Wright et al. on the Process of Mutation

If I was a referee on that paper I would have never allowed them to publish that statement. A citation from at least the 1950's should have been used, at least somewhere after the discovery of DNA. I agree. I think it fits more into false dichotomy where anything that counts against evolution is automatically evidence for ID.

Yes. The only specificity here is to ssDNA.If it was found that a specific base, and only that base, was mutated in response to the presence of leucine and the lack of a functional leuB gene then that would be incompatible with the Modern Synthesis. However, this is not what we see here.

The problem seems to be that you ignore the answers to these questions. I even chose a primary research paper for discussion written by someone that you claim supports your views.I have met people like yourself before. You are married to a conclusion, the data be damned. I have been very upfront about what random mutations are, how they are tested, and potential falsifications. You, on the otherhand, have not. In your eyes, it doesn't seem to matter what the results of experiments are.If I am wrong then please show that I am wrong. Please explain how specificity to ssDNA is non-random with respect to fitness. Please explain how the bacteria prevent deleterious and neutral mutations through this mechanism. Also, please explain why the leuB- reversion rate is only 1 in every 500 million divisions.Edited by Taq, : No reason given.

That is false. Neo-Darwinism did not exist in 1893. It didn't come to fruition until the 1940's, and it has matured since then. Environmental influences on the random mutation rate is a part of the Modern Synthesis (aka neo-Darwinism). The data shows that the environment changes the random mutation rate in genes based on gene upregulation. It is the ssDNA state of the gene which increases the mutation rate, not the need for a specific mutation in that gene. All genes that are actively transcribed, including vital housekeeping genes like gyrase, will see an increase in beneficial, deleterious, and neutral mutations. The processes which produce these mutations are blind to the effects of these mutations on the fitness of the organism.In fact, we can draw pertinent information from the Lederberg plate replica paper. The Lederbergs' observed that antibiotic resistant mutants arose in the absence of antibiotic. One of those antibiotics binds to the DNA gyrase protein. Mutations in that gene can prevent binding of the antibiotic while preserving gyrase activity. The rate at which these mutants arose is comparable to the leuB- reversion rate as it should be given the fact that gyrase is upregulated at all times. This is equivalent to people in debt buying more lottery tickets. This increases their chances of getting out of debt, but the lottery is still random. Not only that, but the 1 in 200 million odds of winning the lottery make it a desperate stab at survival, not a proven mechanism for specifically curing someone's debt woes.If poor people buy more lottery tickets than rich people causing the lottery to be won more often by poor people than rich people does this mean that the lottery is not random but is instead specific for poor people? Does this negate the random nature of the lottery?

No, I do not. Wright is stating that hypermutation is an increase in the random mutation rate in genes that are upregulated, exactly what I have been saying all along. This is consistent with the Modern Synthesis, but perhaps not consistent with Weissman's definition of the Modern Synthesis before there was a Modern Synthesis.Also, Wright states that this hypermutation increase "the availability of variants most likely to evolve in that environment". Wright et al. are hedging their bets against mutations that would be beneficial in genes that are downregulated. This is certainly a possible outcome. Therefore, this mechanism could also lower the probability of specific beneficial mutations occuring in a given environment. There is absolutely no guarantee that every potential beneficial mutation in a given environment will be found in an upregulated gene. I fully believe that Wright et al. would agree with this as well.If you want to go further down the rabbit hole, you also can not forget that the promoter region of the leuB gene had evolved as a part of a functional leuB gene. If not for the selection of the functional leuB gene and its promoter prior to the experiment there would be no reason for the leuB- gene to be upregulated in the absence of leucine in the first place. If this gene were a sequence that had never been selected for based on past leuB activity then it may have very well been downregulated in an environment lacking leucine.

Fair enough. Nonetheless, I am arguing from the position that mutations are random with respect to fitness, or adaptation as described by Merlin. This seems to conflict with shadow's view of how biology works. A rose by any other name . . . The original Luria-Delbruck paper may actually give us some insight into this. They didn't know it at the time, but the mutations that confer resistance to T1 phage occur in the tonB gene in E. coli. This is a protein that has high turnover and is consitutuitively expressed (i.e. always upregulated). In addition to serving as a binding site for T1 phage it is also a part of the vitamin B12 transport system that moves the vitamin from the environment into the cell (here is a good paper on tonB function). A bacterium without this function will be less adapted than one with this function. At the same time, a dysfunctional tonB gene will allow the bacterium to survive in the presence of T1 phage. Therefore, the selection methods used by Luria and Delbruck actually selected for a deleterious mutation in the environment in which the mutation occurred. This deleterious mutation is produced by the same mechanism as the leuB- reversions, and at a comparable rate.Edited by Taq, : No reason given.

