Does the Darwinian theory require modification or replacement?

If which mutations are nonrandom? If 99.999% of mutations are random with a few examples of specialized systems that insert viral DNA into palindromic sequences would the entire theory need to be rewritten, or would a footnote do?

Kind of, but not really. If we found that in a very specific situation that one species of bacteria had a mutation dictated by the enivronment, then that mechanism should be added to the theory. I suppose that would technically be a "modification", but it wouldn't change the fact that everything else is still evolving via mutation that are random with respect to fitness.

You keep asking for data and mechanisms any time some body expresses ideas diferring from your own. Many times you reject so easily works by serious scientists. In other cases you ask mechanisms for theories, hypothesises or ideas that are new and so are not yet known. Iam not saying this is bad . But everything has its time. To be in a hurry to verdict against , shows biased predetermined unscientific viewing.If a hypothesis or heory is not accompanied by substantial evidence , it will remain just a theory to be forgotten.
Iam courious why do you avoy to anwser my question by me in other thread , which i repeat again:,Lamarckism is known. Darwin shared some of these same views, and Weismann , the father of neo-Darwinism, decided late in his career that directed variation must be invoked to understand some phenomena, as random variation and selection alone are not a sufficient explanation .
Lamarckism is based on in formation. So it seems does Darwin and Weismann on at least some occasions. You and nobody else before did "ask" them to bring their data or the relative mechanisms for this special matter. Maybe they could it. But you
are so rigid for any body proposing same views.--------------------------------------------------------------------------------

Isn't that what a scientist should do? No serious scientist would claim that empathy guides mutations. So you admit that you have no mechanism, not testable hypotheses, and no theory. Why should we take you seriously? Weismann died in 1914. Work since then has shown that he was wrong.If you want to argue against the theory of evolution as it existed at the turn of the 20th century then you are more delusional than I thought. Please join us in the present.

"I didn't mean myself . Imeant Shapiro, B. Wright, Yablonnka,Dobjansky,Darwin, Weisman ect when they bring ideas and often facts that difer fron your ideas. I said everything has its time. Do you thing it is clever to change the meaning of my answers? Isaid that the mechanisms are the same that are accepted by
Darwin and Weismann.My hypothesis is testable. Your blind untestable belief in the singularity of randomness in evolution is the problem.

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Information: It is time its undeservedly neglectet powerful role to evolution to be restored.

How? What would be the protocol?Have you put together experiment plan?Will you share it with us?

Please read my message 643 where I present proof of dedicated, nonrandom, beneficial change and tell me if that is reality.

In message 643 I present evidence of dedicated, nonrandom, beneficial change. Do acknowledge that the papers show that?
What if any effect does this proof have on the modification of the MS?Finally, am I misrepresenting Shapiro in message 643?

In message 643 I presented papers showing dedicated, nonrandom, beneficial change.Do you consider these findings consistent within the Modern Synthesis?If so would you agree that the MS does not rule out a planned process?

Your Message 643 quotes an abstract. There is nothing in the abstract about "dedicated, nonrandom, beneficial change." Going to the paper at The CRISPR system: small RNA-guided defense in bacteria and archaea, the words "beneficial" and "nonrandom" do not appear in the article. And a quick perusal doesn't seem to reveal any mention of such possibilities.Could you read the article and quote those portions you think are describing "dedicated, nonrandom, beneficial change"?--Percy

In message 643 I stated that Shapiro in his book cited these 2 papers as evidence of "dedicated, nonrandom, beneficial change."The following is a quote from the paper I linked to online.
I cannot gain access to the full paper of the Abstract Shapiro cited, but I accept his judgment as to what it means.The CRISPR system is an elegant, effective, and fluid mechanism of defense against foreign genetic elements (Fig. 4). It is rightly described as an adaptive immune system, which evolved long before its famed namesake. Interestingly, CRISPR's ability to acquire a resistance phenotype and pass it to progeny could be construed an example of a soft, or Lamarckian, mode of inheritance. One could also view this from a conventional Darwinian perspective, where pressure exerted by the environment simply selects the fittest. However, armed with knowledge of the molecular basis of this response, CRISPR-cas does seem to fit more firmly with a Lamarckian paradigm, in essence because increases in fitness do not rely on random mutations but on a much more specific acquisition of genetic information from environmental sources.

