) is insufficient to understand the subtleties of biological function. In order to get a handle to function we need to understand how the building blocks at a given level of organization interact with each other: how proteins interact with both genes and proteins to produce molecular circuits; how these circuits interact with each other to allow for cellular function; how cells interact to produce tissues; how tissues form organs; and finally how organs work together to create a living being." http://www.research.ibm.com/FunGen/ Posted by nobody (Member # 145) on 12. November 2002, 02:01:
I have read somewhere that the error correction of DNA is superior to human programming. I'm sorry, but I can't locate the link right now. A question for Mike: How many generations of life, for even a "simple" life form, do you think would be possible without error correction? Posted
by Mike Gene (Member # 149) on 12. November 2002, 08:52: How many generations of life, for even a "simple" life form, do you think would be possible without error correction? Who knows? No one has ever done such a simple experiment because there are no such "simple" life forms to experiment with. The fact that many layers of error correction are biological universals raises the possibility that life, without error correction, either cannot exist or cannot exist very long. But I think error correction goes deeper than this. Posted by Art (Member # 179) on 12. November 2002, 21:46: About MDT and error correction/the cytosine "problem": Off the top of my head, I think that the ideas regarding these subjects do not apply to the RNA World. This would seem to me to be a fertile subject for exploration vis-a-vis MDT, and a likely place where SDT would be less tenable a model than MDT. For example, the "need" of error correction, the multitude of ways that "errors" are avoided, the limited applicability of the parity code concept to mutifunctional RNAs (along with the myriad ways by which the parity is broken) all point to a pretty different mode of design, an entirely different "personality". Posted by nobody (Member # 145) on 13. November 2002,
03:34: quote: What RNA World? I thought that was considered scientifically to be a dead horse. There is no evidence of it, only speculation AFAIK. Mike Gene might be able to help you out. Posted by Art (Member # 179) on 13. November 2002, 08:32: You said: Far from being a "dead horse", the RNA World is alive and well, in many, many more ways than, say, any manifestation of ID theory. As for Mike Gene helping me out, it is precisely his logic that allows us, in this thread, to accept the RNA World as a fact, as more certain than the much fuzzier notions of ID that are bandied around on Brainstorms. Recall that Mike's approach is to equate the usefulness of a concept in guiding productive research with evidence for the veracity of the concept. By this standard, the RNA World is light-years ahead of ID - so much so that, if ID is to be taken as a reasonable hypothesis, the RNA World must be fact. ID theory has given us some interesting but entirely unconfirmed speculation, and not much of anything else (at least by way of wet-bench, nitty-gritty scientific understanding). The RNA World idea has given us the catalytic center of peptidyl transferase, a whole slew of different catalytic RNAs, another whole slew of RNA aptamers that are being developed for research and medical uses, the "micro-RNA World", the catalytic center for pre-mRNA splicing, and the life cycle of viroids, just to name a few examples off the top of my head. Any one of these would constitute an advance that is far greater than anything ID theory has given us; the total package (which is not completely listed in this post) absolutely dwarfs ID. There is simply no comparison. Therefore, if Mike's approach is to be accepted - and, since this is his thread, I would suggest that we not even bother questioning the approach - then we should be willing to follow the application of this logic in other areas to its rightful conclusions, such as this one. IOW, we really should be accepting the RNA World as a pretty solid fact (moreso than origin-of-life researchers, who almost to a person have no problems with the concept, do). But all of this is but a sidetrack to the theme of the thread, and to Mike's latest remarks. I think I am highly justified to raise the issues I raise, and think that your remarks, nobody, are rather out of place and uncalled for. I'd like to see Mike analyze all of the interactions that are seen in RNAs using the parity code concept, and to speculate on the myriad of base modifications and editing events that contribute to RNA functionality. I think MDT is a much better framework for explaining the contrast between RNA and DNA than SDT, but I'd be willing to read alternative POVs. Posted by nobody (Member # 145) on 13. November 2002, 13:08: quote: Far from being a "dead horse", the RNA World is alive and well, -------------------------------------------------------------------------------- I see. So how many RNA World forms of life have been analyzed to reach your conclusion? I am not aware of any, but I am willing to be educated if I missed something. I think having a sample of at least one RNA World life would be a minimal