Does the Darwinian theory require modification or replacement?

I see Shapiro trying to spin the question. He rephrased the question in terms of "with respect to their potential biological utility". That is not fitness. I think this is best seen in how some transposons tend to target areas of the genome with high activity. That is, some transposons tend to insert closer to genes and can affect how they are regulated. These changes can be beneficial, neutral, or detrimental so this is once again random with respect to fitness. I would agree with Shapiro in that transposon mutagenesis has a much better chance of producing a change in phenotype (i.e. "biological utility") compared to point mutations.

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. 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. 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. Random in what respect? Again, you need to phrase random with respect to something in order for it to make sense.

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. 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.

Again, we want to see the data. Theories are not overturned or modified by opinions. Who has taken this position? Shapiro stated quite clearly that the mechanisms he has proposed are entirely natural. I have no problem with disagreement. It is refusal to deal with the data that upsets us.

How can you reach scientific conclusions without data? Then present the data found in those papers and demonstrate how that data supports your interpretation of the authors' conclusions. You also present your misinterpretation of Shapiro's findings. What I want to see is how the data in those papers supports YOUR interpretations.If we were going to compare this to a court of law, you are only presenting the opinions of the forensic scientists without ever presenting the forensic evidence itself. Anyone with access to the papers can use my procedure, scientist and non-scientist alike. Then we are no longer talking about science. What we should not be open to is misinterpretations of the data, which is exactly what you have been presenting.

Are you agreeing that these mechanisms that produce mutations also produce neutral and detrimental mutations?

Don't you need to know the rate of neutral and detrimental mutations compared to beneficial mutations before you can claim that these mutations are non-random with respect to fitness? You seem to be jumping to conclusions.

Then show us the data that supports your interpretations.

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In a court of law I, as the attorney, present the Expert, in this case Shapiro via his papers that contain the data, and then with the evidence admitted into evidence, I interpret his testimony in my argument to the jury. That is what I am trying to do in this thread.

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In a court of law you also have to supply this evidence to the opposing side so that they can examine the evidence themselves. For example, any DNA evidence submitted by a procecutor must also be available to the defense so that they can do their own sequencing if they see fit. You need to supply the data.

Nowhere in that quote can you find the word "fitness". She mentions random mutations, but she does not mention how they are random. Like we have said many times, mutations are not random with respect to time and sequence, but they are random with respect to fitness. It's not as if skydivers acquire mutations that produce wings in their children.

Your interpretation inserts "non-random". Nowhere in the quote does it speak of non-random mutations. You are not interpretting. You are projecting your own biases into the quote. What data does she cite that challenges the Luria and Delbruck's conclusions? In order for them to mount a challenge they need data to support their challenge. What is that data?

I already read it. It is wrong. You don't get to present expert testimony even as a written affidavit. Even worse, you don't get to present your interpretation of the expert testimony as evidence. Expert witnesses have to present the data that supports their conclusion, and they have to be available for cross. That's how it works. That is how it worked in the famous Dover ID trial where ID advocates were not allowed to submit written affidavits. They had to be available for cross. You should know that.Of the questions related directly to fitness and random mutations, Shapiro ducked them. When directly asked if mutations were random with respect to fitness HE CHANGED THE QUESTION. He changed it from "random with respect to fitness" to "probability of biological utility". These are NOT THE SAME THING. This should be a very big clue to someone not blinded by their own biases.The fact of the matter is that the mutational mechanisms described by Shapiro produce beneficial, neutral, and detrimental phenotypes. These processes are blind to what will benefit or harm the organism. I have already shown that one of the mechanisms cited by Shapiro (the E. coli SOS response) produces mutations that are random with respect to fitness as defined by both the fluctuation and plate replica methods. For example, the SOS response increases the number of antibiotic mutants EVEN IN THE ABSENCE OF ANTIBIOTICS. Edited by Taq, : No reason given.

Then please show us the presentation of the evidence. That evidence was first presented by the witnesses who were cross examined.

Swing and a miss.The data is the data. Shapiro's opinions are separate from the data. For example, the results from DNA sequencing is the data. Whether or not this indicates a valid DNA match is the opinion of the expert. You need both. So far you have only presented opinion, not the data.

