Uncommon Descent Serving The Intelligent Design Community

The Sound of Circular Reasoning Exploding

Share
Facebook
Twitter
LinkedIn
Flipboard
Print
Email

Alternate Title: Of Mice and Men and Evolutionary Dogma

Explosion
“There has been a circular argument that if it’s conserved it has activity.” Edward Rubin, PhD, Senior Scientist, Genomics Division Director, Lawrence Berkeley National Laboratory

Recent experiments cause a central tenet of NDE to miss the prediction. Large swaths of junk DNA (non-coding, no known function) were found to be highly conserved between mice and men. A central tenet of NDE is that unexpressed (unused) genomic information is subject to relatively rapid corruption from chance mutations. If it’s unused it won’t do any harm if it mutates into oblivion. If it’s unused long enough it gets peppered with mutations into random oblivion. If mice and men had a common ancestor many millions of years ago and they still have highly conserved DNA in common, the story follows that all the conserved DNA must have an important survival value.

A good experiment to figure out what unknown purpose the non-coding conserved pieces are doing would be to cut them out of the mouse genome and see what kind of damage it does to the mouse. So it was done. Big pieces of junk DNA with a thousand highly conserved regions common between mice and men was chopped out of the mouse. In amazement the mouse was as healthy as a horse (so to speak). The amazed researchers were in such a state because they were confident NDE predicted some kind of survival critical function and none was found.

This is a good avenue for positive ID research. If the function of any of those regions were preserved because they could be of important use in the future… well that would pretty much blow a hole in the good ship NDE the size of the one that sunk the Titanic. Maybe not that big, but it would be taking on water – natural selection can’t plan for the future. Planning for the future with genomic information is the central tenet of ID front loading hypothesis. Lack of any known means of conserving non-critical genetic information is the major objection lobbed at the front loading hypothesis. Evidently there is a means after all.

Life goes on without ‘vital’ DNA

16:30 03 June 2004
Exclusive from New Scientist Print Edition.
Sylvia Pagán Westphal, Boston

To find out the function of some of these highly conserved non-protein-coding regions in mammals, Edward Rubin’s team at the Lawrence Berkeley National Laboratory in California deleted two huge regions of junk DNA from mice containing nearly 1000 highly conserved sequences shared between human and mice.

One of the chunks was 1.6 million DNA bases long, the other one was over 800,000 bases long. The researchers expected the mice to exhibit various problems as a result of the deletions.

Yet the mice were virtually indistinguishable from normal mice in every characteristic they measured, including growth, metabolic functions, lifespan and overall development. “We were quite amazed,” says Rubin, who presented the findings at a recent meeting of the Cold Spring Harbor Laboratory in New York.

He thinks it is pretty clear that these sequences have no major role in growth and development. “There has been a circular argument that if it’s conserved it has activity.”

Use the link above for the full article.

