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Author
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Topic: Implications of Behe and Snoke paper
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Bruce Fast
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Member # 924
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posted 12. July 2006 21:10
Zachriel, your exponents describing both the reproductive rates and population sizes of the prokaryotes are impressive.
My understanding is that ORFan genes are what you might call "new" genes. Are ORFan genes limited to prokaryotes? Are ORFan genes found only in organisms with reproductive rates and population sizes that rival the prokaryotes?
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Jehu
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posted 13. July 2006 03:34
Mesk, you said quote:
As there are ~10^14 prokaryotes in the average human gut, and ~10^30 in the world at any one time.
No kidding. Behe said the same thing in his testimony.
quote:
Q. 10 to the 30th, that is quite a lot, right?
A. Yes. That's roughly what is calculated to be the bacterial population of the Earth in any one year. And so over the course of the billion year, 4 billion year history of the Earth, there would probably be a total of roughly 10 to the 40th.
You also said,
quote:
Bacterial generations can be measured in hours, so 10^8 generations is not such a long period of time. As there are ~10^14 prokaryotes in the average human gut, and ~10^30 in the world at any one time, that means that the evolution of the posited genes occurs thousands of times a second — according to Behe & Snoke's calculations. And they admit to have only considered one very limited type of evolutionary process.
Behe and Snoke have "proved" that evolution of new genes is an inevitability.
Actually, it is a well known fact that bacterial generations can range from 15 minutes to several days. Regardless, what Behe said was that for a minimal MR feature protein (that is two amino acids) it takes a population of 10 to the 14th a time of 10 to the 8th generations.
Big deal, two amino acids gets you nowhere in terms of evolution. The average protein is considered to be about 300 amino acids in length. When you go from two amino acids to three the time and/or population size goes up exponentially. Take for example the odds of mutating even a small functional protein of 100 amino acids. The odds of that are at least 10 to the 65th power. Once you get to 10 to the 40th you have every bacteria that ever lived on earth. And that is just the odds of getting a functional protein, never mind if it is one that is the right protein that will create a selective benefit. That doesn't just take any functional protein it takes the right protein, so the odds are even less. However, since you already past the number of proteins that ever existed it is meaningless. Now the odds of getting an average protein of 300 amino acids is even worse, far worse.
BTW by functional protein I mean a protein that will fold.
[ 13. July 2006, 03:43: Message edited by: Jehu ]
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Zachriel
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posted 13. July 2006 07:30
Jehu: "Behe says that populations of 10 to the 9th or greater are needed to mutate even a minimal MR feature (two amino acids) within 10 to the 8th generations."
Jehu: "Big deal"
I assume that means you consider the Behe paper to be largely irrelevant, then. I think that would be considered a valid response to Jules's original query. There are no implications.
Jehu: "Take for example the odds of mutating even a small functional protein of 100 amino acids. The odds of that are at least 10 to the 65th power."
They didn't make that particluar calculation, though, did they? Apparently, you just took the typical creationist bugaboo 4^100 = 100^60 and assumed that was the correct answer. That begs the question as to why Behe and Snoke went to such efforts, your method being so much easier.
Of course, it's also incorrect. That is the calculation that a random mixture of amino acids, assuming equal probability of combination, would create an exact pre-ordained sequence.
The question at issue is, given a working gene, what are the odds of it mutating in such a way as to create a novel adaptation. The Behe and Snokes paper made some very conservative assumptions, and still indicates that it would only take a few thousand years. So evolution of new genes is not only possible, but inevitable, given their calculations and assumptions.
[ 13. July 2006, 08:14: Message edited by: Zachriel ]
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Zachriel
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posted 13. July 2006 08:12
Bruce Fast: "My understanding is that ORFan genes are what you might call 'new' genes. Are ORFan genes limited to prokaryotes? Are ORFan genes found only in organisms with reproductive rates and population sizes that rival the prokaryotes?"
ORFan means Open Reading Frame and can occur in eukaryotes as well as prokaryotes. Basically, it means a sequence in a genome with no known homolog in other sequences. The keyword there is 'known'.
It is known that most genes do have homologs and that they form the familiar nested hierarchy of descent. So what are these 'orphan' genes?
