Hi All,
The following link:-
CSC - A Response to Dr. Dawkins' "The Information Challenge"
was supplied to me on another forum as an example of some kind, of ID explanatory power and associated research. (You will see that it is nothing more than a critique of ToE and Dawkins and Darwin.)
In this short essay I am concerned with the section Luskin offers about gene duplication and its role in evolution. While accepting gene duplication, Luskin scorns the idea that it is anything significant in evolution.
The relevant section is “Part 2: Does Gene Duplication Increase Information Content?”. I will not critique the whole of part 2, but rather will stick to those parts I am easily familiar with. Demonstrating Luskin’s errors there should cast reasonable doubt on his ability to be correct elsewhere.
Part 2 begins with the stated aim to show “…why merely citing gene duplication does not help one understand how Darwinian evolution can produce new genetic information.”.
In itself, such an aim is sensible. Merely citing a mechanism does nothing to demonstrate its reality. (Do you understand this IDers and YECs? Just like showing ToE to be wrong, does not show ID to be right. Just like showing Darwin to have been a bank robber, does not show ToE to be wrong.)
However, Luskin falls when he goes on to the following two points:-
1) “Duplicating Genes Doesn't Increase Biological Information in Any Important Sense” and
2) “Darwinists Must Give Detailed Accounts of how a Duplicated Gene Acquires its New Function”
So how does Luskin fall?
At point 1) Luskin mocks evolutionists by implying that they essentially argue that to say a sentence twice is to increase information, because, if a gene duplication adds information, then so must a duplicated sentence. Clearly such a statement about sentences is rubbish, therefore the claim by evolutionists about duplicated genes is rubbish.
But who is really talking the rubbish? As I will show, evolutionists go way beyond this, and they were at the time Luskin wrote his piece.
Luskin tackles point 2) with the following statement:-
“The Darwinist would probably reply to my objection by saying, "Well, it isn't just gene duplication that increases the genetic information — such information is increased when gene duplication is coupled with the subsequent evolution of one of the new copies of the gene." Aye, there's the rub.”
And what is the rub according to Luskin? Well according to him, evolutionists must be able to show, in detail, how either of the pair of duplicated genes can evolve to acquire a new function. Hence he writes:-
“But the new genetic information must somehow be generated during that subsequent evolution of the gene. To explain how Darwinian processes can generate new and meaningful genetic information, Darwinists must provide a detailed account of how a duplicate copy of a gene can evolve into an entirely new gene. But ask Darwinists for details as to how the duplicate copy then starts to perform some new function, and you probably won't get any. At least, Dawkins didn't given us any details (as I explain below) about this in his "The Information Challenge" article, which I am rebutting here.”
And just to show that Dawkins is not alone in being unable to do this, Luskin offers the following sentence from an abstract in Nature
“A recent study in Nature admitted, "Gene duplication and loss is a powerful source of functional innovation. However, the general principles that govern this process are still largely unknown." (Ilan Wapinski, Avi Pfeffer, Nir Friedman & Aviv Regev, "Natural history and evolutionary principles of gene duplication in fungi," Nature, Vol. 449:54-61 (September 6, 2007).) Yet the crucial question that must be answered by the gene duplication mechanism is, exactly how does the duplicate copy acquire an entirely new function? “
So there we have it. Dawkins could not explain how it is done and even Nature admits that this cannot be done. (Don’t you just love that word “admit” when creationists use it?)
THE WHOLE ABSTRACT IS MORE REVEALING THAN LUSKIN LETS ON.