Comments
Fifth, mice breed like rabbits. They made 250 of the things before they published these things. However, Mesk over on TT suggests that the real test would be a more natural environment than a lab. I would suggest taking knock-out mice, and non-knock out mice of similar breeding, and put them in an old barn with a cat and an owl. Lets see if after a year or two the non-knock out dominate over the knock-out. That would be an interesting study that even I could do -- given grant money, of course. Hmmm, I think I know where I can get the barn.bFast
December 9, 2006
December
12
Dec
9
09
2006
01:52 PM
1
01
52
PM
PDT
fifth Bacteria don't have junk dna so this really doesn't apply to them. Fruit flys don't have these CNGs in common with vertebrates. Fish and birds have a number of them in common with mammals. You've got the right idea though. Insects probably have CNGs like these in common with arthropods and those would be two good candidates for comparison with much faster life cycles than vertebrates. That said, there's probably more of practical interest to be found in figuring out what these CNGs are doing in mammals as it could lead to finding cures for disease and genetic disorders in humans.DaveScot
December 9, 2006
December
12
Dec
9
09
2006
01:36 PM
1
01
36
PM
PDT
"He suggests that if a mutation has a deleterious effect as small as 0.0001%, it will not fix in the population." Fine we experiment with bacteria or fruit flies instead of mice and this can still be settled quickly. In the mean time I would expect to see special reports on Fox News and in The New York Times. This is a big deal.fifthmonarchyman
December 9, 2006
December
12
Dec
9
09
2006
12:54 PM
12
12
54
PM
PDT
fifthmonarchyman The plain consensus is that any conserved DNA sequence between organisms that diverged in the distant past must have an "important" function. Greater or lesser conservation of conserved sequences in the same two species implies either greater or lesser tolerance to mutation while still maintaining function or greater or lesser importance or both. Ultra conserved DNA implies both importance and intolerance to change. The sequences in question here are highly conserved but not ultra-conserved if by ultra-conserved we mean greater than 95% similarity in sequence. These are not coding genes so we don't know if synonymous substitutions are possible or not. It would appear not as the sequences exhibit far more absolute similarity than do coding genes between mice and men. If just a few highly conserved regions were knocked out and nothing happened to the mouse it wouldn't be a big deal but in this case a thousand highly conserved regions where knocked out and nothing happened. If there isn't important function associated with these regions then there's a mechanism other than natural selection at work conserving DNA sequences. The jury is still out on what naturally selectable advantage all these conserved bits have but it's looking rather grim right now for finding anything important.DaveScot
December 9, 2006
December
12
Dec
9
09
2006
11:29 AM
11
11
29
AM
PDT
bfast "Immediate" in an evolutionary sense can be a number of generations. The difference between a day and a thousand years is next to nothing on an evolutionary timescale. Thus the difference between a mutation that causes spontaneous abortion and one that causes a genetic disorder that impairs but doesn't kill the organism will both be "weeded out" in an eyeblink of evolutionary time.DaveScot
December 9, 2006
December
12
Dec
9
09
2006
11:10 AM
11
11
10
AM
PDT
m7 "1) Are regulatory functions uniform in mice and men?" To a large extent but less so than coding genes. "2) Are large areas of non-coded regions part of any search space besides the copying process which is essential to reproductive inheritance?" IIUC the answer is yes. "3) Besides number of base pairs deleted without function in the mice. Is it not also another problem for possible search space issues by regulatory functions? Or is the search simply halted or abreviated by a specific type of “stop codon” in a particular location?" If something is badly broken in a gene or its regulatory region such that it is either no longer expressed or kills the organism when it does express then searching, if I understand what you are saying, necessarily halts as part of the "search" is testing new formulations or expression patterns. "4) What is the economic cost of efficiency considered for keeping and copying such large spaces of non-coded regions if they serve no purpose?" The cost is size of the cell and speed of reproduction. For organisms that rely on great numbers of progeny produced in a small amount of time (prokaryotes) the economic cost of DNA baggage is extreme and they use just about every last bit of sequence and squeeze it down to the smallest possible size. Eukaryotes appear to have a lot more flexibility in that regard. Some simple organisms have much more DNA than we do. Amoeba dubia, a huge single celled organism, has 200 times more DNA than we do. All the plants and animals with huge amounts of DNA all seem to thrive just fine with all that baggage. There's a readily identifiable pattern we know about for genes (the genetic code) which makes them easy to understand. There is no genetic code for non-coding regions we know about so we don't don't have a very good idea yet how they operate. The genetic code is like a Rosetta Stone for coding genes. For prokaryotes that's really all we need. Prokaryotes have virtually no non-coding regions in comparison to eukaryotes. For eukaryotes we need to find more Rosetta Stones to decipher what's going on in non-coding regions. The coding gene is king in the prokaryote world. In our world variation in coding gene expression by non-coding instruction are king.DaveScot
