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Author
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Topic: Testable ID hypothesis
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mturner
Member
Member # 190
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posted 28. September 2002 06:12
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quote:
Take the worm C. elegans. You can induce mutations in the genome of elegans by radiation or chemical mutagenesis. This leads to a vast enhancement in the generation of biological novelties. This can be a selection protocol- e.g. enabling elegans to grow in adverse thermal, biological or chemical conditions. These mutants simply are not found in normal populations.
Thus random mutation does lead to the creation of biological novelty.
yours
per
Hi per,
Please point me to links where it can be verified that such "enhancements", (by which I suppose you to mean, 'adaptive organismic novelties'), were randomly/stochastically, (as opposed to intelligently/heuristically), engendered.
This would be the first example I have ever come across where any genetic mutation, induced by a genomic alteration brought on by an externally applied, randomly operating, mutagen, resulted in an adaptive organismic novelty. That is, one which was engendered without a specific artificial selection criterion ("protocol"?) being maintained over generations by human intelligence, (as this would turn it into an heuristic teleological process).
To avoid this, I think your example would have to demonstrate an *immediate*, single generation, adaptive organismic innovation resulting directly and solely from randomly applied mutagens.
More importantly, you would have to *demonstrate*, not merely assume, that any adaptive organismic novelty arose from an 'indirect' action of a mutagen upon the genome, and not from a 'direct', (that is, ecological), action of an artificially created environment upon the organism itself. To do that you would have to note specific organismic alterations in individuals that clearly are the result of genetic mutation brought on by your randomly operating mutagens, and then randomly insert these various individuals into several ecologically unfamiliar artificial environments in order to see if any of these 'originals' are, in fact, *immediately* better adapted to their new environment/s than the 'old-fashioned' organism is, in their place.
Unless your example can do this, I'm afraid it proves nothing in support of 'randomness' as a mechanism for adaptive novelty. It would only be another instance of intelligently directed, teleological modification. (The 'intelligence' being found either in the human experimenter, or in the organism itself, or both.)
Thanks,
mturner
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Frances
Member
Member # 169
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posted 28. September 2002 06:31
Mturner,
YOu seem to overlook another possibility, the 'intelligence' of the environment of the organism enforcing a selective pressure.
In fact all the parts of the Neo-Darwinian theory have been subjected to observation and testing. And these observations and tests all support the theory. Mutations, variation, selection all have been found to act in nature. Any experiment requires intelligence thus that seems an easy way of rejecting science but imho not very convincing. For instance the c-elegans experiments make it hard to argue that the mutations were selectively applied. Through selection some of the ''lucky'' mutations spread more quickly through the population than others.
Mutations, selection all are very well known and observed facts.
What also would be helpful is if you could show any evidence supporting an alternative hypothesis and show that this hypothesis explains the observations better.
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peroxisome
unregistered
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posted 28. September 2002 13:17
quote:
Please point me to links where it can be verified that such "enhancements", (by which I suppose you to mean, 'adaptive organismic novelties'), were randomly/stochastically, (as opposed to intelligently/heuristically), engendered.
Well, the answer is no, because I cannot be bothered to go find the original references. However, I will tell you that it is straightforward textbook biology that both radiation and chemical mutagens interact randomly with DNA to produce mutations. Each mutagen has its own spectrum of mutations (e.g. strand breaks, deletions, nucleotide preference), and areas of the genome that are less affected, but the mutations are fairly random within these constraints.
The phenotypes result directly from these random mutations in the genome. I really don't understand how you can make any case that this is a non-random process.
quote:
To avoid this, I think your example would have to demonstrate an *immediate*, single generation, adaptive organismic innovation resulting directly and solely from randomly applied mutagens.
this is of course a difficult barrier to jump. Mutations are normally heterozygous and recessive, and so require multiple generations of breeding to see the recessive phenotype.
quote:
More importantly, you would have to *demonstrate*, not merely assume, that any adaptive organismic novelty arose from an 'indirect' action of a mutagen upon the genome, and not from a 'direct', (that is, ecological), action of an artificially created environment upon the organism itself. To do that you would have to note specific organismic alterations in individuals that clearly are the result of genetic mutation brought on by your randomly operating mutagens, and then randomly insert these various individuals into several ecologically unfamiliar artificial environments in order to see if any of these 'originals' are, in fact, *immediately* better adapted to their new environment/s than the 'old-fashioned' organism is, in their place.