What percentage of these mutations produce beneficial adaptations? That is the part you are leaving out. The fact of the matter, as I will show in a subsequent post, is that we are talking about a mutation that occurs once or twice per billion bacteria. Even more, the same mechanism that Wright points to is just as capable of producing neutral or detrimental mutations. Let's take a look at this paper.From the introduction in that paper:

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Our data indicate that transcription
(starvation-induced derepression) is unique in augmenting
variant availability in a specific manner, i.e., by stimulating
rates of transcription (and associated phenomena such as RNA
polymerase pausing) in targeted operons, thereby increasing
the concentration of single-stranded DNA (ssDNA), which is
more vulnerable to mutations than double-stranded DNA.
Although the mutations per se are random, as described above
for background mutations, the mechanisms that target operons
for increased rates of transcription are highly specific. This
specificity is not compatible with current neo-Darwinian
dogma.
[my note: sorry for formatting, but copying and pasting from a .pdf is a pain]

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What Wright is really arguing for is that transcription of a gene increases the random mutation rate in that gene. Other investigators have found that single stranded DNA (ssDNA) is more susceptible to random mutation. Therefore, any stretch of DNA that is actively transcribed will be more susceptible to mutation.So what types of beneficial mutation rates are we talking about? Wright et al. looked at the reversion rate for a broken leuB gene in E. coli. All it takes to make this gene functional is the conversion of a specific C to a T.Take a look at Table 1. We are talking about 0.2 to 2.5 beneficial mutations PER BILLION BACTERIA (1 per 10(9) for our misguided British friends who use the wrong definition for billion ). Not only that, but the conversion needed (C to T) is highly favored by the mechanisms that causes mutations in ssDNA. Wright also discusses other environmentally unrelated mechanisms, such as transcription pause sites, that further enhance random mutation of ssDNA.I would also argue that the system that Wright et al. use is highly artificial and colored by bias. First, the proposed mechanisms requires upregulation of the DNA sequence in question in an environment where mutations within that DNA sequence would be beneficial. If a mutation in a downregulated or repressed gene would be beneficial in a given environment then this mechanism actually tips towards detrimental. For example, if a mutation in an enzyme within the de novo proline biosynthesis pathway could mutate to also fill a role in the broken leucine de novo biosynthesis pathway such mutations would be repressed in an environment rich in proline but lacking leucine.Secondly, it is not the lack of leucine in the environment that guides the mutations. This is supported by the finding that replacing the wild type leuB promoter with an IPTG driven tac promoter produces the same number of leuB- revertants. When IPTG is added to the growth media the transcription of the leuB- gene is increased like that seen in wild type conditions where it requires the absence of leucine. What did they observe? Close to the same rate of mutation as seen in the wild type. It is not the lack of leucine in the environment that guides the mutation of the leuB- gene. It is the state of the gene (ssDNA) that increases the random mutation rate.It is also worth mentioning that the classic examples of random mutations discussed by Lederberg, Luria, and Delbruck occur in actively transcribed genes. For the antibiotic resistance in the Lederberg plate replica experiment the mutations happen in the DNA gyrase gene. In the Luria-Delbruck fluctuation assay the mutations occur in the high turnover tonB gene. When antibiotic and bacteriophage resistance mutations occur in these genes it is not in response to the presence of antibiotics or bacteriophage. They are random with respect to fitness, just like the mutations in the leuB- gene in the Wright et al. paper.Edited by Taq, : No reason given.Edited by Taq, : No reason given.

Ernst Mayr said it best:

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By the end of the 1940s the work of the evolutionists was considered to be largely completed, as indicated by the robustness of the Evolutionary Synthesis. But in the ensuing decades, all sorts of things happened that might have had a major impact on the Darwinian paradigm. First came Avery's demonstration that nucleic acids and not proteins are the genetic material. Then in 1953, the discovery of the double helix by Watson and Crick increased the analytical capacity of the geneticists by at least an order of magnitude. Unexpectedly, however, none of these molecular findings necessitated a revision of the Darwinian paradigmnor did the even more drastic genomic revolution that has permitted the analysis of genes down to the last base pair.
Just a moment...

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As an aside, the whole essay is a great read. It is a short synopsis of Ernst Mayr's view of his career over 80 years. He wrote it to commemorate his 100th birthday:

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Having reached the rare age of 100 years, I find myself in a unique position: I'm the last survivor of the golden age of the Evolutionary Synthesis. That status encourages me to present a personal account of what I experienced in the years (1920s to the 1950s) that were so crucial in the history of evolutionary biology.

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Edited by Taq, : No reason given.