December 9, 2006
December
12
Dec
9
09
2006
10:55 AM
10
10
55
AM
PDT
fifthmonarchyman
If I understand Evo-Devo correctly in order for something to be functional it must provide immediate reproductive advantage. No other function counts.
My discussions with Mesk over at telicthoughts (he's clearly an evolutionist, but he's got some humility in his bones, and a scientist's curiosity) this is not so. He suggests that if a mutation has a deleterious effect as small as 0.0001%, it will not fix in the population. If it doesn't fix in the population, it will weed out. Contrary to what you have stated, he shows that disease producing mutations, for instance, can persist for a significant number of generations, but still find themselves weeded out of the genome.bFast
December 9, 2006
December
12
Dec
9
09
2006
10:39 AM
10
10
39
AM
PDT
Dave, Some simple questions from the peanut gallery. I don't understand how all the regulatory functions work with regards to non-coding regions. Geneticist have discovered some non-coded areas do get expressed, by different mechanisms in the human genome, correct? And some are tied to disease. So... 1) Are regulatory functions uniform in mice and men? 2 Are large areas of non-coded regions part of any search space besides the copying process which is essential to reproductive inheritance? 3) Besides number of base pairs deleted without function in the mice. Is it not also another problem for possible search space issues by regulatory functions? Or is the search simply halted or abreviated by a specific type of "stop codon" in a particular location? 4) What is the economic cost of efficiency considered for keeping and copying such large spaces of non-coded regions if they serve no purpose? I comprehend the copying mechanism for transfer during reproduction matters of inheritance. But it appears regulatory functions are still quite an enigma, or they're growing in scope and complexity. From a programmatic perspective, I can entertain the thought of code compressed and packaged, but left unused until the correct licensing key is utilized to unlock more code. From the viewpoint of someone unfamiliar with this process, they'd see the code and think it is "junky" and inefficient. From a practical perspective as a delivery mechanism from the intelligent coder however, it is not. When a user decides to license a new program, the key they purchase unlocks the existing code delivered earlier in compressed format, which then unfolds and communicates with existing internal and external programs, updates accordingly to the environmental surroundings(PC type, hardware, MS version) and distributes itself. That is strictly a commercial perspective. But, then... to extend this to nature. A DNA "program" is delivered in multiple areas across distant shores. The core has components unfold as different nutrients allow them to proceed. Each unfolds differently based upon the input factors of surrounding environments. So, color, length, height, beak size, etc., are all reactive to the environmental factors as to how the "coded" regions unfold. Whereas the non-coded regions exist as contingencies and to unfold more in the future given new input. But even this does not explain some issues like sexual differences. Like the horned beetle male and female which both need the horn at birth. But the female loses it afterwards. hattip; creationsafaris.com. So, last question that must be asked. Why is this not perceived as "vestigial" DNA?Michaels7
December 9, 2006
December
12
Dec
9
09
2006
09:31 AM
9
09
31
AM
PDT
“the function of ultra-conserved elements is the subject of a raging debate.” Ok, if that is true we need hold and opposition to some clear definitions of what is required for super-conserved DNA to be considered functional. The Darwinist does not have the same freedom that ID does in ascribing function to a section of DNA. If I understand Evo-Devo correctly in order for something to be functional it must provide immediate reproductive advantage. No other function counts. This sort of thing could easily be tested. Simply put the knockout organism in a controlled environment with wild stock and see what happens. The function or lack there of could be determined in one generation. After all natural selection only sees the present generation and can not look to the future. Any “function” not seen in the first generation is by definition “Telic” and we win. This sort of experiment could be done with frogs or fish or any thing else with super-conserved DNA. We could know the results in a matter of months not years. It almost sounds like a high school science project.fifthmonarchyman