But what did Nature really say about the matter. The abstract (which Luskin quoted from, actually goes as follows:-
”Gene duplication and loss is a powerful source of functional innovation. However, the general principles that govern this process are still largely unknown. With the growing number of sequenced genomes, it is now possible to examine these events in a comprehensive and unbiased manner. Here, we develop a procedure that resolves the evolutionary history of all genes in a large group of species. We apply our procedure to seventeen fungal genomes to create a genome-wide catalogue of gene trees that determine precise orthology and paralogy relations across these species. We show that gene duplication and loss is highly constrained by the functional properties and interacting partners of genes. In particular, stress-related genes exhibit many duplications and losses, whereas growth-related genes show selection against such changes. Whole-genome duplication circumvents this constraint and relaxes the dichotomy, resulting in an expanded functional scope of gene duplication. By characterizing the functional fate of duplicate genes we show that duplicated genes rarely diverge with respect to biochemical function, but typically diverge with respect to regulatory control. Surprisingly, paralogous modules of genes rarely arise, even after whole-genome duplication. Rather, gene duplication may drive the modularization of functional networks through specialization, thereby disentangling cellular systems.”
Now a read of the above will reveal that the aticle to follow is from people who are beginning to work things out, and after having done their research, it is not as if they still have no ideas.
If you doubt me YECs and IDers then read the darn abstract for once, and think about the wording on offer.
BUT RESEARCHERS WERE ALREADY BEGINNING TO DO WHAT LUSKIN DENIES
But what is worse for Luskin, is that he wrote his article late 2007, months after the above mentioned research. However in earlier years one could already find several articles dealing with blow by blow descriptions of plausible mechanistic details by which new functionality in duplicated genes evolved. How were the mechanisms made plausible? Well the researchers tested the ideas in their laboratories.
Yet according to Luskin, this was not happening. Dawkins admitted to it and so did Nature.
Here are a couple of those papers Lusking implicitly claims do not exist. (Note the dates, all before 2007? And even though gene duplication may not be mentioned, they are about what happened following such events. I read the Nature article reporting on them*):-
1) Jamie T. Bridgham, Sean M. Carroll, Joseph W. Thornton, “Evolution of Hormone-Receptor Complexity by Molecular Exploitation”, Science, 312, 7-April-2006, pages 97-101.
The abstract is:-
According to Darwinian theory, complexity evolves by a stepwise process of elaboration and optimization under natural selection. Biological systems composed of tightly integrated parts seem to challenge this view, because it is not obvious how any element's function can be selected for unless the partners with which it interacts are already present. Here we demonstrate how an integrated molecular system—the specific functional interaction between the steroid hormone aldosterone and its partner the mineralocorticoid receptor—evolved by a stepwise Darwinian process. Using ancestral gene resurrection, we show that, long before the hormone evolved, the receptor's affinity for aldosterone was present as a structural by-product of its partnership with chemically similar, more ancient ligands. Introducing two amino acid changes into the ancestral sequence recapitulates the evolution of present-day receptor specificity. Our results indicate that tight interactions can evolve by molecular exploitation—recruitment of an older molecule, previously constrained for a different role, into a new functional complex.
The whole paper is concerned with what happened following a gene duplication.
2) Poelwijk FJ, Kiviet DJ, and Tans SJ, “Evolutionary potential of a duplicated repressor-operator pair: simulating pathways using mutation data.”, PLoS computational biology 2(5):e58, 2006 May -
The abstract is:-
Ample evidence has accumulated for the evolutionary importance of duplication events. However, little is known about the ensuing step-by-step divergence process and the selective conditions that allow it to progress. Here we present a computational study on the divergence of two repressors after duplication. A central feature of our approach is that intermediate phenotypes can be quantified through the use of in vivo measured repression strengths of Escherichia coli lac mutants. Evolutionary pathways are constructed by multiple rounds of single base pair substitutions and selection for tight and independent binding. Our analysis indicates that when a duplicated repressor co-diverges together with its binding site, the fitness landscape allows funneling to a new regulatory interaction with early increases in fitness. We find that neutral mutations do not play an essential role, which is important for substantial divergence probabilities. By varying the selective pressure we can pinpoint the necessary ingredients for the observed divergence. Our findings underscore the importance of coevolutionary mechanisms in regulatory networks, and should be relevant for the evolution of protein-DNA as well as protein-protein interactions.