Let me digress a bit. Intelligent Design, as usually constituted, is an argument from ignorance, and has been continually pushed back by the light of evidence. Now, Intelligent Design has been pushed all the way back to the Cambrian and before, to the origin of cellular mechanics. Because these events are so distant in time, it is a wonder we know anything about the epoch at all!
That ORFan genes do not constitute recognizable families is not to claim that they cannot constitute families. There are significant limitations to the process of sequencing and analyzing genomes. Ignorance is not evidence of anything other than ignorance. But not surprisingly, as more genomes have been sequenced, most ORFan's have been put into families. Many others undoubtedly will be also.
Of course, some may be truly novel genes that were created by recombination, artifacts, frame-shifts or other known and unknown mechanisms. Determining the origin of these genes may be very difficult. But again, ignorance is not evidence.
[ 13. July 2006, 09:58: Message edited by: Zachriel ]
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Jehu
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posted 13. July 2006 13:49
Mesk,
quote:
Jehu: "Take for example the odds of mutating even a small functional protein of 100 amino acids. The odds of that are at least 10 to the 65th power."
Mesk: They didn't make that particluar calculation, though, did they?Apparently, you just took the typical creationist bugaboo 4^100 = 100^60 and assumed that was the correct answer.
I have no idea where you came up with this comment.
Behe made the calculation based on the findings in a publication by Sauer. Reidhaar-Olson, J. F., & Sauer, R. T. (1990) "Functionally Acceptable Substitutions in Two -Helical Regions of Repressor", Proteins: Structure, Function, and Genetics 7, 306-316.
Here is what Behe wrote regarding the calculation.
quote:
Sauer's laboratory, in order to answer questions about protein structure that interested them, took the genes for several viral proteins, systematically took out small pieces of them (corresponding to instructions for three amino acids at a time) and inserted altered pieces back in the genes. They did this, three amino acids 'codons' at a time, for the whole length of the gene. By clever manipulation of the altered pieces they were able to screen codons for all twenty amino acids at each position of the protein. This is like trying all 26 letters of the alphabet in turn at each position of a word. The altered genes were then placed in bacteria, which read the DNA code and produced chains of amino acids from them. It turns out that bacteria quickly destroy proteins that are not folded, so Sauer's group looked for the altered proteins that were not destroyed. By determining their sequences they could tell which amino acids in a given position were compatible with producing a folded, functional protein. And what did they see?
In some positions of the protein Sauer's group saw that a great deal of amino acid diversity could be tolerated. Up to 15 of the twenty amino acids could occur at some positions and still yield a functional, folded protein. However, at other positions in the amino acid sequence very little diversity could be tolerated. Many positions could accomodate only 3 or 4 different amino acids. Other positions had an absolute requirement for a particular amino acid; this means that if, say, a P does not appear at position 78 of a given protein the protein will not fold regardless of the proximity of the rest of the sequence to the natural protein. In terms of our sentence analogy, this is like saying that, yes, all vowels are interchangeable, but that if the last `r' is changed to any other letter, such as 's' ("Drop the anchor in one hous"), the protein sentence is no longer understandable.
Sauer's results can be used to calculate the probability of finding a given protein structure (6). We proceed in the following manner. If any of ten amino acids can appear in the first position of a given functional protein sequence then the odds are 1 in 2 that a nondirected search will place one of the allowed group there. If any of four amino acids can appear in the second position then the odds are 1 in 5 of finding one of that group, and the odds of finding the correct amino acids next to each other in the first two positions are one-half times one-fifth, which is one-tenth. Suppose in the third position there is an absolute requirement for G. Then the odds of getting a G at that position are one in twenty and the odds of getting the first three amino acids right are now up to one in two hundred. In this aspect it is like winning a trifecta in horse racing. Over the course of 100 amino acids in our small protein the odds quickly reach astronomical numbers.
From the actual experimental results of Sauer's group it can easily be calculated that the odds of finding a folded protein are about 1 in 10 to the 65 power.
You also wrote: quote:
The question at issue is, given a working gene, what are the odds of it mutating in such a way as to create a novel adaptation. The Behe and Snokes paper made some very conservative assumptions, and still indicates that it would only take a few thousand years. So evolution of new genes is not only possible, but inevitable, given their calculations and assumptions.
To begin with, a working gene has to come from somewhere and the odds of ever getting a functional protein by chance are impossible, especially when you realize that you don't get proteins without DNA and you don't get DNA without proteins.