December 9, 2006
December
12
Dec
9
09
2006
09:28 AM
9
09
28
AM
PDT
Unlikely but it should be considered. A retrovirus that can jump from mice to men should have little problem jumping to any mammal. One that can jump from birds to men (re avian flu virus) even less problem infecting a wide range of mammals.
From what I've read on the subject retroviruses can have target preferences so I'd consider that an open possibility for explaining the homology present here.Patrick
December 9, 2006
December
12
Dec
9
09
2006
08:35 AM
8
08
35
AM
PDT
"But once we deeply imbibe the fundamental truth that an organism is a tool of DNA, rather than the other way around, the idea of ’selfish DNA’ becomes compelling, even obvious." Its really that easy to drink in... Thus is the bottom up, materialist strategy unleashed in a survival of the fittest DNA mode. As multi-cellular organisms, we serve DNA, ultimately some tube worm I suspect that morphed into FSM. Then it is reasonable we should kneel to the high priest of DNA, like Dawkins and become drunk with his glorifying the spirit of DNA. Now I know where Dawkin's authority comes from. Our bodies, our minds, our souls serve Gaia-FSM, DNA goddess of scientism and the high Priest of Genetics, well, in this case, a Zoologist.Michaels7
December 9, 2006
December
12
Dec
9
09
2006
07:33 AM
7
07
33
AM
PDT
DaveScot #87, I did not at all dismiss the possibility of gene flow. I said that conservation would leave a signature that gene flow would not. If you recall from Denton's discussion of the cytochrome C gene (if not, you really need to read that book) the mutational distance between organisms produces a (near) perfect mapping of the phylogenic tree. (Chimp is close to man, mouse is somewhat different, tree is more different, amoeba is way different.) If we had been attacked by rabid mosquitos, say 3 million years ago, the phylogenic tree would still not show up. Chimp DNA would be as different from man's as the mouse's is. #88, I think that there are two factors in the level of conservation. Certainly the importance of the gene is one of them. However, I think that the "precision" of the gene is actually a greater factor. If one gene is highly important -- an essential atp synthase gene, for instance, and another gene is much less important -- say it allows us to see color -- if the former gene works just as well with a variety of mutations, and the latter gene ceases function no matter what the change, the latter will drift more slowly. fifthmonarchyman, "what am I missing." If Mesk, over on on Telic Thoughts is correct, this issue, and the ultra-conserved gene question "the function of ultra-conserved elements is the subject of a raging debate." We must not let 'em forget this one, but science does have to wiggle and squirm a bit before they are content that they have explored every avenue to save their baby. I think that's fair.bFast
December 9, 2006
December
12
Dec
9
09
2006
07:30 AM
7
07
30
AM
PDT
Yes, I'd like to know what's going on, too.Douglas
December 9, 2006
December
12
Dec
9
09
2006
07:25 AM
7
07
25
AM
PDT
What am I missing? It looks to me like this is the death blow to Neo Darwinism. This is the bacterial flagellum times one thousand. Yet no other Id website that I know of has picked up on it yet and no one on the other side has seriously tried to discredit this. What is going on ?fifthmonarchyman
December 9, 2006
December
12
Dec
9
09
2006
05:05 AM
5
05
05
AM
PDT
ds: "Yes, it does indeed follow when the theory of natural selection is applied to the observations. This is the basis of natural selection. The less critical the sequence is to survival the less selection pressure to preserve it, the more critical the more pressure." Wait. Richard Dawkins now says:
Cows and pea plants (and, indeed, all the rest of us) have an almost identical gene called the histone H4 gene. The DNA text is 306 characters long... Cows and peas differ from each other in only two characters out of these 306. We don't know exactly how long ago the common ancestor of cows and peas lived, but fossil evidence suggests that it was somewhere between 1,000 and 2,000 million years ago... Histone H4 is vitally important for survival. It is used in the structural engineering of chromosomes... The histone gene's conservatism over the aeons is exceptional by genetic standards. Other genes change at a higher rate, presumably because natural selection is more tolerant of variations in them. For instance, genes coding the proteins known as fibrinopeptides change in evolution at a rate that closely approximates the basic mutation rate. This probably means that mistakes in the details of these proteins (they occur during the clotting of blood) don't matter much for the organism. Haemoglobin genes have a rate that is intermediate between histones and fibrinopeptides. Presumably natural selection's tolerance of the errors is intermediate. Haemoglobin is doing an important job in the blood, and its details really matter; but several alternative variants of it seem capable of doing the job equally well. (The Blind Watchmaker (1986), p. 123-125.)
