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Author | Topic: About New Lamarckian Synthesis Theory | |||||||||||||||||||||||||||||||||||||||
zi ko Member (Idle past 3650 days) Posts: 578 Joined: |
Then what are they related to?
We have in front of us the reality of life.This is what they are related to.
So guided mutations are indistinguishable from random mutations? And here you are accusing random mutations of being unfalsifiable. It appears that it is guided mutations that are unfalsifiable.
Random and guided mutations are equally unfalsifiable. Your example of falcification of random mutatations could easily be used to falsify guided mutations as well, unless you could bring reliable works favoring randomness about time needed to have the present life diversity. Edited by zi ko, : No reason given.
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dayalanand roy Junior Member (Idle past 3615 days) Posts: 18 Joined: |
I am extremely grateful to you for following my all posts, even if you don't find anything noticeable in them. I am further grateful to you for pointing out my problem. I would love to keep in touch with you.
deepest regards. dayala
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Taq Member Posts: 10085 Joined: Member Rating: 5.6
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We have in front of us the reality of life.This is what they are related to. So mutations are guided with respect to life? What does that even mean?
Random and guided mutations are equally unfalsifiable. I spent an entire paragraph demonstrating that random mutations (with respect to fitness) are falsifiable. Perhaps you could do the honest thing and actually address what I said? Are are you saying that random mutations are unfalsifiable simply because you say so?
Your example of falcification of random mutatations could easily be used to falsify guided mutations as well, Why? Because you say so?
unless you could bring reliable works favoring randomness about time needed to have the present life diversity. Already did that in multiple posts. I discussed the Luria-Delbruck flucutation test, the Lederberg's plate replica experiment, and the pocket mice. You ignored all of it and just kept claiming that mutations are guided without ever addressing the points that I made. Your entire argument boils down to "mutations are guided because zi ko says so".
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zi ko Member (Idle past 3650 days) Posts: 578 Joined: |
So mutations are guided with respect to life? What does that even mean?
You talk about mutations not related to fitness. I talk about mutations related to the reality of life.
I spent an entire paragraph demonstrating that random mutations (with respect to fitness) are falsifiable. Perhaps you could do the honest thing and actually address what I said? Are are you saying that random mutations are unfalsifiable simply because you say so?It is falsifiable. If mutations are not random then we would expect a large portion of a single generation to share the de novo beneficial mutation. IOW, their parents would not have this mutation, but a large portion of the subsequent generation would have this mutation, and it would be shown to be triggered by an environmental cue.
You just relate unsupported conlusions, taking for granted that guided mutations would lead to what you like to be. You use inthe pocket mice example the highily unreliable notions of mutation rates and relative time frames to reach to your conclusions.The Luria-Delbruck flucutation test and the Lederberg's plate replica experiment are referring one cell organisms. I asked for for evidence about metazoans. So what do we observe? We do not observe the environment triggering the same beneficial mutation in multiple individuals at a rate beyond that expected from random mutations. What we do observe is the same mechanism of mutation producing mutations throughout the genome, including detrimental mutations that lead to genetic diseases such as achondroplasia and hemophilia. We observe that these mechanisms produce mutations in junk DNA where it has no effect on fitness.
Here is a work that i would like you to coment on: Journal of Theoretical BiologyVolume 78, Issue 4, 21 June 1979, Pages 573—591 Beyond neo-Darwinisman epigenetic approach to evolution M.W. Ho Department of Biology, Open University, Walton Hall, Milton Keynes, MK7 6AA, England AbstractWe argue that the basic neo-Darwinian frameworkthe natural selection of random mutationsis insufficient to account for evolution. The role of natural selection is itself limited: it cannot adequately explain the diversity of populations or of species; nor can it account for the origin of new species or for major evolutionary change. The evidence suggests on the one hand that most genetic changes are irrelevant to evolution; and on the other, that a relative lack of natural selection may be the prerequisite for major evolutionary advance. Contrary to the neo-Darwinian view, we point out that the variations of the phenotype, on which natural selection could act, do not arise at random; they are produced by interactions between the organism and the environment during development. We propose, therefore, that the intrinsic dynamical structure of the epigenetic system itself, in its interaction with the environment, is the source of non-random variations which direct evolutionary change, and that a proper study of evolution consists in the working out of the dynamics of the epigenetic system and its response to environmental stimuli as well as the mechanisms whereby novel developmental responses are canalized.We postulate that large evolutionary changes could be the result of the canalization of novel developmental responses which arose from environmental challenges under conditions of relaxed natural selection, and moreover, that the canalization of novel developmental responses might involve cytoplasmic inheritance or maternal effects at least in the initial stages.
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Taq Member Posts: 10085 Joined: Member Rating: 5.6
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You talk about mutations not related to fitness. No, I don't. I am saying that mutations are RANDOM relative to fitness.
I talk about mutations related to the reality of life.
What does that mean?