I find some of the concepts here difficult. The mutations arise from a direct interaction of mutagen on the genome, leading to a gene mutation. This seems to be a direct action on the genome. It does not arise from the environment, because you have to demonstrate first that the selection procedure completely discriminates against wild-type worms.
I don't see the point of putting individuals randomly into different environments; but the experiment has been done anyway. People make large deletion libraries of elegans. These are stored, and people phone up, and test the library against all sorts of environments. Sometimes you find a mutant phenotype, sometimes you don't...
Anyways, I really don't understand your case. The radiation/ chemical induces mutations randomly. You sort the library until you find a mutant worm that survives in your circumstances of interest. You isolate the mutation, and demonstrate the mutation/ deletion that leads to the phenotype. You can easily demonstrate that it is the deletion that leads to the phenotype. The only question is whether radiation/ chemicals act stochastically, and that's clear.
yours
per
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Berthajane Vandegrift
Member
Member # 272
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posted 28. September 2002 14:26
First, I want to apologize for confusing Eva Jablonka’s name as “Jablonski“. earlier in this thread. The following article discusses some of the scientific details that would be involved if evolution were viewed as a process of adaptive change in living organisms -- rather than being viewed as accidental, meaningless changes in a genome. This teleological approach is new, and if it is not valid the research will eventually show that. However, I predict that more and more evidence of directed mutation and epigenetic inheritance will be confirmed. (Thanks to mturner for the article.)
Berthajane Vandegrift
http://www.wikipedia.org/wiki/Epigenetic_inheritance
excerpt
The source of the variation that is necessary in Darwin's theory of evolution is the random variation in the sequence of the DNA bases that constitute the genes. The environment can influence these variations slightly (for example, radioactivity is known to influence the structure of DNA), but only in a random manner.
In recent years, however, scientists are realising the role of the environment in the story of life has been underrated. Some stressful conditions lead to mutations that are adaptive to the environment inducing them.
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peroxisome
unregistered
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posted 28. September 2002 15:11
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Some stressful conditions lead to mutations that are adaptive to the environment inducing them.
you could give as an example here the RAG recombinase system which cause somatic mutation in antibody producing cells, thereby allowing for somatic selection of cells with high-affinity antibody for a particular antigen. Some of these examples are quite well known.
cheers
per
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charlie d.
Member
Member # 159
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posted 28. September 2002 15:49
quote:
In recent years, however, scientists are realising the role of the environment in the story of life has been underrated. Some stressful conditions lead to mutations that are adaptive to the environment inducing them.
Augh, how many times have references to the list of articles which debunk "directed" mutations appeared here and at ARN? Why don't people seem to notice? Do they think that evidence simply disappears, if it's repeatedly ignored? This is getting really tedious.
Patricia Foster, one of the original Cairns collaborators, has written already in 1998 a review of the issue (tellingly titled "Has the Unicorn landed?") that basically turns out the lights on the "lamarckism" of stationary-phase mutations for good. Here's an excerpt: quote:
IN 1988, JOHN CAIRNS and his collaborators published an article entitled "The Origin of Mutants" (CAIRNS et al. 1988 ) that has changed our thinking about how spontaneous mutations arise. Drawing upon their own and others' results, they argued that mutations arise in nondividing bacterial cells subjected to nonlethal selective pressure. Additional evidence suggested that only selected mutations, not deleterious or neutral mutations, appeared in a population during selection. Obviously, this phenomenon would have profound implications for evolution and for carcinogenesis. In 1989, CAIRNS and I began a collaboration to further study the phenomenon, which was dubbed "directed mutation" by the editors of Nature and "a unicorn in the garden" by STAHL 1988 .