j
December 9, 2006
December
12
Dec
9
09
2006
04:47 AM
4
04
47
AM
PDT
j I'm glad you added the laughing icon. At least one fatal flaw in applying selfish genes to this problem is that the sequences in question aren't genes.DaveScot
December 9, 2006
December
12
Dec
9
09
2006
04:18 AM
4
04
18
AM
PDT
geomor The point of my last comment was that, merely from the observation that sequence X is conserved at higher percent identity than sequence Y, it does not follow that sequence X must have a “more important” function than sequence Y, and vice versa. Yes, it does indeed follow when the theory of natural selection is applied to the observations. This is the basis of natural selection. The less critical the sequence is to survival the less selection pressure to preserve it, the more critical the more pressure. If you don't know that I question whether you should be contributing to this thread.DaveScot
December 9, 2006
December
12
Dec
9
09
2006
04:13 AM
4
04
13
AM
PDT
bfast re horizontal gene flow Unlikely but it should be considered. A retrovirus that can jump from mice to men should have little problem jumping to any mammal. One that can jump from birds to men (re avian flu virus) even less problem infecting a wide range of mammals.DaveScot
December 9, 2006
December
12
Dec
9
09
2006
04:07 AM
4
04
07
AM
PDT
Richard Dawkins has the resolution of our dilemma. This DNA doesn't need to have anything to do with function in the real world, just so long as it's selfish!:
While awaiting evidence for and against [other hypotheses], the thing to notice in the present context is that they are hypotheses made in the traditional mold; they are based on the idea that DNA, like any other aspect of an organism, is selected because it does the organism some good. The selfish DNA hypothesis is based on an inversion of this assumption: phenotypic characters are there because they help DNA to replicate itself, and if DNA can find quicker and easier ways to replicate itself, perhaps bypassing conventional phenotypic expression, it will be selected to do so. Even if the editor of Nature (Vol. 285, p. 604, 1980) goes a bit far in describing it as 'mildly shocking', the theory of selfish DNA is in a way revolutionary. But once we deeply imbibe the fundamental truth that an organism is a tool of DNA, rather than the other way around, the idea of 'selfish DNA' becomes compelling, even obvious. (The Extended Phenotype (1982), p. 158.)
:lol:j
December 9, 2006
December
12
Dec
9
09
2006
04:03 AM
4
04
03
AM
PDT
DaveScot, What you wrote about synonymous substitutions sounds right to me. I'm not sure exactly what message we were to take from it. The point of my last comment was that, merely from the observation that sequence X is conserved at higher percent identity than sequence Y, it does not follow that sequence X must have a "more important" function than sequence Y, and vice versa. Jehu, | With a mutation rate of 2.22 x 10^-9 per year per base pair, the chances of having sequences of 100 bp with 70 identy by chance is not likely, especially after 70 - 90 million years. By those exact numbers, you'd expect most of the genome to be greater than 70% identity between mouse and the human-mouse ancestor. Just multiply 2.22e-9 subs/site/yr by 90Myr = 0.2 subs/site or 80% identity. Between human and mouse (140-180Myr of divergence), you'd expect tens of thousands of 100-bp sequences to have 70% or better identity in a 3e9-bp genome. That one is a little more complicated to work out. Anyway, I'm not trying to argue that there were not many "truly" conserved sequences in the deleted regions -- this discussion was a sidetrack about why we need to keep sequencing genomes in order to distinguish the conserved sequence with greater precision, so that we know what we're going after. Again, NDE's prediction here remains that the conserved deleted sequences are functional and have conferred a selective advantage. The Nobrega paper is certainly some evidence against this prediction, and that's fair to point out for the time being. To investigate the question further, we'll need a better general understanding of the biological mechanisms that involve conserved non-coding sequences, which is more or less what most genome scientists are working on these days. We might succeed or we might fail.GeoMor
December 9, 2006
December
12
Dec
9
09
2006
12:19 AM
12
12
19
AM
PDT
#72, Dave, When I initially posted here. I was compared to a "Crackpot" for thinking there were libraries in the Genome. But then, I was taking it one step farther, seeing it as active, functional libraries are carried along with each species as it interacts with the environment. And mostly what we see is now deleterious. What we started with was fully functional unfolding plan. What we see today is a hodge-podge of plans and mutations eating away at the original blueprint. We see this most pronounced thru the embryo development of Crack babies who have to forever be put on some form of amphetamine to keep them calm and focused. It is an immediate impact of "evolution" if ToE's want to call it such. Reading Spetner's notes re: repositories in Not by Chance, and now this is encouraging to say the least.Michaels7
