Future Risk Assessment in the Genome
| November 9, 2007 | Posted by Dave S. under Intelligent Design |
I found the following research quite intriguing. It has far reaching implications of interest to IDists. One implication requires a front-loading IDist to appreciate. Basically what the researchers found is that there are risk assessments in the promoter regions of genes. If a gene is critical and random mutations to it would be bad news it is marked as high risk and isn’t subject to mutation. If it’s not so critical it is marked low risk and exposed to experimentation.
How does this apply to front-loading? A major problem for front-loading is no known mechanism for conservation of genomic information other than natural selection. Information stored for a distant future that isn’t used in the present is ostensibly destroyed by deep time and random mutation. Other research we’ve blogged here showed compelling evidence that a mechanism for conserving unexpressed information exists. This is even more compelling – tags saying “conserve this”. Now all we need to find is the enhanced error detection and correction mechanism that is employed to conserve information tagged for conservation and there’s our mechanism for presevation of front-loaded genomic information over deep time.
Evolution: When Are Genes ‘Adventurous’ And When Are They Conservative?
ScienceDaily (Nov. 8, 2007) — Taking a chance on an experiment – this is one of the impulses that drive evolution. Living cells are, from this angle, great subjects for experimentation: Changes in one molecule can have all sorts of interesting consequences for many other molecules in the cell. Such experiments on genes and proteins have led the cell, and indeed all life, on a long and fascinating evolutionary journey.
Prof. Naama Barkai of the Weizmann Institute’s Molecular Genetics Department recently took a look at gene expression – the process in which the encoded instructions are translated into proteins – and the evolution of mechanisms in the cell for controlling that expression. Changes in genes, and thus in protein structure, are a double-edged sword: They can give cells new abilities or advantages for survival, but they can also spell disease or death for the organism. Not all genes evolve at the same rate. Indeed, some have been conserved through long stretches of evolution: Similar versions of some genes are found in yeast, plants, worms, flies, and humans.
When do cells hold on to specific gene sequences, and when do they allow evolution to experiment with them? Clearly, highly conserved genes fulfill some basic, universal function for all life, and changes in their sequences have drastic consequences, involving death or the inability to multiply. How does evolution “decide” which genes need to be conserved, and which it can change freely? What keeps these genes safe from the ongoing experimentation that’s constantly carried out on other genes?
Barkai and her team discovered a sort of “risk distribution law” for evolution. They found that a genetic “phrase” that regularly shows up in the promoter region of genes (the bit of genetic code responsible for activating the gene) contains a key to gene conservation: The expression of a gene that contains the sequence TATA in its promoter is more likely to have evolved than that of a gene that does not have TATA in its promoter.
In other words, the level of risk appears to written in the gene code, in a way that’s similar to financial risk analysis: When the cost of error is high, an investor’s willingness to chance the risk is low, but if the cost of a mistake is negligible, even if the chance of making one is high, the possibility of gain may make the risk worthwhile. Evolution, it seems, discovered this principle millions of years before Wall Street.
Read the rest of the article at the source here
79 Responses to Future Risk Assessment in the Genome
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DaveScot:
I’m just getting myself up to speed on all of the details in this debate, but doesn’t ToE predict that we shouldn’t necessarily see the kind of changes you’re looking for in organisms that are successful in a given environment? From what I’ve read so far, it seems that there have been significant changes that Behe didn’t account for, although I readily admit that I don’t have the kind of knowledge necessary to sort out these claims very effectively. That’s one reason I was glad to find this site, where there seems to be a proper ID perspective on things.
Bob O’H,
I hope this does not sound rude, as I am not face to face with you, but for the 5th time, please go get the book Bob.
getawitness,
I believe that Dr. Sanford, being a more than highly qualified, Geneticist, is interpreting the evidence, presented by Gerrish and Lenski, exactly as he sees it, and you, not being privy to what he knows intuitively to be true, interpret their evidence very differently from his highly educated and more qualified perspective.
Thus, I stand by what he wrote and will not retract it.
bFast:
To play devil’s advocate for a moment (and perhaps the word “devil” is instructive here)it seems that while the Darwinist’s search for the mechanism isn’t the point, but certainly the search for a cause is. Even if we grant Darwinists’ claims of knowledge regarding mechanisms, we know that materialism has barred the door marked “Cause.” I think that even Dr. Dembski has said that ID is not a mechanistic theory, so why not give the Devil his due wrt mechanisms, and emphasize the dearth of research into cause?
bornagain77,
Please calm down. I’m not attacking Dr. Sanford. In fact, I thought I was just offering a minor and friendly correction to you, since your original comment gave the impression that you’d read Gerrish and Lenski yourself. Now I realize that you were citing that paper secondhand, from Dr. Sanford’s book.