The above abstracts give the clue. The following articles are all about mechanism following gene duplication, and how this leads to new function. AND GUESS WHAT? THEY EVEN BOTHER TO WRITE THESE ARTICLES BASED ON ACTUAL LABORATORY RESEARCH.
QUOTING MEYER
Luskin goes on to quote Steven Meyer, "The origin of biological information and the higher taxonomic categories," Proceedings for the Biological Society of Washington, Vol. 117(2):213-239 (2004):-
This scenario has the advantage of allowing the genome to vary through many generations, as mutations "search" space of possible base sequences. The scenario has an overriding problem, however: the size of the combinatorial space (i.e., the number of possible amino acid sequences) and the extreme rarity and isolation of the functional sequences within that space of possibilities. Since natural selection can do nothing to help generate new functional sequences, but rather can only preserve such sequences once they have arisen, chance alone—random variation—must do the work of information generation—that is, of finding the exceedingly rare functional sequences within the set of combinatorial possibilities. Yet the probability of randomly assembling (or "finding," in the previous sense) a functional sequence is extremely small.
All very well for Meyer to write in 2004 perhaps. I do not know though, because I am a mere layman. However, not so excusable for a fellow from the DI to write in 2007.
The above kind of research I have noted, does exactly the kind of thing Meyer requires.
This is not to say that the above mentioned research is widespread and has reached its full potential. As the articles make clear, it is only just underway, thanks to advances in genetic tools and computational analysis.
However, Luskin is wrong – even at the time he wrote his piece. His mocking is simply silly when put into context of the research he claimed or insinuates is not being done.
And given that the Luskin link was given to me as an example of ID science and research, I can offer more papers if needed, showing the role of gene duplication in:-
1) speciation and
2) untangling of a genetic network.
So back to you any YEC or IDer who thinks Luskin’s article was correct:-
1) When he wrote it, it was undermined by earlier work, as I have shown.
2) His quote of Nature simply ignored the remainder of the abstract which, had he read it, should have given him pause for thought.
3) When the context provided by 1) and 2) above is considered, then his mocking about the duplicated sentences reveals an inability to understand what was already happening around him with regards to evolution and genetics.
Regards, Roland
* Another article which described the above two papers I reported:-
Frank J. Poelwijk, Daniel J. Kiviet, Daniel M. Weinreich & Sander J. Tans “Empirical fitness landscapes reveal accessible evolutionary paths”, Nature, 445, 383-386 (25 January 2007)
The Abstract:-
”When attempting to understand evolution, we traditionally rely on analysing evolutionary outcomes, despite the fact that unseen intermediates determine its course. A handful of recent studies has begun to explore these intermediate evolutionary forms, which can be reconstructed in the laboratory. With this first view on empirical evolutionary landscapes, we can now finally start asking why particular evolutionary paths are taken.”
By the way
Here is the link to the above mentioned PLoS article:-
PLoS Computational Biology: Evolutionary Potential of a Duplicated Repressor-Operator Pair: Simulating Pathways Using Mutation Data
Have a scan of it and you will see the kind of stuff that now comes out of research labs.
This is something I am still waiting for any ID advocate to provide.
Grab two genes, any two genes, providing they are look-a-likes in sequence and structure, that the Disc. Inst. has explored, and provide me with the mechanism by which ID made these two look-a-like genes.
Conventional evolutionary theory has been doing this for several years now, despite what Luskin writes. Yet on several occasions I have had ID folk say that ID does a better job at explaining.
Yet they never offer the example, other than to assert that ID offers a better explanation for natural complexity.
They do not know this. It is simply an undemonstrable assertion and at the end of the day, it does not do as Luskin demands, provide an explanation as to how two look-a-like genes came to be.
OTOH, ToE is beginning to provide just such explanations, thanks to recent advances in both technology and the understanding of genetics.