However, moving to the hope that after you have a functional protein you can migrate from one function to another via gene duplication and point mutations, Behe and Snokes said that a mininum number of nucleatide substitutions take 10^8 generation in a population of 10^11 organisms under selective pressure with a fixed duplicated gene. Only when you are discussing bacteria with a very fast generation time is that a few thousand years. I would assume that evolution requires other organisms besides bacteria to mutate novel protein functions? Remember we are talking minimal distances in function. According to the calculations of Behe and Snoke, if just three nucleotide substitutions are required (which is unrealisticly low) it would require a population of 100 billion (under selective pressure with a duplicate gene waiting to be mutated) 100 million generations. These numbers are obviously not achievable by most organisms.
Now we are just talking three nucleotide substitutions. Behe and Snokes give an example of a real world example of a very simple transition of function quote:
In a recent in vitro study intended to mimic evolution, a recombinant amphioxus insulin-like peptide was altered by site-directed mutagenesis at seven nucleotide positions to contain five altered amino acid residues that would allow interaction with mammalian insulin receptor (Guo et al. 2002). In order for such a process to occur in vivo by gene duplication and point mutation within a hundred million generations would be expected on average to require >10^25 organisms.
Okay, so to simulate the evolution of a similar protein in lancets to a protein that will interact with mammalian insulin it would take a population of >10^25 organisms 100 million generations. And that is for only seven nucleotide changes. Again, very minimal.
Remember also, in order to explain the gaps in the fossil record the concept of punctuated equilibrium has become the concensus view that states that evolution happens in small isolated populations not in large populations. So you cannot have incredibly large populations to help you get around the mathmatical improbabilities of mutating a novel gene and at the same time have small populations to explain the lack of fossil evidence to support evolution.
I certainly would not call this paper meaningless or insignificant. Behe and Snoke correctly conclude: quote:
[G]ene duplication and point mutation may be an effective mechanism for exploring closely neighboring genetic space for novel functions where single mutations produce selectable effects, this conceptually simple pathway for developing new functions is problematic when multiple mutations are required. Thus, as a rule, we should look to more complicated pathways, perhaps involving insertion, deletion, recombination, selection of intermediate states, or other mechanisms, to account for most MR protein features.
[ 13. July 2006, 14:04: Message edited by: Jehu ]
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Bruce Fast
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posted 13. July 2006 13:55
Yet, Zachriel, you carefully avoided answering my question, did you not? It is very convenient to point to the mass population numbers in the prokaryotes, but when you look at the long generations and small numbers in humans and chimps it becomes more difficult to find the necessary organism count to account for significant evolution.
Further, Zachriel, my understanding is that your science is to a huge extent still in its infancy? Isn't it true that in the simplest known independantly living organism, the function of over half of the essential genes is not known? Isn't it also true that recent research has suggested that significantly more of the genes in said organism are essential than first thought -- has something to do with the dear thing having redundant genes. (Oooh, PB has clarified a significant evolutionary challenge to redundant genes.) Further, isn't it true that recent research indicates that the eukaryotes did not descend from the simpler forms? Though ID makes a lot of claims "in the gaps" there seem to be gaping gaps, much bigger gaps than you imply.
About the fossil record, my understanding is that once fossilization happens, time is brought to a complete standstill. While fossil beds may be eroded to mush, those that are not eroded contain image quality as good as existed once fossilization was complete. My understanding is that the fossil beds which document the cambrian explosion have stunning detail, even imaging extensive soft tissue. Its easy to say that the cambrian was a long time ago, but when time is frozen completely, as it is in the fossil record, it makes little difference.
Further, though I am not a scientist, I have followed this ID argument extensively over the past couple of years. Though IDers do present the abiogenesis challenge, and the cambrian explosion challenge as issues of point, that is hardly the beginning and end of the IDer's case. For instance, over on Uncommon Descent there is currently a raging discussion of the convergence found between the marsupials and the placentals. It is a discussion of positive evidence, and a discussion of living organisms. Maybe you should go over there and convince those guys that ID should limit itself to abiogenesis and the cambiran explosion.
[ 13. July 2006, 13:57: Message edited by: Bruce Fast ]
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Jehu
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posted 13. July 2006 15:35
Zach,
You said quote:
Behe and Snoke have "proved" that evolution of new genes is an inevitability.
