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Member (Idle past 2960 days) Posts: 706 From: Joliet, il, USA Joined: |
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Author | Topic: Does the Darwinian theory require modification or replacement? | |||||||||||||||||||||||||||
NoNukes Inactive Member |
The following quote from Dr. Wright's paper makes clear that Dr. Wright is merely describing a Lamarckian (and naturalistic) modification to Neo-Darwinistic evolution.
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jar Member (Idle past 420 days) Posts: 34026 From: Texas!! Joined: |
shadow71 writes: jar writes;
What utter crap you post. First, as has been pointed out to you several times, this has absolutely nothing to do with religion or atheism and certainly nothing to do with Christianity Have you missed the many posts that ridicule "creationists"? There are many on this board that hold the belief that anyone who opposes the modern synthesis, do so on religious beliefs, and therefore must be ridiculed and dismissed as believers and therefore not intelligent assayers of the theory. Did you say:
quote: You really can't get anything straight can you? YOU inserted religion and even said that you began with the conclusion. YOUR posts are more than enough to prove beyond a shadow of a doubt that Creationism and Intelligent Design are NOT science but only an attempt to palm the pea, con the rube, sell the snake oil. The fact is, the Theory of Evolution has been modified and will continue to be modified when the weight of evidence warrants it. But YOU seem to start with the conclusion you want and then try to find support for your position. Sorry Charlie, that is NOT how science works. Anyone so limited that they can only spell a word one way is severely handicapped!
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Wounded King Member Posts: 4149 From: Cincinnati, Ohio, USA Joined: |
When you are talking about bacteria then pretty much everything is lamarckian since there is only a single cell involved. A mutation in the main chromosomal DNA of the cell will have as much effect as a mutation during mitosis wuld on the daughter cell.
In a very real sense the majority of bacterial evolution is Lamarckian. It is only with the establishment of a germline/soma distinction that offspring stop inheriting virtually all the mutations that their parent organisms acquired. TTFN, WK
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jar Member (Idle past 420 days) Posts: 34026 From: Texas!! Joined: |
As I said back in Message 3 this thread seems to be pretty much pointless from the git-go, but that doesn't mean that I can't learn from the posts even if they are unrelated to the topic.
So I have a few questions. Looking at sexual critters ... mutations happen. In some cases, for example under stress, mutation rates increase. BUT, those mutations are only selected in the next generation. Now at the next generation the selection filter may or may not be the same as what caused the mutation rate increase. Is that correct so far? Anyone so limited that they can only spell a word one way is severely handicapped!
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NoNukes Inactive Member |
Wounded King writes: In a very real sense the majority of bacterial evolution is Lamarckian. It is only with the establishment of a germline/soma distinction that offspring stop inheriting virtually all the mutations that their parent organisms acquired.WK Thanks WK, that's helpful information. What I don't understand is why Wright and Shapiro believe that their peers are resistant to those concepts? I also find hard find it hard to understand how the mechanisms discussed by Dr. Wright can explain the evolution of the sophisticated organs in animals. Lamarckian changes in animals shouldn't end up in their offspring. Dr. Wright's paper says the following:
quote: Yet it would not seem that anything she says would be helpful in speeding the formation of a human eye.
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Wounded King Member Posts: 4149 From: Cincinnati, Ohio, USA Joined: |
Hey Jar,
The thing is there is actually very little in the way of evidence that these mechanisms operate in most sexual organisms, certainly in most metazoa. We can certainly see the effects of transposable elements in mammalian genomes, for instance, and the inherent mutational biases and hotspots are apparent. But there is no equivalent stress response which would affect the mutational spectrum of germline cells. The closest thing is perhaps the effect that heat shock can have in some organisms, Fly (Rutherford and Lindquist, 1998) and C. elegans are the model most work has been done on, which can reveal previously hidden conditional mutations. But in this case the stress response is revealing the mutations to natural selection, by removing normally present stabilising elements, rather than modifying the mutation rate. TTFN, WK Edited by Wounded King, : No reason given.
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Dr Adequate Member (Idle past 311 days) Posts: 16113 Joined: |
In a very real sense the majority of bacterial evolution is Lamarckian. It is only with the establishment of a germline/soma distinction that offspring stop inheriting virtually all the mutations that their parent organisms acquired. But Lamarckism does not merely require that somatic changes should also be changes in the germ-line; it also requires that they should be reactive adaptations to the environment.
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Dr Adequate Member (Idle past 311 days) Posts: 16113 Joined: |
I admit that I accept the work of Shapiro, a world renown molecular biologist at the University of Chicago, who happens to be outfront of the old dogma defenders of a theory that is being devasted by molecular biology discoveries. ("Devastated", of course, in a way that has gone completely unnoticed by molecular biologists.)