The following link:-
CSC - A Response to Dr. Dawkins' "The Information Challenge"
was supplied to me on another forum as an example of some kind, of ID explanatory power and associated research. (You will see that it is nothing more than a critique of ToE and Dawkins and Darwin.)
In this short essay I am concerned with the section Luskin offers about gene duplication and its role in evolution. While accepting gene duplication, Luskin scorns the idea that it is anything significant in evolution.
The relevant section is “Part 2: Does Gene Duplication Increase Information Content?”. I will not critique the whole of part 2, but rather will stick to those parts I am easily familiar with. Demonstrating Luskin’s errors there should cast reasonable doubt on his ability to be correct elsewhere.
Part 2 begins with the stated aim to show “…why merely citing gene duplication does not help one understand how Darwinian evolution can produce new genetic information.”.
In itself, such an aim is sensible. Merely citing a mechanism does nothing to demonstrate its reality. (Do you understand this IDers and YECs? Just like showing ToE to be wrong, does not show ID to be right. Just like showing Darwin to have been a bank robber, does not show ToE to be wrong.)
However, Luskin falls when he goes on to the following two points:-
1) “Duplicating Genes Doesn't Increase Biological Information in Any Important Sense” and
2) “Darwinists Must Give Detailed Accounts of how a Duplicated Gene Acquires its New Function”
So how does Luskin fall?
At point 1) Luskin mocks evolutionists by implying that they essentially argue that to say a sentence twice is to increase information, because, if a gene duplication adds information, then so must a duplicated sentence. Clearly such a statement about sentences is rubbish, therefore the claim by evolutionists about duplicated genes is rubbish.
But who is really talking the rubbish? As I will show, evolutionists go way beyond this, and they were at the time Luskin wrote his piece.
Luskin tackles point 2) with the following statement:-
“The Darwinist would probably reply to my objection by saying, "Well, it isn't just gene duplication that increases the genetic information — such information is increased when gene duplication is coupled with the subsequent evolution of one of the new copies of the gene." Aye, there's the rub.”
And what is the rub according to Luskin? Well according to him, evolutionists must be able to show, in detail, how either of the pair of duplicated genes can evolve to acquire a new function. Hence he writes:-
“But the new genetic information must somehow be generated during that subsequent evolution of the gene. To explain how Darwinian processes can generate new and meaningful genetic information, Darwinists must provide a detailed account of how a duplicate copy of a gene can evolve into an entirely new gene. But ask Darwinists for details as to how the duplicate copy then starts to perform some new function, and you probably won't get any. At least, Dawkins didn't given us any details (as I explain below) about this in his "The Information Challenge" article, which I am rebutting here.”
And just to show that Dawkins is not alone in being unable to do this, Luskin offers the following sentence from an abstract in Nature
“A recent study in Nature admitted, "Gene duplication and loss is a powerful source of functional innovation. However, the general principles that govern this process are still largely unknown." (Ilan Wapinski, Avi Pfeffer, Nir Friedman & Aviv Regev, "Natural history and evolutionary principles of gene duplication in fungi," Nature, Vol. 449:54-61 (September 6, 2007).) Yet the crucial question that must be answered by the gene duplication mechanism is, exactly how does the duplicate copy acquire an entirely new function? “
So there we have it. Dawkins could not explain how it is done and even Nature admits that this cannot be done. (Don’t you just love that word “admit” when creationists use it?)
THE WHOLE ABSTRACT IS MORE REVEALING THAN LUSKIN LETS ON.