That is nonsense, at the most their paper shows that single point mutatioins in duplicate gene may be capable of searching very closely related protein space, and then only in extremely large populations with rapid generation times.
The difficulty in evolving a non-closely related protein function by single point mutation has been described in the literature elswhere as well. quote:
[M]oving from one family to another requires crossing a high-energy frustration barrier along which the protein does not fold into a stable structure and is therefore incapable of performing biological functions.
The implication, then, is that moving from one family to another will require more than just one small change at a time (a gradual walk). The evolutionary process must leap over the nonfunctional frustration barriers in order to produce new protein families.
"Proposed Mechanism for Stability of Proteins to Evolutionary Mutations," Erik Nelson and Jose Onuchic (PNAS, vol. 95, issue 18, 10682-10686, Sept 1, 1998)
quote:
We address here, from a theoretical point of view, the question of how protein space can be searched efficiently and thoroughly, either in the laboratory or in Nature. We demonstrate that point miutation alone is incapable of evolving systems with substantially new protrein folds. We demonstrate further that even the DNA shuffling approach is incapable of evolving substantially new protein folds.
"A Hierarchical Approach to Protein Molecular Evolution", Bogarad and Deem (PNAS Vol. 96, Issue 6, 2591-2595, March 16, 1999)
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Jules
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posted 13. July 2006 17:22
As a non-scientist, I need to ask how we define a significant change to a duplicated gene. Would 10 new amino acids (in key positions) be considered "significant"? If so, then I think the Behe/Snoke paper would show that we can expect bacteria to have evolved several new genes in their long history, by the mechanism of single point neutral mutations in duplicated genes.
Perhaps we need to know how big a difference there are between the proteins that make up a flagellum, and their precursors, if there are any.
Though I haven't tried finding information on times for generations of eukaryotes, I'm guessing they are considerably longer, perhaps even for unicellular eukaryotes.
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Jehu
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posted 13. July 2006 20:57
Jules,
You said, quote:
As a non-scientist, I need to ask how we define a significant change to a duplicated gene. Would 10 new amino acids (in key positions) be considered "significant"? If so, then I think the Behe/Snoke paper would show that we can expect bacteria to have evolved several new genes in their long history, by the mechanism of single point neutral mutations in duplicated genes.
The issue generally isn't the number of amino acids, what is significant is whether there is a novel function.
I have no idea how you have come to the conclusion that the Behe/Snoke papers supports the idea that bacteria will evolve new genes if 10 amino acids is significant. Certainly the Behe/Snoke paper does not support the conclusion that a bacteria can evolve a function that is ten amino acids away if that is what is required for the new function. According to their paper a change of 7 nucleotides requires a population of 10^25 organisms a time of 100 million generations. Remember in the real world you are not ever going to get a population of bacteria that is 10^25 with a fixed dupilcate gene under selective pressure, so it is going to take you a lot longer. That is just for 7 substitutions, 10 would be way out of reach, even for bacteria. And a change in 10 amino acids is almost certainly going to take more than 10 nucleotide substitutions.
As I mentioned in my post to Zach, Behe/Snoke are not the only ones to come to this conclusioin regarding point mutations. The difficulty in evolving a non-closely related protein function by single point mutation has been described in the literature elswhere as well. quote:
[M]oving from one family to another requires crossing a high-energy frustration barrier along which the protein does not fold into a stable structure and is therefore incapable of performing biological functions.
The implication, then, is that moving from one family to another will require more than just one small change at a time (a gradual walk). The evolutionary process must leap over the nonfunctional frustration barriers in order to produce new protein families.
"Proposed Mechanism for Stability of Proteins to Evolutionary Mutations," Erik Nelson and Jose Onuchic (PNAS, vol. 95, issue 18, 10682-10686, Sept 1, 1998)
quote:
We address here, from a theoretical point of view, the question of how protein space can be searched efficiently and thoroughly, either in the laboratory or in Nature. We demonstrate that point miutation alone is incapable of evolving systems with substantially new protrein folds. We demonstrate further that even the DNA shuffling approach is incapable of evolving substantially new protein folds.