Early in the project, we established that the mutational process was not "directed" toward specific targets (i.e., there was no reverse information flow) (FOSTER and CAIRNS 1992 ), and we renamed the phenomenon "adaptive mutation" (FOSTER 1993 ). ...
Because nonselected mutations arise and persist in the population during selection, a stress-associated general mutational state, strictly speaking, does not meet the original definition of adaptive mutation. However, here I will continue to call the selected mutations "adaptive" to distinguish them from mutations occurring during nonselective growth and from nonselected mutations occurring during selection. This meaning of "adaptive mutation" is the same as that used by evolutionists to distinguish beneficial from neutral or deleterious mutations. [my emphasis]
Recently, much progress has been made into defining the actual process underlying "adaptive" mutations in bacteria:
Hendrickson H, Slechta ES, Bergthorsson U, Andersson DI, Roth JR. Amplification-mutagenesis: evidence that "directed" adaptive mutation and general hypermutability result from growth with a selected gene amplification. Proc Natl Acad Sci U S A. 2002 99:2164-9, and references therein.
quote:
When a particular lac mutant of Escherichia coli starves in the presence of lactose, nongrowing cells appear to direct mutations preferentially to sites that allow growth (adaptive mutation). This observation suggested that growth limitation stimulates mutability. Evidence is provided here that this behavior is actually caused by a standard Darwinian process in which natural selection acts in three sequential steps.
Finally, I would caution everybody to take Wikipedia with a grain of salt. Although it's an interesting project, as an "open" encyclopedia it is very prone to errors and mischaracterizations.
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charlie d.
Member
Member # 159
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posted 28. September 2002 15:51
quote:
In recent years, however, scientists are realising the role of the environment in the story of life has been underrated. Some stressful conditions lead to mutations that are adaptive to the environment inducing them.
Augh, how many times have references to the list of articles which debunk "directed" mutations appeared here and at ARN? Why don't people seem to notice? Does evidence simply disappear, if it's repeatedly ignored? This is getting really tedious.
Patricia Foster, one of the original Cairns collaborators, has written already in 1998 a review of the issue (tellingly titled "Has the Unicorn landed?") that basically turns out the lights on the "lamarckism" of stationary-phase mutations for good. Here's an excerpt: quote:
IN 1988, JOHN CAIRNS and his collaborators published an article entitled "The Origin of Mutants" (CAIRNS et al. 1988 ) that has changed our thinking about how spontaneous mutations arise. Drawing upon their own and others' results, they argued that mutations arise in nondividing bacterial cells subjected to nonlethal selective pressure. Additional evidence suggested that only selected mutations, not deleterious or neutral mutations, appeared in a population during selection. Obviously, this phenomenon would have profound implications for evolution and for carcinogenesis. In 1989, CAIRNS and I began a collaboration to further study the phenomenon, which was dubbed "directed mutation" by the editors of Nature and "a unicorn in the garden" by STAHL 1988 .
Early in the project, we established that the mutational process was not "directed" toward specific targets (i.e., there was no reverse information flow) (FOSTER and CAIRNS 1992 ), and we renamed the phenomenon "adaptive mutation" (FOSTER 1993 ). ...
Because nonselected mutations arise and persist in the population during selection, a stress-associated general mutational state, strictly speaking, does not meet the original definition of adaptive mutation. However, here I will continue to call the selected mutations "adaptive" to distinguish them from mutations occurring during nonselective growth and from nonselected mutations occurring during selection. This meaning of "adaptive mutation" is the same as that used by evolutionists to distinguish beneficial from neutral or deleterious mutations. [my emphasis]
Recently, much progress has been made into defining the actual process underlying "adaptive" mutations in bacteria:
Hendrickson H, Slechta ES, Bergthorsson U, Andersson DI, Roth JR. Amplification-mutagenesis: evidence that "directed" adaptive mutation and general hypermutability result from growth with a selected gene amplification. Proc Natl Acad Sci U S A. 2002 99:2164-9, and references therein.
quote:
When a particular lac mutant of Escherichia coli starves in the presence of lactose, nongrowing cells appear to direct mutations preferentially to sites that allow growth (adaptive mutation). This observation suggested that growth limitation stimulates mutability. Evidence is provided here that this behavior is actually caused by a standard Darwinian process in which natural selection acts in three sequential steps.