Wright didn't show that in this paper, and it was never stated outright in the section you quoted.Even more importantly, the data does not support non-random mutations. Wright's opinion does not trump the data.

Opinions do not trump data. Please support your arguments with data, not opinions. Actually, I think the term was "daft" which is an apt description. We keep telling you that your opinion of another's opinion does not trump the data. Instead of focusing on the data, you restate your opinion of another's opinion in almost the same words. What more are we supposed to say before you actually focus on the data? You don't understand his findings, as you have stated before. You have never delved into Shapiro's data in any of his papers, and you refuse to delve into data produced by Wright in this thread. Opinions do not trump data. Yes, the school of thought where opinions do not trump data. Based on what data?

Then it is off topic. In this thread we are interpretting the data in the Wright paper. Wright's opinion is irrelevant. What matters is the data that you refuse to deal with. What is wrong with the paper in the OP?

Then show that it exists with reference to the data in the paper. Show how a 1 in 500 million success rate evidences a type of intelligence. Show how a mechanism that produces deleterious and neutral mutations is an intelligent way to produce a beneficial mutation in 1 out of every 500 million individuals. Proof of what? That everything else is intelligent too just because man is? That has to be the worst argument you have used yet. It is certainly absent from the mechanism of mutation described in Wright's paper.

Actually, I do have an objection. The suggested paper is a review paper where no data is presented. I would agree to a new paper as long as:1. It is an original research paper where the data and methods are presented, not a review paper. The suggested paper has many references to Wright's own original research papers. Shadow should choose one of those papers for further discussion.2. Shadow agrees that there is no evidence for directed mutations in the paper currently under discussion. If Shadow does think that there is evidence for directed mutations in the data presented in the current paper then there is no reason to move on.Edited by Taq, : No reason given.

I fully agree. Like Percy says, start interpreting. That is what I have been asking you to do from the very start.

If Wright has interpreted the leuB- reversion findings as evidence of directed mutations then Wright has misinterpreted the findings. That is the whole point of this thread. Let's even agree, for the sake of argument, that Wright does think that these findings indicate directed mutations. With that out of the way, it is now time for you to address my arguments as to why these findings do not indicate directed mutations.1. These are not directed mutations because the beneficial reversion only occurs once in every 500 million divisions. If this was a directed process then at least 1-10% of the population should have the needed mutation.2. Wright's own findings show that the mechanism responsible for the directed mutations in the leuB- gene would also produce neutral and deleterious mutations in all genes that are upregulated in a given environment, including vital housekeeping genes.3. Wright also demonstrated that changing the leuB- promoter and promoter alone changed the rate of hypermutation. This indicates that hypermutation is not specific to the function of the gene, but rather it's physical state as single stranded DNA.If this does not disprove Wright's conclusion* of directed mutations, then what would?*this conclusion is only being linked to Wright for this discussion only. This does not indicate that Wright holds this conclusion in real life, but only for the purposes of this discussion.

Doesn't matter. In this experiment the probability of a bacterium surviving the conditions in the environment is 1 in 500 million. Out of 500 million bacteria a single bacterium will survive, and it will be a random bacteria. There is no way you could ever predict beforehand which bacterium is going to get the needed mutation. If you have 100 bacteria then the chances of any of those bacteria survivng is 100 in 500 million, or 1 in 5 million if you want to get rid of some zeros. Life perserverance is determined by random probabilities when it comes to the appearance of beneficial mutations.

I'm with WK on this one. I don't read books on biology. I read the primary lit (and even help write some of it). If I do read a book it is more along the lines of Netter's Infectious Diseases (btw, I know one of those authors personally). When I am curious about something in that book I order the primary lit paper that is referenced in the interesting bit.So, are we done discussing Wright's paper? Do you agree with the rest of us that there is no evidence of directed mutations in the paper (your opinion, not Wright's)?