"A Hierarchical Approach to Protein Molecular Evolution", Bogarad and Deem (PNAS Vol. 96, Issue 6, 2591-2595, March 16, 1999)
[ 13. July 2006, 22:06: Message edited by: Jehu ]
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Zachriel
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posted 14. July 2006 10:56
Jehu: "I have no idea where you came up with this comment.
Behe made the calculation based on the findings in a publication by Sauer."
I would note that it would take 10000x longer than just taking random bases and trying to match a single specified sequence. In any case, Behe purports 'to calculate the probability of finding a given protein structure', a telelogical goal at an ambiguous distance.
Jehu: "To begin with, a working gene has to come from somewhere and the odds of ever getting a functional protein by chance are impossible"
Irrelevant to the evolution of existing life, and irrelevant to the study in question.
Jehu: "Behe and Snokes said that a mininum number of nucleatide substitutions take 10^8 generation in a population of 10^11 organisms under selective pressure with a fixed duplicated gene."
From the abstract: "We conclude that, in general, to be fixed in 10^8 generations, the production of novel protein features that require the participation of two or more amino acid residues simply by multiple point mutations in duplicated genes would entail population sizes of no less than 10^9."
Jehu: "Only when you are discussing bacteria with a very fast generation time is that a few thousand years."
That is the study in question. However, it is known that recombination is an important source of novelty in sexually reproducing eukaryotes. It may not always take multiple point-mutations. And the calculations may be faulty by a few orders of magnitude. Their calcuation of ρ is suspect.
Jehu: "Remember we are talking minimal distances in function."
Evolution proceeds by *small* steps, whether point mutations, recombination events, or other such processes.
Behe & Snokes: In most models of the development of evolutionary novelty by gene duplication, it is implicitly assumed that a single, albeit rare, mutation to the duplicated gene can confer
a new selectable property (Ohta 1987, 1988a,b; Walsh 1995).
Jehu: "Okay, so to simulate the evolution of a similar protein in lancets to a protein that will interact with mammalian insulin it would take a population of >10^25 organisms 100 million generations."
Guo et. al. don't appear to claim in their paper that any such process occurred or that such a calculation makes any sense.
Jehu: "So you cannot have incredibly large populations to help you get around the mathmatical improbabilities of mutating a novel gene and at the same time have small populations to explain the lack of fossil evidence to support evolution."
Strawmen don't evolve in small populations, that's correct. However, that is not what the Theory of Evolution proposes. Rather, small changes accumulate in isolated populations.
Bruce Fast: "Yet, Zachriel, you carefully avoided answering my question, did you not?"
Not at all. I answered your question directly. ORFan's are not confined to prokaryotes.
Bruce Fast: "Further, Zachriel, my understanding is that your science is to a huge extent still in its infancy?"
Quite so.
Bruce Fast: "Further, isn't it true that recent research indicates that the eukaryotes did not descend from the simpler forms?"
Correct again. Though no one knows for sure at this point, it is believed that Common Descent may not apply properly to the origin or evolution of cellular life.
Bruce Fast: "Though ID makes a lot of claims 'in the gaps' there seem to be gaping gaps, much bigger gaps than you imply."
Of course the gap is large. There is no complete theory of abiogenesis. There may never be. There is no complete theory of how cellular machinary arose. There may never be. These events are very distant in time and have been overshadowed by the changes that have occurred since then. It's amazing we know anything!
However, the more scientists examine the evidence, the more they discover natural mechanisms as explanations. And there are scientifically valid ways to determine where to look for these explanations and to put limits on what is scientifically plausible.
Meanwhile, you are welcome to put your Creator in the ever-shrinking gap in human knowledge. But he seems to be a very pale imitation of the God I know.
Bruce Fast: "Maybe you should go over there and convince those guys that ID should limit itself to abiogenesis and the cambiran explosion."
Their stated policy specifically precludes criticism of Intelligent Design.
Jehu: "The issue generally isn't the number of amino acids, what is significant is whether there is a novel function."
As novel proteins have been observed to evolve by known evolutionary mechanisms (e.g. nylonase), it would seem that the entire exercise by Behe and Snokes would be suspect.