Finally, I would caution everybody to take Wikipedia with a grain of salt. Although it's an interesting project, as an "open" encyclopedia it is very prone to errors and mischaracterizations.
[ 28. September 2002, 22:05: Message edited by: charlie d. ]
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mturner
Member
Member # 190
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posted 28. September 2002 17:12
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peroxisome
quote:
Well, the answer is no, because I cannot be bothered to go find the original references.
**
I expected as much.
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However, I will tell you that it is straightforward textbook biology that both radiation and chemical mutagens interact randomly with DNA to produce mutations.
**
Yes, we all know that. Just as we all know that if you hit a man's knee with a baseball bat, you will alter his manner of locomotion. We have, after more than 70 years of chemical and radioactive mutagens, nothing more than horribly deformed fruitflies and other poor creatures to show for it. Unless your claim re 'c. elegans' is true. But then, you can't be bothered proving it's true, can you?
quote:
Each mutagen has its own spectrum of mutations (e.g. strand breaks, deletions, nucleotide preference), and areas of the genome that are less affected, but the mutations are fairly random within these constraints.
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Hmmm!?! "spectrum", "area", "constraints"!!??!!
"fairly random"?? Sorry, but this does not fit my definition of stochastic "randomness". Sounds pretty darn 'selected and directed', to me. Purely artificial. Like Darwin's pigeon breeding.
quote:
this is of course a difficult barrier to jump. Mutations are normally heterozygous and recessive, and so require multiple generations of breeding to see the recessive phenotype.
**
Yes, it is a difficult barrier to jump. But unless and until you jump it, you have no stochastic randomness producing viable adaptations. You have nothing but an unsupported assumption, and that's not science, that's "faith". Or you have, as I keep repeating, artificial "breeding", which has nothing to do with 'randomness', by very definition.
quote:
The only question is whether radiation/ chemicals act stochastically, and that's clear.
**
No, that is certainly not "the only question". Let me see if I can rephrase the question so that you can understand it. It is this. Do you have proof that your assertion that a purely stochastic, random application of mutagens to the genome of the worm 'c.elegans' can produce, directly and immediately, in the next generation, mutant varieties of 'c.elegans' that are better adapted to certain strange, (to them), environments than the untreated, unmodified variety? You've already admitted that your mutagens are not applied with true stochastic randomness, so your example has already been refuted and discarded.
Further to that, if you ever do find a purely stochastic application of mutagens to a genome, you will still have to *prove* that that random mutation was the sole and only causal agent responsible for any *** viably adaptive*** organismic mutation, and in order to do that you must eliminate any possibility of 'intelligence' as a causal agent; be that 'intelligence' endogenous or exogenous to the organism itself. Any experiment which fails to do this is worthless to your pro 'stochastic randomness as *the* causal agent for viable organismic adatations' argument. You are left shouting an empty assertion of blind faith. Much like a muezzin in his minaret. Or any other religious proclamation.
mturner
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mturner
Member
Member # 190
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posted 28. September 2002 17:44
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charley d.
quote:
Finally, I would caution everybody to take Wikipedia with a grain of salt. Although it's an interesting project, as an "open" encyclopedia it is very prone to errors and mischaracterizations.
**
Hi chuck;
More ad hom arguments? I would caution everybody to take your tendencious assessment with a grain of salt, and I would urge you to deal directly with the material, instead of merely maligning the source.
As for the rest of your post, it is getting truly tiresome to hear you make the same empty argument over and over again. When are you going to catch on to the fact that 'description' is not 'explanation', and that 'behaviour' is not automatically, 'cause', but just as easily, 'effect'? Whether you like it or not, the observed phenomenon is quite simply this:
Ecological imbalance between an organism and its environment that is chronic and life-threatening may induce organismic mutation in that particular organism which may enable it to generate a viable adaptation to the specific alteration in its environment, thus restoring its ecological balance.