First, however, let me correct something you wrote about me. You wrote:
“This reflects your belief that some mutations are not deleterious but could be neutral and as such have some hypothetical future beneficial effect.”
I said no such thing. I’ve said nothing about my beliefs regarding mutation but only about the claims of Gerrish and Lenski. They’re the ones who assume not all mutations are negative. Frankly, you’re assuming a lot about me.
Let me explain why I think Dr. Sanford uses the source wrongly. It has nothing to do with intuition or what Dr. Sanford knows to be true; it has to do with treating sources fairly. That’s the first rule of citation.
Imagine that Gerrish and Lenski cite Sanford’s book, and they say “Sanford has argued that most or all mutations are neutral or deleterious.” Sanford would be hopping mad at such a misuse of his book, and rightly so! Such a statement claims that Sanford believes in neutral mutations, when he clearly does not! The proper way to disagree with Sanford would be to write, “Sanford has argued that most or all mutations are deleterious, but he should consider neutral mutations more carefully.”
So my point is simply that Sanford gives the false impression that Gerrish and Lenski were intending to estimate the rate of bad to good mutations. What Sanford should have said was something like this:
“I have seen estimates of the incidence of beneficial mutations which range from one in one thousand up to one in one million. The best estimates seem to be one in one million (Gerrish and Lenski, 1998) Since neutral mutations almost never occur, then the ratio of deleterious to beneficial mutations seems to be one million to one.”
That would be a fair use of the source.
Finally, let me offer again a suggestion, in all friendship: You should not give the impression that you’ve read a primary source when you’ve gotten that material through a secondary source.
getawitness,
For me to even discuss such high level matters on the web is extremely humorous to the highest degree, for I was a homeless alcoholic for over 12 years, before I managed, with a lot of help from the Lord, to turn my life around. What is extremely funny is that even though, I should not be able to so easily refute such high level critics of ID, I do so (albeit as you have pointed out, rather clumsily) with relative ease. Hopefully I am getting better in my use of sources and appreciate your constructive criticism.
But the main point being that my faith in God has not been compromised in the least by these high level debates but has been rewarded and strengthened remarkably.
Shoot, I am even confident enough to make this following prediction for the Theistic position of ID.
Further deciphering of the human genome will reveal 100% functionality with severe polyfunctionality revealed throughout the entire genome. As well I predict the complexity of the genome will severely stress if not exceed man’s ability to completely understand it.
If you are a betting man, That is sure money the way I see things getawitness!
SR:
As far as the theory of evolution “predicting”, well, Darwin formally predicted that we would see a multitude of transitional forms. However, the modern theory makes allowance for holes in the rock record. However, there are other records to contend with, most noteably the record of the DNA. Haldane, a noted evolutionist, presented the dilemma that man has many more mutations compared to chimps than can possibly be accounted for by means of RV+NS. This is a sore spot in the tale of ToE. For ToE to be validated, it must be able to account for the reasonable statistical possibility of all changes in DNA. Currently it is far from being able to do so.
SR:
I would suggest that cause and effect are both subject to modern science. The only issue of “cause” that is barred is the issue of “first cause”. The ToE presents a formula of causation, namely RV+NS. These two mechanisms — variations in DNA from replication errors, damage etc., plus variation in environment caused by unrelated phenomenon (asteroids, etc.) and interaction of organisms filtered through the great “if it works” mechanism of selection.
The ID hypothesis seeks to “detect evidence of design”. As such, the ID hypothesis, at least within biology, does not suggest that that the designer(s) be “super-natural.” If the designer(s) are not super-natural, then, by definition, their effects can be detected and studied by a fully materialistic science. If the effects of a non-supernatural designer can be studied by a fully non-materialistic science, then the effects of a designer supernatural or not should by no means be beyond the scope of science.
“Since neutral mutations almost never occur, then the ratio of deleterious to beneficial mutations seems to be one million to one.”
To be fair to Gerrish and Lenski they never say they think “neutral mutations almost never occur”, given that they cite Kiumra so heavily I suspect they would say many mutations are neutral.