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Zachriel
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posted 14. July 2006 11:04
Jehu: "The difficulty in evolving a non-closely related protein function by single point mutation has been described in the literature elswhere as well... A Hierarchical Approach to Protein Molecular Evolution", Bogarad and Deem (PNAS Vol. 96, Issue 6, 2591-2595, March 16, 1999)"
No one posits that point-mutation is the only mechanism of evolution. From Bogarad and Deem:
"Random assembly and base substitution are ideally suited for searching local regions of polypeptide space, as demonstrated experimentally"
But...
"However, the difficulty of making the transition from one productive tertiary fold to another limits evolution by means of base substitution and homologous recombination alone."
"More generally, it seems likely that organization into higher-order fundamental units such as nucleic acids, the genetic code, secondary and tertiary structure, cellular compartmentalization, cell types, and germ layers allows systems to escape complexity barriers and potentiates explosions in diversity."
But let's assume that point-mutation was the only known mechanism of novelty in genomes. And it was determined that point-mutation was not sufficient to account for the variation found in genomes. The scientific conclusion would not be that an Intelligent Designer did it. That's a fallacious argument from ignorance, angels pushing planets on crystal spheres. Rather, additional mechanisms would be sought after, whether these were mechanisms of design or natural contingency. The mechanisms found thus far are all natural processes, and there is no reason to suspect design other than people's intuition and desire for science to ratify their metaphysical and religious beliefs.
You may believe that the Earth is the center of God's physical Creation. You may intuit that the Earth is fixed. Eppur si muove.
[substantial edits]
[ 14. July 2006, 11:20: Message edited by: Zachriel ]
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Eric Anderson
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posted 14. July 2006 12:27
quote:
But let's assume that point-mutation was the only known mechanism of novelty in genomes. And it was determined that point-mutation was not sufficient to account for the variation found in genomes. The scientific conclusion would not be that an Intelligent Designer did it. That's a fallacious argument from ignorance, angels pushing planets on crystal spheres."
Fortunately, ID theorists do not take this approach. Neither did Behe and Snoke in their paper.
quote:
. . . there is no reason to suspect design other than people's intuition and desire for science to ratify their metaphysical and religious beliefs.
You may believe that the Earth is the center of God's physical Creation. You may intuit that the Earth is fixed. Eppur si muove."
This is good stuff. A prime example of how, when the "scientific" critique of ID fails, there is fallback to general accusations about religious motives.
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Jules
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posted 14. July 2006 16:05
Jehu wrote: quote:
I have no idea how you have come to the conclusion that the Behe/Snoke papers supports the idea that bacteria will evolve new genes if 10 amino acids is significant.
I got the idea from looking at the last graph in their paper, combined with Behe's testimony that there are 10<30> bacteria present at any one time. The graph says that it would take a population of 10<30> and 10<12> generations (200 million years) to produce a protein with 10 new amino acids. I assumed that we could include the entire world population of bacteria in making our calculation. Perhaps that's a bad assumption?
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Zachriel
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posted 14. July 2006 18:08
Eric Anderson: "Fortunately, ID theorists do not take this approach."
Asserting that known natural mechanisms are not sufficient to explain evolution is certainly put forth as evidence of Intelligent Design by some ID 'theorists'.
Eric Anderson: "Neither did Behe and Snoke in their paper."
That is correct. The Behe and Snoke paper does not argue for Intelligent Design.
Jules: "The graph says that it would take a population of 10<30> and 10<12> generations (200 million years) to produce a protein with 10 new amino acids."
Not to mention all sorts of other novel sequences at closer distances. Of course, other evolutionary processes are also at work.
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Zachriel
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posted 14. July 2006 23:11
Jules: "The graph says that it would take a population of 10<30> and 10<12> generations (200 million years) to produce a protein with 10 new amino acids."
Zachriel: "Not to mention all sorts of other novel sequences at closer distances. Of course, other evolutionary processes are also at work."
Now consider the situation where it takes just a
few sequence changes to create a new gene. And there may be more than a single novel gene within the distance of a few sequence changes. The search will find many of these other genes in about the same time. And of course, there may be plenty of variations discovered that are even closer.
Let's say it took ~100K years to find these genes. Now each of these genes forms a stable point to start a new search. And within ~100K years, it would again have the opportunity to search the available space for even more genes.
In a few million years, some of the genes may differ from others by large numbers of basepairs. You now have a diversifying and branching family of genes. Oh, and they will form a nested hierarchy (within the limitations of stochastic processes).
Of course, other evolutionary processes are at work.
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