You just relate unsupported conlusions, taking for granted that guided mutations would lead to what you like to be. That is not a conclusion. That is the definition of guided mutations. To reiterate what I stated before, this is what guided mutations look like: ". . .the environment triggering the same beneficial mutation in multiple individuals at a rate beyond that expected from random mutations."
You use inthe pocket mice example the highily unreliable notions of mutation rates and relative time frames to reach to your conclusions. Why are they unreliable? Are they unreliable just because you say so?
The Luria-Delbruck flucutation test and the Lederberg's plate replica experiment are referring one cell organisms. I asked for for evidence about metazoans. That's strange, because you then use references that mention the CRISPR system in one celled organisms as an example of guided mutations. Perhaps you should follow your own advice? Also, the two experiments mentioned demonstrate how random mutations are falsifiable. The Luria and Delbruck paper specifically describes exactly how to falsify random mutations using specific math equations. I strongly suggest that you read the actual paper: http://www.genetics.org/content/28/6/491.full.pdf+html They specifically tested for Lamarckian type acquisition of immunity to bacteriophage. That is, they directly tested for guided mutations. The same ideas can be applied to all species, including metazoans. A human corrolary to bacteriophage resistance in E. coli is human HIV resistance. People with a missing portion of their CCR5 gene are strongly resistant to HIV. Just like the Luria and Delbruck experiment, this mutation occurred independently of HIV. This mutation did not occur as a guided response to the presence of HIV. The mutation does offer a benefit to those exposed to HIV, but it came about by a random mutation before HIV even existed. This mutation was random with respect to fitness as modeled in the Luria and Delbruck experiment. If mutations were guided, then we would expect to see this de novo mutation occuring at high rates in children born in areas with high levels of HIV infection. We don't.
Here is a work that i would like you to coment on: You first. It is your reference, so YOU need to show how the evidence in the article supports YOUR arguments. Edited by Taq, : No reason given.
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zi ko Member (Idle past 3650 days) Posts: 578 Joined: |
We propose, therefore, that the intrinsic dynamical structure of the epigenetic system itself, in its interaction with the environment, is the source of non-random variations which direct evolutionary change, and that a proper study of evolution consists in the working out of the dynamics of the epigenetic system and its response to environmental stimuli as well as the mechanisms whereby novel developmental responses are canalized.
It is clear that the wrighters believe that environmental stimuli causeWe postulate that large evolutionary changes could be the result of the canalization of novel developmental responses which arose from environmental challenges "large" evolutionary changes which are the result of canalization, which is not negated by random mutations that can follow. They talk also about mechanisms of canalization, which clearly reminds me about that "epigenetic changes pave the way to guided deep genome mutations" i had insisting of
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Taq Member Posts: 10085 Joined: Member Rating: 5.6
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It is clear that the wrighters believe that environmental stimuli cause "large" evolutionary changes which are the result of canalization, which is not negated by random mutations that can follow. Again, epigenetic changes do not explain the differences between species. The differences between humans and chimps is not due to epigenetics, it is due to a difference in the DNA SEQUENCE of their genomes. Any explanation of why species are different MUST explain how differences in sequence arise.
They talk also about mechanisms of canalization, which clearly reminds me about that "epigenetic changes pave the way to guided deep genome mutations" i had insisting of So they are the same thing because you say so? Why don't you actually SHOW how epigenetics guides mutations instead of putting words in other peoples' mouths. After all, the paper is from 1979 well before DNA methylation and epigenetics was understood. Edited by Taq, : No reason given. Edited by Taq, : No reason given.
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zi ko Member (Idle past 3650 days) Posts: 578 Joined: |
Epigenetic programming of differential gene expression in development and evolution
Taq here you maybe find the answer of your questions to me.Marilyn Monk* Based on our data, a picture of the inheritance of methylation imprints and speculation on the significance of the Xist imprint in development is presented. On a more general level, an hypothesis of evolution by adaptive epige-netic/genetic inheritance is considered. This proposes modification of germ line DNA in response to a change in environment and mutation at the site of modification (e.g., of methylated cytosine to thymine). Epigenetic inheritance could function to shift patterns of gene expression to buffer the evolving system against changes in environment. If the altered patterns of gene activity and inactivity persist, the modifications may become fixed as mutations; alternatively, previously silenced gene networks might be recruited into function, thus appearing as if they are acquired characteristics. An extension of this hypothesis is foreign gene acquisition and sorting (selection or silencing of gene function according to use). Kidnapping and sorting of foreign genes in this way could explain the observation that increased complexity in evolution is associated with more junk DNA. Adaptive epigenetic/genetic inheritance challenges the central dogma that information is unidirectional from the DNA to protein and the idea that Darwinian random mutation and selection are the sole mechanisms of evolution. 1995 Wiley-Liss, Inc.
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Taq Member Posts: 10085 Joined: Member Rating: 5.6 |
Taq here you maybe find the answer of your questions to me. Why don't YOU show me where those answers are.
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