“A model is a lie that helps you see the truth” - Howard Skipper (biochemist/oncologist)
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Then please restate them the way you think is appropriate.
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@swamidass. @T_aquaticus. @Patrick. @Art
You are all smart people. When we set things up in the lab we do everything possible to maximize the chances of success. Nasvall did th same . The only deck they did not stack was the vector they used, which was very low copy. Would this work in the wild? Under the right selections and fortuitous regulatory mutations yes.
What about Schmidt and OSBS? I am less sanguine because of the very low level of expression
Νοw, I see no point in continuing. I have said what I wanted to,since you seem determined not to understand…(Good bye).
So you think this will work in the wild, in the right circumstances great. I’m just left wondering how the initial objections could be salien then.
Perhaps this is just example of conceding without conceding?
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A “noncession”?
Absolutely not. Properly done, experiments are designed to get answers, not “maximize the chances of success” (which, in @Agauger’s eyes in this case, is the production of enzymes with differing functionalities) . Nasvall designed their experiments to ask three questions, NOT to optimize their chances to generate enzymes with differing functionalities. Their hypotheses could very well have been wrong, and their experiments would have been successful.
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Really? Is that what you and Doug Axe did in your experiments? Maximized the “chances of success”? i.e. That the functions you were investigating would be as likely as possible to arise thru mutations?
I don’t think so.
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Even Darwin understood the difference between artificial selection and natural selection. It’s been 150 years, and you guys still haven’t gotten as far as him. Strange.
You should change your name to the Evangeleical Atheist.
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@Agauger
I agree with all of this. What we were scratching our heads over was the initial criticism that lab experiments don’t count. We thought that was a bit strange, and there is always the chance that we misread your criticisms.
Can random mutations switch HisA activity to TrpF activity if the gene is being expressed and in the right environment? Yes. Would we expect the same to happen in the wild if the same conditions are met? Yes. If we can agree on these points, I think we could move on to more general questions about protein evolution.
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I tend to view ‘getting good answers’ as what a ‘successful’ experiment does.
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In that sense every experiment is a success.
In my view . . .
A successful experiment is one where you get a strong yes or a strong no. The unsuccessful experiments are the ones where you get a maybe, or a “can’t tell”.
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Did they show that the mutations were random with respect to fitness as they had defined fitness for the purpose of the experiment?
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Given the rate at which these mutants appear, it would be consistent with random mutation. If you had 1 million bacteria and 500,000 of them had the mutation after one generation then that would certainly cast doubt on random mutation. However, if you only see one positive mutant out of billions or trillions of bacteria, that supports the conclusion of random mutations.
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Not really, I have personally done quite a few experiments that didn’t give good answers (one way or the other) and needed to be tweaked and repeated - often numerous times.
Ditto.
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You are now using a different definition of random mutation than the one you gave in your OP on random mutation.
It’s the same definition. If memory serves, the standard mutation rate in E. coli is about 1 mutation in every 2 to 3 divisions. In the Luria and Delbruck fluctuation assay and the Lederberg’s plate replica experiment they were seeing a specific mutant 1 in every 100 to 500 million divisions. It is true that the specific experiments we are discussing in this thread did not use these methods to determine if the mutations were truly random, but the number of mutants is consistent with previous experiments that did demonstrate random mutations. That’s why I said the number of mutants was consistent with random mutation. In addition, I also described what non-random mutation would look like in these experiments.
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