I also note Gerrish and Lenski do witness a series of fitness improvements in the evolving E. coli they study? Where is the entropic decay in this model?
bornagain77,
Thank you for sharing some aspects of your life with me; that was very touching. I’m sure not going to take that bet even if I were a betting person! You should know that I agree with you on more than you may think, including the fundamentally Theistic implications of ID.
Sorry if I sound like a old hen with a ruler sometimes. I want ID to make the best case possible!
Pantrog,
In my suggested revision, Sanford does not attribute the absence of neutral mutations to Gerrish and Lenski. That’s pretty clearly Sanford’s claim.
BFast,
I’m not sure how what you are saying answered the question, which was directed to DaveScot’s contention that in “billions of trillions” of replications, we should see significantly more change than we do in p.falciparum. My point was (and I’m a neophyte, don’t forget) that ToE doesn’t expect such changes in organisms well-adapted to their environments. Once again, I’m not making any claims of my own here, I’m just trying to understand the argument and hoping that those here who have more experience and knowledge than I do can help me along.
Pantrog you stated,
I also note Gerrish and Lenski do witness a series of fitness improvements in the evolving E. coli they study? Where is the entropic decay in this ?
I guess your referring to this statement:
Based on three sudden fitness increases during 1400 natural generations
(Lenski & Travisano, 1994),
I think this paper has part of the answer:
http://www.answersingenesis.or.....vation.asp
Of special note:
“Scientists used the MG1655 strain of E. coli K-12 bacteria that has been cultured in the lab environment for approximately 80 years. This strain has adapted well to the lab setting of growing on rich media full of carbon sources (unlike that found in natural environments). MG1655 was grown in a minimal medium containing the sole carbon source glycerol for a period of 44 days. The strain already has the pathway to catabolize (breakdown) glycerol so the “evolution” that occurred did not originate the pathway to utilize glycerol. MG1655 did not utilize glycerol well initially (as evidenced by a slow growth rate) but it was found that mutant strains developed that could utilize glycerol better (faster growth rate) than the original strain over time. The entire genome (all the DNA) from these strains was sequenced to observe mutations that led to the better utilization of glycerol. Do these mutations provide evidence that the bacteria evolved?
One strain had a mutation in a gene for the enzyme glycerol kinase which is important in the first step of glycerol breakdown. This mutation reduced the ability of glycerol kinase to be inhibited by fructose-1,6-bisphosphate (FBP). FBP is important in limiting the rate at which glycerol is catabolized. This is important since a side reaction during glycerol breakdown results in the production of a metabolite which is toxic at high concentrations. No gain of information took place as required by evolution, only loss leading to dysregulation of this pathway. In the wild, versus the rather comfy lab environment, this could be extremely detrimental.”
This study is typical of every study I’ve looked claiming fitness increase Pantrog,
Thus they can claim fitness increase while ignoring the fact that they have really broken something in the e-coli, and have in fact created a e-coli that would be “less fit” in the wild and would soon be out-competed into oblivion by the original e-coli.
Are you beginning to get the picture at how foundational Genetic Entropy truly is to biology Pantrog?
getawitness,
Since, Gerrish and Lenski most likely used a incomplete measure of fitness, I maintain that their, one in a million, estimate is skewed. I maintain that when taking into account a complete picture of fitness for mutated e-coli (loss of information from original strain as well as compared complete robustness to original strain), there will NEVER be a beneficial mutation that will both increase fitness and information at the same time.
Thus holding to the foundational principle of Genetic Entropy:
The rule can somewhat be stated like this:
All adaptations away from a parent species for a sub-species, which increase fitness to a particular environment, will always come at a loss of information from the original parent species.
This overriding principle, drawn directly from Genetic Entropy, is substantiated for all adaptations I have looked at from “simple” micro-organisms to complex higher organisms.
It is a solid inference, all the way down to the second law and the conservation of information.
Thus it most likely is a rule that will hold across the board for all of biological life forms!
Getawitness,
I’ve revised my study notes to reflect your objection, I would like to know if the revision passes your inspection:
The primary thing that is crushing to the evolutionary theory is this fact. Of the random mutations that do occur, and have manifested traits in organisms that can be measured, at least 999,999 out of 1,000,000 (99.9999%) of these mutations to the DNA have been found to produce traits in organisms that are harmful and/or fa^tal to the life-form having the mutation!