But what did Nature really say about the matter. The abstract (which Luskin quoted from, actually goes as follows:-
”Gene duplication and loss is a powerful source of functional innovation. However, the general principles that govern this process are still largely unknown. With the growing number of sequenced genomes, it is now possible to examine these events in a comprehensive and unbiased manner. Here, we develop a procedure that resolves the evolutionary history of all genes in a large group of species. We apply our procedure to seventeen fungal genomes to create a genome-wide catalogue of gene trees that determine precise orthology and paralogy relations across these species. We show that gene duplication and loss is highly constrained by the functional properties and interacting partners of genes. In particular, stress-related genes exhibit many duplications and losses, whereas growth-related genes show selection against such changes. Whole-genome duplication circumvents this constraint and relaxes the dichotomy, resulting in an expanded functional scope of gene duplication. By characterizing the functional fate of duplicate genes we show that duplicated genes rarely diverge with respect to biochemical function, but typically diverge with respect to regulatory control. Surprisingly, paralogous modules of genes rarely arise, even after whole-genome duplication. Rather, gene duplication may drive the modularization of functional networks through specialization, thereby disentangling cellular systems.”
Now a read of the above will reveal that the aticle to follow is from people who are beginning to work things out, and after having done their research, it is not as if they still have no ideas.
If you doubt me YECs and IDers then read the darn abstract for once, and think about the wording on offer.
BUT RESEARCHERS WERE ALREADY BEGINNING TO DO WHAT LUSKIN DENIES
But what is worse for Luskin, is that he wrote his article late 2007, months after the above mentioned research. However in earlier years one could already find several articles dealing with blow by blow descriptions of plausible mechanistic details by which new functionality in duplicated genes evolved. How were the mechanisms made plausible? Well the researchers tested the ideas in their laboratories.
Yet according to Luskin, this was not happening. Dawkins admitted to it and so did Nature.
Here are a couple of those papers Lusking implicitly claims do not exist. (Note the dates, all before 2007? And even though gene duplication may not be mentioned, they are about what happened following such events. I read the Nature article reporting on them*):-
1) Jamie T. Bridgham, Sean M. Carroll, Joseph W. Thornton, “Evolution of Hormone-Receptor Complexity by Molecular Exploitation”, Science, 312, 7-April-2006, pages 97-101.
The abstract is:-
According to Darwinian theory, complexity evolves by a stepwise process of elaboration and optimization under natural selection. Biological systems composed of tightly integrated parts seem to challenge this view, because it is not obvious how any element's function can be selected for unless the partners with which it interacts are already present. Here we demonstrate how an integrated molecular system—the specific functional interaction between the steroid hormone aldosterone and its partner the mineralocorticoid receptor—evolved by a stepwise Darwinian process. Using ancestral gene resurrection, we show that, long before the hormone evolved, the receptor's affinity for aldosterone was present as a structural by-product of its partnership with chemically similar, more ancient ligands. Introducing two amino acid changes into the ancestral sequence recapitulates the evolution of present-day receptor specificity. Our results indicate that tight interactions can evolve by molecular exploitation—recruitment of an older molecule, previously constrained for a different role, into a new functional complex.
The whole paper is concerned with what happened following a gene duplication.
2) Poelwijk FJ, Kiviet DJ, and Tans SJ, “Evolutionary potential of a duplicated repressor-operator pair: simulating pathways using mutation data.”, PLoS computational biology 2(5):e58, 2006 May -
The abstract is:-
Ample evidence has accumulated for the evolutionary importance of duplication events. However, little is known about the ensuing step-by-step divergence process and the selective conditions that allow it to progress. Here we present a computational study on the divergence of two repressors after duplication. A central feature of our approach is that intermediate phenotypes can be quantified through the use of in vivo measured repression strengths of Escherichia coli lac mutants. Evolutionary pathways are constructed by multiple rounds of single base pair substitutions and selection for tight and independent binding. Our analysis indicates that when a duplicated repressor co-diverges together with its binding site, the fitness landscape allows funneling to a new regulatory interaction with early increases in fitness. We find that neutral mutations do not play an essential role, which is important for substantial divergence probabilities. By varying the selective pressure we can pinpoint the necessary ingredients for the observed divergence. Our findings underscore the importance of coevolutionary mechanisms in regulatory networks, and should be relevant for the evolution of protein-DNA as well as protein-protein interactions.