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Dr Adequate Member (Idle past 311 days) Posts: 16113 Joined: |
And pray tell how does the enviroment direct in a random world? A moot question, since we don't live in one.
Non-random means directed or planned. Of course not, don't be silly.
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jar Member (Idle past 420 days) Posts: 34026 From: Texas!! Joined: |
So is what is being discussed (Shapiro and inferences based on Shapiro) unrelated to sexual organisms from the git-go?
Anyone so limited that they can only spell a word one way is severely handicapped!
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Taq Member Posts: 10073 Joined: Member Rating: 5.2 |
It says that the feedback is sensitive and directed, and that it might facilitate and accelerate the ADAPATION OF ORGANISMS TO NEW ENVIROMENTS. The facilitation and acceleration is due to the increase in the random mutation rate, including random transposon mutagenesis which can have more of an effect on gene regulation than point mutations.
That means that the mutations are sensitive and directed for non-random fitness. No, it doesn't. Your lack of scientific knowledge is causing you to read things into the conclusions that aren't there. The rate and timing of mutations is non-random, but the mutations themselves are still random with respect to fitness.
It is mysterious in that nature per the theory is not non-random and directed for fitness. We scientists have this strange monster to deal with. It's called data. All of the data demonstrates that mutations are random with respect to fitness. When transposon mutagenesis is induced (per Shapiro and Wright) these transposons insert all over the genome with no mind towards what will benefit or hurt the organism. That is what makes them random.
And pray tell how does the enviroment direct in a random world? Random in what respect? Again, you need to phrase random with respect to something in order for it to make sense.
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Taq Member Posts: 10073 Joined: Member Rating: 5.2 |
How can anyone challenge our precious modern systhesis beliefs which we accept as dogma?
You could actually present the data from experiments. That would be a refreshing change in tactics. You know, do some actual science instead of lawyering.
I admit that I accept the work of Shapiro, How can you accept something that you don't understand? What is this work? Can you please point to the data that Shapiro has produced which demonstrates nonrandom mutations with respect to fitness? No more "I read his conclusions". I want to see you present the data, figures, and tables found in the results section of his papers and show us how these results point to nonrandom mutations with respect to fitness.
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Wounded King Member Posts: 4149 From: Cincinnati, Ohio, USA Joined: |
Not necessarily, it is just that there is no evidence for such mechanisms operating in metazoa, and such mechanisms would need a radically different operation in large multicellular organisms compared to unicellular ones.
If we look at Wright's mechanism for instance it rapidly becomes clear that in an organisms with a sequestered germline you aren't going to see the same interaction of genome to environment in terms of de-repression of genes in response to a challenge. Consequently the bias for mutations in transcriptionally active sites will not be towards metabolic genes triggered by the response. Instead we might expect to see a pattern of bias towards genes transcriptionally active in germline development and early embryonic development. Such genes would be likely to affect survival of the particular cell lineage in which a mutation arose and, arising early, such a lineage would be likely to have a chance of contributing substantially to the germline. TTFN, WK
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jar Member (Idle past 420 days) Posts: 34026 From: Texas!! Joined: |
Wounded King writes: Not necessarily, it is just that there is no evidence for such mechanisms operating in metazoa, and such mechanisms would need a radically different operation in large multicellular organisms compared to unicellular ones. If we look at Wright's mechanism for instance it rapidly becomes clear that in an organisms with a sequestered germline you aren't going to see the same interaction of genome to environment in terms of de-repression of genes in response to a challenge. Consequently the bias for mutations in transcriptionally active sites will not be towards metabolic genes triggered by the response. Instead we might expect to see a pattern of bias towards genes transcriptionally active in germline development and early embryonic development. Such genes would be likely to affect survival of the particular cell lineage in which a mutation arose and, arising early, such a lineage would be likely to have a chance of contributing substantially to the germline. TTFN, WK When you say "Such genes would be likely to affect survival of the particular cell lineage in which a mutation arose and, arising early, such a lineage would be likely to have a chance of contributing substantially to the germline.", does that mean only an increased chance for survival or do you mean that those changes that happen to be towards increased survival will have a greater chance of contributing substantially to the germline? Anyone so limited that they can only spell a word one way is severely handicapped!
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Wounded King Member Posts: 4149 From: Cincinnati, Ohio, USA Joined: |
does that mean only an increased chance for survival or do you mean that those changes that happen to be towards increased survival will have a greater chance of contributing substantially to the germline? Neither really, what I meant was that mutations occurring at such early embryonic stages, say pre-gastrulation for example, have a good chance of contributing significantly to the germline cells. Also since those early embryonic stages can be quite sensitive to mutation there would be strong negative selection against deleterious mutants occurring at that stage. So if transcriptionally active/derepressed genes are more liable to mutation then at these early stages that bias would be towards genes associated with early development which are prime candidates for being subject to strong selective pressures due to the sensitivity of early development. TTFN, WK
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