“I have seen estimates of the incidence of beneficial mutations which range from one in one thousand up to one in one million. The best estimates seem to be one in one million (Gerrish and Lenski, 1998) Since neutral mutations can be inferred to almost never occur in a genome, then the ratio of deleterious to beneficial mutations seems to be one million to one.” (Sanford; Genetic Entropy, page 38: Note: this statement has been revised to reflect the evolutionary belief of some totally neutral mutations of Gerrish and Lenski)
http://myxo.css.msu.edu/lenski.....Lenski.pdf
Even if there were totally neutral mutations, which is highly unlikely given the overwhelming interrelated complexity of the genome, Gerrish and Lenski most likely used a incomplete measure of fitness/information in order to arrive at their one in a million number for beneficial mutations. I maintain that their, one in a million, estimate is flawed and that ALL mutations to a genome will be found to be harmful/fatal when using a correct measure of fitness/information. The following article points out this flaw, in measuring the total fitness/information of a organism, by evolutionary scientists and thus skewing the already crushing mutational studies:
http://www.answersingenesis.or.....vation.asp
In fact, from consistent findings such as these, it is increasingly apparent that Genetic Entropy is the overriding foundational rule for all of biology with no exceptions:
The foundational rule for biology can be stated like this:
All adaptations away from a parent species for a sub-species, which increase fitness to a particular environment, will always come at a loss of information from the parent species.
SR, “ToE doesn’t expect such changes in organisms well-adapted to their environments.” Oh, I see what you are suggesting. The reason Behe points to p.falciparum’s mutation rates is because it is not “well-adapted” to its environment. Man, in his wisdom, has done everything we can to make a toxic environment for malaria (p.falciparum). In doing so, we have created a situation where malaria should feel poorly adapted, and should adapt. That said, malaria has adapted somewhat, but always by lessening itself, rather than by becoming something greater. With more organisms being so challenged than there ever has been quadrupeds, one would think that the malaria should have been able to pull off at least one progressive (rather than regressive) mutation by now.
bornagain77,
The short answer is “I’m not sure,” because in the paragraph beginning “I have seen estimates,” I’m not sure what are your words and what are Sanford’s. (It would be easier for me to tell if I had Sanford’s book. I’ll get a copy, though, and tell you when I find out.) Thanks for taking the objection seriously, however. As I mentioned before, I’m not arguing against genetic entropy or against Sanford: I’m arguing for a good use of sources.
bFast, how can something that’s not well adapted to its environment go through, as DaveScot puts it, “billions of trillions” of replications?
getawitness, “I’m arguing for a good use of sources.”
I have been watching your debate with BA77, and agree with you that as the underdog we need to be particularly cautious to use sources carefully. Further, I agree that a source should be presente from the source’s perspective, even if we then suggest that said perspective is in error.
SR, if well adapted is confirmed by “billions of trillions” of replications, then the fact that humans have only replicated about ten billion times would indicate that we are not well adapted
Surely one would agree that if the organism replicates billions of times per acre per day — which malaria does — that if an otherwise fertile acre becomes toxic, and replication rates drop to near zero, those malaria find themselves in an environment for which they are not well adapted. As the microbe can reproduce more in an acre per year than there are humans in history, they should be able to make changes that somewhat match the difference between man and chimp — at least 2% of DNA. Why have they made NO progressive mutational changes even in toxic environments?
DaveScot and all,
You may find this study interesting;
Protein stability imposes limits on organism complexity and speed of molecular evolution
Konstantin B. Zeldovich, Peiqiu Chen, and Eugene I. Shakhnovich
http://www.pnas.org/cgi/conten.....4/41/16152
of special note:
Here we study population dynamics in a where fitness can be inferred from physical properties of proteins under a physiological assumption that loss of stability of any protein encoded by an essential gene confers a lethal phenotype…..
It establishes a universal speed limit on rate of molecular evolution by predicting that populations go extinct (via lethal mutagenesis) when mutation rate exceeds approximately six mutations per essential part of genome per replication for mesophilic organisms and one to two mutations per genome per replication for thermophilic ones.
Although I don’t know the details yet, this seems that evolutionists are themselves in the foot again, since evolutionists are required to have rapid speciation events that occur within 5 to 50,000 years to explain the gaps in the fossil record.
Thus on one hand, because of the fossil record, they must have a certain rate of rapid speciation, yet on the other hand, because of functional properties of proteins, they are limited to the amount of change they can incur per generation..
Though the study is technically a bit beyond me right now…I do smell another rat in evolutionary thinking with this particular study!
bornagain77 –
What about synonymous substitutions?
I’m also curious if you’re read this article. If not, I can try and get a copy to email you.
Bob