The above abstracts give the clue. The following articles are all about mechanism following gene duplication, and how this leads to new function. AND GUESS WHAT? THEY EVEN BOTHER TO WRITE THESE ARTICLES BASED ON ACTUAL LABORATORY RESEARCH.
QUOTING MEYER
Luskin goes on to quote Steven Meyer, "The origin of biological information and the higher taxonomic categories," Proceedings for the Biological Society of Washington, Vol. 117(2):213-239 (2004):-
This scenario has the advantage of allowing the genome to vary through many generations, as mutations "search" space of possible base sequences. The scenario has an overriding problem, however: the size of the combinatorial space (i.e., the number of possible amino acid sequences) and the extreme rarity and isolation of the functional sequences within that space of possibilities. Since natural selection can do nothing to help generate new functional sequences, but rather can only preserve such sequences once they have arisen, chance alone—random variation—must do the work of information generation—that is, of finding the exceedingly rare functional sequences within the set of combinatorial possibilities. Yet the probability of randomly assembling (or "finding," in the previous sense) a functional sequence is extremely small.
All very well for Meyer to write in 2004 perhaps. I do not know though, because I am a mere layman. However, not so excusable for a fellow from the DI to write in 2007.
The above kind of research I have noted, does exactly the kind of thing Meyer requires.
This is not to say that the above mentioned research is widespread and has reached its full potential. As the articles make clear, it is only just underway, thanks to advances in genetic tools and computational analysis.
However, Luskin is wrong – even at the time he wrote his piece. His mocking is simply silly when put into context of the research he claimed or insinuates is not being done.
And given that the Luskin link was given to me as an example of ID science and research, I can offer more papers if needed, showing the role of gene duplication in:-
1) speciation and
2) untangling of a genetic network.
So back to you any YEC or IDer who thinks Luskin’s article was correct:-
1) When he wrote it, it was undermined by earlier work, as I have shown.
2) His quote of Nature simply ignored the remainder of the abstract which, had he read it, should have given him pause for thought.
3) When the context provided by 1) and 2) above is considered, then his mocking about the duplicated sentences reveals an inability to understand what was already happening around him with regards to evolution and genetics.
Regards, Roland
* Another article which described the above two papers I reported:-
Frank J. Poelwijk, Daniel J. Kiviet, Daniel M. Weinreich & Sander J. Tans “Empirical fitness landscapes reveal accessible evolutionary paths”, Nature, 445, 383-386 (25 January 2007)
The Abstract:-
”When attempting to understand evolution, we traditionally rely on analysing evolutionary outcomes, despite the fact that unseen intermediates determine its course. A handful of recent studies has begun to explore these intermediate evolutionary forms, which can be reconstructed in the laboratory. With this first view on empirical evolutionary landscapes, we can now finally start asking why particular evolutionary paths are taken.”
By the way
Here is the link to the above mentioned PLoS article:-
PLoS Computational Biology: Evolutionary Potential of a Duplicated Repressor-Operator Pair: Simulating Pathways Using Mutation Data
Have a scan of it and you will see the kind of stuff that now comes out of research labs.
This is something I am still waiting for any ID advocate to provide.
Grab two genes, any two genes, providing they are look-a-likes in sequence and structure, that the Disc. Inst. has explored, and provide me with the mechanism by which ID made these two look-a-like genes.
Conventional evolutionary theory has been doing this for several years now, despite what Luskin writes. Yet on several occasions I have had ID folk say that ID does a better job at explaining.
Yet they never offer the example, other than to assert that ID offers a better explanation for natural complexity.
They do not know this. It is simply an undemonstrable assertion and at the end of the day, it does not do as Luskin demands, provide an explanation as to how two look-a-like genes came to be.
OTOH, ToE is beginning to provide just such explanations, thanks to recent advances in both technology and the understanding of genetics.
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