December 8, 2006
December
12
Dec
8
08
2006
11:02 PM
11
11
02
PM
PDT
But as I suspect you know it doesn’t quite work out that way because different proteins acquire synonymous substitutions at different rates in the same species. There’s a whole cottage industry sprung up trying to calibrate molecular clocks so they agree with one another.
Would that be the special pleading industry?Jehu
December 8, 2006
December
12
Dec
8
08
2006
03:33 PM
3
03
33
PM
PDT
Jehu:
I expect they will argue that some sequences are not subject to random genetic drfit like the other sequences.
And if they can come up with a GOOD explanation, fine enough. I've rolled a dice often enought to suggest that they have their work cut out for them. However, they have had two years. They need to get to work to save their baby!!bFast
December 8, 2006
December
12
Dec
8
08
2006
03:21 PM
3
03
21
PM
PDT
geomor Your spin isn't working. A thousand sites ranging from average to very highly conserved had the plug pulled and nothing happened. Deal with it. Me, you, Rubin and most of those on this thread understand synomous substitutions in coding genes and what that means for comparative purposes. You underestimate the difference in coding genes because of them. There are 64 possible codes for 20 amino acids. Take an example of a protein with two monomers monomer A - can be either code 1, 2, or 3 through degeneracy monomer B - can be either code 4, 5, or 6 through degeneracy Only 2 unique polymers can be generated; AB and BA. Yet there are 9 unique codes that can generate each polymer. If you compared them through sequence data alone you will get 0% match in 9 yet they generate exactly the same protein. Taking into account synonymous mutations in comparing protein coding sequences is a necessity otherwise they'd be all over the map and wouldn't make any sense at all. However, synomous substitutions in coding genes should (in theory) be quite accurate molecular clocks for divergence when the same protein is compared between species. But as I suspect you know it doesn't quite work out that way because different proteins acquire synonymous substitutions at different rates in the same species. There's a whole cottage industry sprung up trying to calibrate molecular clocks so they agree with one another. *Edited to correct typo in second monomer list. DaveScot
December 8, 2006
December
12
Dec
8
08
2006
02:54 PM
2
02
54
PM
PDT
I am waiting for the special pleading from the Darwinists to start. I expect they will argue that some sequences are not subject to random genetic drfit like the other sequences.Jehu
December 8, 2006
December
12
Dec
8
08
2006
02:32 PM
2
02
32
PM
PDT
Finally, to the problem of distinguishing conserved sequences. You can construct a mathematical model of sequence evolution and work out how many sequences of length N you expect to be preserved just by chance in a 3-billion base genome. With sophisticated models and only two mammalian genomes, the number is quite large even for N on the order of 100. There is a great figure on this in the original mouse genome paper, which is the basis for the oft-repeated claim that about 5% of the human genome is under selection. It’s not that there is only 5% of the sequence shared: it’s much higher than that. 5% is the excess amount of conservation above what you would expect by chance. We need more mammalian genomes to continue intersecting (a crude terminological approximation there) to distinguish what is really under selection.
Basically you are saying the identity might be a conincedence and the genes are not actually conserved. Well I respect the fact that at least you are taking a shot at it. However, my literature search hasn't shown anything where it is suggested that sequences of a minimum of 100 bp and 70% identity might be the result of homoplasy instead of homology. At this point I don't find your position credible. With a mutation rate of 2.22 x 10^-9 per year per base pair, the chances of having sequences of 100 bp with 70 identy by chance is not likely, especially after 70 - 90 million years. It gets even worse when the gene has > 90% identity, and is > 400 bp long and is conserved in chicken, frog, mouse, and human as some of the sequences were in the Nature article. I have to conclude that this is strong evidence that highly conserved sequences have not function. And apparently, as discussed above, even ultraconserved sequences can have no function.Jehu
December 8, 2006
December
12
Dec
8
08
2006
02:26 PM
2
02
26
PM
PDT