requirement to call anything alive and well. As I said earlier, Mike can help you out on this topic much more than I can. He's spent years on things like this. However, your RNA claims appear to be hijacking the thread away from Mike's original post so we should not continue our discussion here. You can always choose to begin a thread of your own to explain your current support for the RNA World hypothesis. This thread is about error correction. Posted by Mike Gene (Member # 149) on 24. November 2002, 10:11: Art writes: Therefore, if Mike's approach is to be accepted - and, since this is his thread, I would suggest that we not even bother questioning the approach - then we should be willing to follow the application of this logic in other areas to its rightful conclusions, such as this one. IOW, we really should be accepting the RNA World as a pretty solid fact (moreso than origin-of-life researchers, who almost to a person have no problems with the concept, do). I don't think my approach can deliver "facts," let alone "solid facts," whether we're talking about ID, FLE, or the RNA World. It's merely a heuristic approach that delivers research guidance with the potential to render any scenario intellectually plausible. That is, one might have reason to think a particular scenario intersects with the truth (as this would nicely explain the success of an approach), but I don't think this can be established in any factual sense. Now, yes, I think the RNA World is plausible and is supported by the success of the metaphor and some circumstantial evidence. I don't think it is a "dead horse." But ironically, RNA World proponents are in the same boat as teleologists, in that it's not clear that the success of their metaphor translates as valid historical insight, as there are complicating factors. The success of the metaphor needs to be balanced with the history of science. Nucleic acids have always been underestimated. Since biochemistry matured by studying proteins and protein enzymes, and biochemists were intrigued by their abilities, it was only natural proteins would be on the pedestal. The first ones to get to the party can often define the mood of the party. Do not forget the biologists originally thought that proteins were the genetic material. They knew the nucleus contained proteins and DNA, but they originally thought the DNA played some type of inert structural role and assigned proteins another "glory role." Yet when it was determined in the 40s and 50s that DNA was indeed the genetic material, this did not lead to a "DNA World," where each advance, to this day, in understanding the importance and activity associated with DNA was seen as reflecting it as the first biological molecule to enter the stage of history. As for the comparison between the success of ID and the RNA World, there are two more factors to consider. First, I think it more appropriate to compare the RNA World as metaphor with the Design as metaphor. And it sure seems to me that teleological metaphors have delivered just as much, even more, than the RNA metaphor. Secondly, the concept of "ID" comes with immense historical and sociological baggage. While a good idea may be a necessary ingredient for a fruitful research program, it is not sufficient. It has been pointed out by many that science proceeds as a communal activity. And then 9/10 scientists think the concept of ID is inherently religious, one can see a very real sociological obstacle that the RNA World never really had to face. Sociological factors (and other considerations) simply cannot be excluded if such a comparison is to be made. Keep in mind that I have no a priori reason to reject the RNA World, as an RNA World is clearly front-loaded to become like modern organisms. I'd like to see Mike analyze all of the interactions that are seen in RNAs using the parity code concept, and to speculate on the myriad of base modifications and editing events that contribute to RNA functionality. I'll put it on my incredibly large "to do" list. I think MDT is a much better framework for explaining the contrast between RNA and DNA than SDT, but I'd be willing to read alternative POVs. On the contrary, I think you underscore the inherent handicap of the MDT approach. While it would view the contrasts between DNA and RNA as a launching pad to begin reverse engineering the psychology of the designers, an SDT approach would stay ground in biotic reality and reverse engineer it , looking for the design logic that weaves the contrast into a coherent whole. Science is often about finding patterns and relationships between things that appear unconnected, or even that appear to be in tension with each other. Thus, while an MDT approach would entail an RNA designer and a DNA designer, an SDT approach would allow us to understand the logic of using both RNA and DNA. I would think the SDT framework is much better. Keep in mind that I invited MDT "proponents" to this thread to apply their model to the choice of cytosine as a nitrogenous base. And while I have found the SDT approach to be fruitful (as shown in my latest web page essay), the MDT "proponents" still offer only promissory notes. There is no evidence to think the MDT approach is a better framework. Keep in mind also that I have no inherent