Please point out where your quote:

quote:

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The CRISPR system is an elegant, effective, and fluid mechanism of defense against foreign genetic elements (Fig. 4). It is rightly described as an adaptive immune system, which evolved long before its famed namesake. Interestingly, CRISPR's ability to acquire a resistance phenotype and pass it to progeny could be construed an example of a soft, or Lamarckian, mode of inheritance. One could also view this from a conventional Darwinian perspective, where pressure exerted by the environment simply selects the fittest. However, armed with knowledge of the molecular basis of this response, CRISPR-cas does seem to fit more firmly with a Lamarckian paradigm, in essence because increases in fitness do not rely on random mutations but on a much more specific acquisition of genetic information from environmental sources.

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mentions "dedicated, nonrandom, beneficial change"?

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Anyone so limited that they can only spell a word one way is severely handicapped!

"..., CRISPR-cas does seem to fit more firmly with a Lamarckian paradigm, in essence because increases in fitness do not rely on random mutations but on a much more specific acquisition of genetic information from environmental sources."Dedicated =specific acquistion of genetic information.
nonrandom=do not rely on random mutations.
beneficial= inceases in fitness.

Does the term "dedicated, nonrandom, beneficial change" appear in your quote.A simple yes or no should suffice.Edited by jar, : appalin spallin

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Anyone so limited that they can only spell a word one way is severely handicapped!

If you merely accept what Shapiro tells you the paper means instead of understanding what it actually says then you can't really discuss it, can you. All you can do is go off and find more Shapiro to quote at us. Your whole approach in this thread isn't that you've examined Shapiro's references and concluded that he's correct. Your approach is merely, "Shapiro's claims agree with what I already believe, so I'll just assume he's correct without trying to understand the evidence he cites."But if you don't understand Shapiro's references, how are you going to discuss them? Seriously, this is a big problem for you. How are you going to convince other people that Shapiro is right about something you don't understand? This isn't due to any shortcomings on your part. How would anybody anywhere ever convince other people of things they don't themselves understand? All they can do is hope the people they are talking to can become convinced without understanding what it is they are being convinced of.But the people you're discussing with here aren't willing to accept things they don't understand. If you want to convince anyone here then you're going to have to understand Shapiro first. That means understanding not just his claims, which you have a fair grasp of, but also the evidence and rationale behind his claims.Here the link to that paper again: The CRISPR system: small RNA-guided defense in bacteria and archaea. Let's see if we can find where Shapiro might think it supports his claim of "dedicated, nonrandom, beneficial change."The word "nonrandom" or "non-random" or even "non random" never appears in the paper.But search for "random" and we can find two occurrences, so let's try to get a handle on why Shapiro thinks the paper supports his position.First we need to understand what CRISPR's are. Looking up CRISPR at Wikipedia (I recommend reading at least the introductory paragraph and giving the diagram a good, long look) we see that it stands for Clustered Regularly Interspaced Short Palindromic Repeats. CRISPR's are specific gene locations in DNA "containing multiple short direct repeats...CRISPR functions as a prokaryotic immune system..."Okay, enough of that excerpt, it's pretty technical. But I've looked up the terms and boiled it down, and in lay terms I can tell you that CRISPR's are one type of a bacteria's defense mechanism against infection by viruses.So let's quote a small portion of the article that includes the first appearance of the word "random": This says that the sequences that are inserted as spacers are not selected at random, so let's see if we can figure out how the selection is not random. This article itself is pretty tough for me to follow, we need WK's help, but I think I can figure out some of this.The article uses the term "proto-spacer" to refer to a DNA sequence in the virus genome of the virus that is attempting to infect the bacteria (they use the term phages in the article, instead of viruses). The authors think their evidence suggests that the spacers inserted at a CRISPR location are selected by a process driven by proteins that can recognize the specific sequences in viruses that confer immunity.Is this a "dedicated, nonrandom beneficial change" to the bacteria's genome? I would answer, "Yes."Is it a genetic mechanism that evolved over time through a process of descent with modification and natural selection (in particular, the recognition proteins)? I would again answer, "Yes."We've known for a very long time about viruses' ability to insert genetic material into cells that adds to or replaces DNA in the cell's nucleus to take over the cell's machinery, usually to produce more copies of the virus. This detailed understanding we're developing of the CRISPR mechanisms that allow bacteria to develop resistance to viral infection is new, but it seems to fit perfectly within both modern genetics and evolutionary theory.--Percy