The conceptual principle that "more important function means better conserved" is basically right. However, it is not necessarily the case that "importance of function" correlates with conservation as measured by sequence percent identity (or similar metrics based solely on the sequence), which is how the conserved elements have been defined. For example, many transcription factors bind DNA through physical contact at several locations spatially separated by perhaps 3-12 bases. This means that the DNA is constrained to be a certain sequence at several "footprints", interleaved with stretches where there may be only very weak constraints. Even on the footprints, DNA-binding proteins can be more or less picky about what the sequence there has to be; they may need certain bases to be only A or C, for example, and the binding efficiency is pretty equivalent. These are just a few examples of a general principle, which indicate tht strength of selection need not correlate with sequence identity. To pick up the TF example, a modestly important factor may only bind a very specific sequence, which will therefore be preserved at high identity, while a crucial factor may bind a rather degenerate sequence, which is therefore free to vary somewhat. In this case, "percent identity" is dictated both by strength of selection on the factor's activity and the biophysics of the factor itself, and you can't gauge the former without specifically accounting for the latter. TFs are just one example here of a very general principle; two protein-coding genes, for example, need only be about 70% identical at the DNA sequence level to code for exactly the same protein, because of degeneracy in the genetic code. We can write some programs that sort of distinguish what is conserved and what is not, but without specific mechanistic knowledge of what processes use the sequences, we cannot correlate sequence identity with importance of function. Thus, NDE's prediction is only that there is a function for the conserved sequences that confers "sufficient" selective advantage, without any claim about how advantageous it is. Finally, to the problem of distinguishing conserved sequences. You can construct a mathematical model of sequence evolution and work out how many sequences of length N you expect to be preserved just by chance in a 3-billion base genome. With sophisticated models and only two mammalian genomes, the number is quite large even for N on the order of 100. There is a great figure on this in the original mouse genome paper, which is the basis for the oft-repeated claim that about 5% of the human genome is under selection. It's not that there is only 5% of the sequence shared: it's much higher than that. 5% is the excess amount of conservation above what you would expect by chance. We need more mammalian genomes to continue intersecting (a crude terminological approximation there) to distinguish what is really under selection. This is all very much more complicated than I've explained it, but I hope it is interesting.GeoMor
December 8, 2006
December
12
Dec
8
08
2006
02:01 PM
2
02
01
PM
PDT
bFast,
There is no way on God’s green earth that the RM+NS model can support “ultraconserved” for a over half a billion years when there is no function (fish/amphibian common ancestor * 2). This data seems to be clearly understood within the halls of science. Why are they not admitting that the theory so badly does not fit the data! This is a conspiracy that makes the galileo thing look pretty insignificant.
I agree this data contradicts the NDE paradigm and I don't see how "evo-devo" can account for it either. IMO the data is shocking. I think the only available answer to Darwinists is to disbelieve the results, not unlike the situation with the discovery of soft tissue in a dinosaur bone. I found a discussion outline sheet for a Ph.D. course in genomics as Stanford. It seems to question whether the gene knockouts were really achieved but makes no mention of the conservation of nonfunctioning genes. I wonder if it came up in the class? I would have liked to have heard that discussion. http://www.stanford.edu/class/bio203/NobregaPollard.pdfJehu
December 8, 2006
December
12
Dec
8
08
2006
01:42 PM
1
01
42
PM
PDT
Jehu:
Those two studies tested in vivo a total of 36 ultraconserved non-coding sequences and did not find function in 9 of them, or 25% of the ultraconserved sequences.
Wow! I don't care how many untra-conserved sequences has function, if any of the untraconserved sequences do not have function RM+NS is DOOMED!! There is no way on God's green earth that the RM+NS model can support "ultraconserved" for a over half a billion years when there is no function (fish/amphibian common ancestor * 2). This data seems to be clearly understood within the halls of science. Why are they not admitting that the theory so badly does not fit the data! This is a conspiracy that makes the galileo thing look pretty insignificant.bFast
December 8, 2006
December
12
Dec
8
08
2006
01:19 PM
1
01
19
PM
PDT
bFast: “What I really want to see is a mouse where one of the “untra-conserved” non-coding segments is knocked out. If you can knock out the ultra-conserved stuff too, it’ll just be more nails in the ‘ol coffin.” The authors address your question in that paper: “The small fraction of elements conserved across several vertebrates but not fish with enhancer activity in this study (1 of 15) contrasts with the results obtained when human–fish conserved non-coding sequences were previously tested with the same in vivo assay. In those studies a significant fraction of human–fish conserved non-coding sequences present in gene deserts were shown to be functional, with 5 of 7 elements in one study and 22 of 29 in a second study.”ofro
December 8, 2006
December
12
Dec
8
08
2006
01:04 PM
1
01
04
PM
PDT
1 2 3 4 5

Leave a Reply