bias against the MDT approach. Instead, I have merely highlighted some of its problems which render it useless for my interests. For example, I am more the willing to entertain the proposition that the designers are some form of ETI, and this speculation is heuristically productive. But when I asked MDT "proponents" about when we use humans as "single-designers" vs. "multiple-designers," they had no answer. If they cannot make this distinction when it comes to well-known designers, it seems the whole approach crumbles if the designers are some form of ETI. Posted by Art (Member # 179) on 24. November 2002, 16:05: quote: Since I’ll be out-of-pocket wrt this discussion for awhile, I’ll expand on my introductory remarks and then see if the MD Theorists are of a mind to explore the idea. Briefly, Mike, my take on your ideas vis-a-vis cytosine is that you rationalize the seemingly untoward “choice” of cytosine in terms of the novel expectations that C->U demethylation events (in DNA) would lead to. Such expectations have no analogies in the RNA World (pre-biotic or extant - remember that the RNA World is very much a part of all living things). It follows that, when it comes to speculation as to the significance of the use of cytosine in living things, we have two basic positions: cytosine was “chosen” for two different reasons, or your ideas about cytosine in DNA are wrong, and there is in fact a single “reason”. Granting the veracity of your ideas, then two functions is the pretty obvious conclusion. I think that MDT proponents can easily make a case, given this multiplicity of proposed functions. Posted by Mike Gene (Member # 149) on 24. November 2002, 23:27: My hypothesis deals with deamination, not demethylation events. And in this case, there is something better than an analogy in the "RNA World," namely, an example. In mammals, apolipoprotein B (apoB) is involved in transporting lipids in the aqueous plasma. Given its relationship to atherosclerosis, it has received immense attention from the research community. It has been determined that apoB exists in two forms - a full length apoB100 form, which synthesized in the liver and used in the plasma, and a truncated apoB48 version, which is synthesized in the small intestines and used to form chylomicrons (structures that transport dietary lipids). The two forms exist because of RNA editing , where small intestinal cells express an editosome, including a cytidine deaminase (apobec-1) that modifies the RNA, where a specific CAA codon is converted into a premature UAA stop codon. This may only be the tip of the iceberg. A related deaminase, apobec-2, was recently found to be expressed only in cardiac and skeletal muscle. I have a couple of other interesting examples I'll try to discuss tomorrow. Posted by Art (Member # 179) on 25. November 2002, 00:05: quote: Oops - my bad. Thinking deamination, typing demethylation. Oh well.
In mammals, apolipoprotein B (apoB) is involved in transporting lipids
in the aqueous plasma. Given its relationship to atherosclerosis, it
has received immense attention from the research community. It has
been determined that apoB exists in two forms - a full length apoB100
form, which synthesized in the liver and used in the plasma, and a
truncated apoB48 version, which is synthesized in the small intestines
and used to form chylomicrons (structures that transport dietary lipids).
The two forms exist because of RNA editing , where small intestinal
cells express an editosome, including a cytidine deaminase (apobec-1)
that modifies the RNA, where a specific CAA codon is converted into
a premature UAA stop codon. This may only be the tip of the iceberg.
A related deaminase, apobec-2, was recently found to be expressed only
in cardiac and skeletal muscle. I have a couple of other interesting
examples I'll try to discuss tomorrow. First and foremost, this example (and others like it) are not really pertinent to the RNA World. What I am speaking about is the applicability of the idea that cytosine is special to RNA functionality. For your proposal to have such an analogy, Mike, you would have to be shown that spontaneous cytosine deamination (got it right this time ) has an evolutionary "effect" on RNA structure and function analogous to the one you propose for cytosine deamination in DNA. I am very skeptical of this, because the same "rules" that apply to the matter in DNA simply have no analogy in RNA. Second, the specific case you mention, Mike, does not seem to be relevant to error correction, or to the proposal you make on your web page. Third, off the
top of my head, I think that RNA editing kind of eliminates the "need" for cytosine in a design sense. This is because
C->U editing is not the only sort of editing that occurs, and any
of the alternatives that are known could do the same job as C->U
editing in terms of mRNA coding. Which makes the special property of
cytosine - a propensity to deamination - irrelevant, and reduces cytosine
to a "position" no more favored than any other base. IOW,
more of a "frozen accident" than a conscious choice. (Or,
maybe, a rather nondescript product of the work of an RNA designer
that was modified for a more clever purpose by a DNA designer .)
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