That is quite simply not RM&NS. That is not stochastic randomness. Why do you keep pretending that it is?
mturner
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charlie d.
Member
Member # 159
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posted 28. September 2002 18:52
mturner,
Either the mutations occurring in the bacterial genome during these experiments are random wrt to fitness (increased as their rate may be), or they aren't. Scientists have looked, and the mutations fall pretty much everywhere, striking adaptive sites and non-adaptive sites alike. The mutations are random. Random mutations happen to strike adaptive sites at low frequency, and the bacteria with random mutations that happen to be adaptive survive. Ergo, random mutations can be adaptive, just like darwinian mechanisms posit. Simple as that. The Unicorn has landed.
I'll pass on the rest, this is supposed to be a serious forum.
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peroxisome
unregistered
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posted 28. September 2002 20:04
Dear mturner
I am really unsure of what you are trying to argue. You seem to accept that radiation and chemical carcinogens act randomly to mutate DNA ("yes we all know that"). Then you suggest that the action of mutagens is 'selected and directed'. These viewpoints seem discordant.
I am not clear what you mean by random. Benzo(a)pyrene- for example- principally results in point mutations in G residues. However, it attacks all G residues in DNA. Although chemical reactions with other nucleotides are less important for mutagenesis, mutations are induced in individual genes by Benzo(a)pyrene in a random manner.
If you think that the RM&NS paradigm specifically involves mutations at an equal rate at all four residues, then I have to say that this is not a perception shared by biologists or chemists.
If you want examples of C elegans being used for selection, this is again textbook stuff. Try C elegans by Wood et al., but any elegans textbook should explain this to you. For a live example, try: (A neomorphic syntaxin mutation blocks volatile-anesthetic action in Caenorhabditis elegans. van Swinderen B, et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 96 (5): 2479-2484 MAR 2 1999)
quote:
I think your example would have to demonstrate an *immediate*, single generation, adaptive organismic innovation resulting directly and solely from randomly applied mutagens.
I am even more befuddled by your requirement for instant adaptations. As I explained, mutations are heterozygous, and typically recessive. Nonetheless, the genetic mutant is present in the F1 generation. The mutant will be seen in just one generation further on- the homozygous F2. This is conventional Mendelian genetics, it has been known for hundreds of years. Do you understand Mendelian genetics ? Do you understand what a recessive, or dominant, is ? It is not, contrary to your suggestion, selective breeding. What is more, your contention makes no sense; the RM&NS theory makes no reference to genes only working on heterozygotes, or excluding recessive characteristics.
It is also trivially easy to prove ( or ***PROVE***) that the mutagenesis protocol is necessary for the mutation; no mutagenesis protocol, and the number of mutants is drastically reduced. The mutation is responsible for the phenotype.
So what I am saying is, to repeat:
1) radiation or chemical mutagens produce mutations in individual genes in a *random* manner
2) the resulting mutants are seen in a homozygous state in the *******F2 generation *******
3) the mutagenesis procedure is **solely** and ***directly*** responsible for the induction of the mutations
4) the selection protocol is not necessary for the generation of homozygous mutants !!!!!!!
I hope the punctuation helps you
per
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Moderator
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Member # 1
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posted 28. September 2002 21:20
2 warnings:
1. A general warning that this thread is quickly slipping.
2. A warning to mturner for fostering hostility. If it continues, you will be banned for 30 days.
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mturner
Member
Member # 190
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posted 28. September 2002 22:20
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I'm sorry that the moderator thinks that I am the one "fostering hostility". I admit that I do have a bad habit of returning stroke for stroke. Therefore I will erase my response to charlie d.
mturner
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mturner
Member
Member # 190
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posted 28. September 2002 22:36
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Same goes double for peroxisome. Somehow his posts strike me as "fostering hostility", but then, that's only my opinion. Probably nobody else sees it that way. At least, no moderators, since neither he nor charley were given warnings.
Thats fine. I don't like debating people with 'attitude' anyway, especially when that 'attitude' is invisible to the moderators.
I'll just go back to reading the opinions of intelligent, articulate posters, and forget about debating the others.
mturner
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