Wouldn’t that apply equally to experimenters changing residues in proteins?
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… and it’s associated MIC? Why didn’t he do that? No, he does not explain this anywhere.
Then why does he not use the wt enzyme against it’s associated MIC? No, he doesn’t say this anywhere.
Whoah, HIGHER? You’re correct, but then why does Axe say it would be lower?
Remember what Axe writes:
According to Hunt, I “molded a variant that would be exquisitely sensitive to mutation.” [2] Venema expressed the same concern, that the starting sequence I used was “intentionally ‘hamstrung’ with multiple mutations to render it far less functional than its natural counterpart.” [7]
Both Hunt and Venema seem to think the outcome would have been more favorable (i.e., functional sequences would have been more prevalent) had I used the highly proficient natural enzyme as a starting point rather than the handicapped version. Actually, as a demonstration will show, the opposite is true.
So here Axe says functional sequences would have been the opposite of more prevalent. That means lower than 38%.That means a lower per-position pass rate of 38%. A calculated fraction even less than 10-77. So why does Axe say that when even you can see that isn’t true?
The analogy Axe goes on to make doesn’t even show that the “opposite” would happen. Rather he tries to make a case that the result would be invalid, because, he argues, the result would imply the sequence is more tolerant to mutations than he thinks it is.
Why didn’t Axe perform this experiment, then? What would be wrong with doing that?
No it implies his answer does not actually constitute an answer. I want you to engage your brain and realize this, rather than engaging in absent-minded copy-pastings of his words. What is occurring right now is exactly why I began this whole exchange by insisting you should show a willingness to think.
And that’s how the obfuscation occurs. Because he has broken up the two factors into separate parts of his analogy, you lose sight of the question and seem to think he has actually answered why he didn’t test the wt enzyme against the wt-enzyme’s MIC even when he has not actually done so.
Axe only explains why he didn’t use the wt enzyme against the temp-sensitive MIC with his analogy (he says this would produce a misleading result). His response doesn’t ever provide an answer to why he didn’t use the wt enzyme against the wt MIC.
If you disagree with me, please tell me where Axe explains why he didn’t use the wt enzyme against the wt MIC. The thing you agreed above you can’t know the results of until measurements are made.
I replied that laboratories are part of nature, and the distinction is synthetic.
Which we know is false.
Are things like putting basic nutrients bacteria routinely encounter in the wild, into flasks, and letting them consume them. They use basic KB medium. This contains such naturally occurring compounds as amino acids and peptides (exist in enormous quantities as both secreted products by other organisms, or the decay products they leave behind after they die), glycerol (a ubiquitous carbon and energy source), and a few salts like potassium phosphate and magnesium sulfate, which are simply sources for K, Mg, P, and S. Elements also found in the natural world.
Furthermore, the salts partially act as buffering solutions suppressing the magnitude of pH fluctuations, which reduces stress on the bacteria, which reduces the chance that mutation-inducing stress responses are at play.
If anything, in fact, the experiment does the opposite of what you are suggesting.
You’re just making shit up now out of desperation dude.
Are those dark oily stains in your armpits from desperation sweating?
Gene fusions are results of mutations, not mutations themselves. The mutations that can result in gene-gene fusions are insertions or deletions.
Many insertions and deletions have occurred in the LTEE, at least one insertion of which produced a gene-gene fusion as a byproduct (I already told you about it in an earlier post). It is not known to have been an adaptive fusion (it isn’t known whether the fusion protein has any function). But they have definitely occurred in the LTEE.
Another desperate fail response.
The “probability of finding a nearby functional peak” can only make sense in light of a certain mechanism. If the claim is that generating a novel functional protein de novo by accumulation of point mutations is exceedingly unlikely, and then this is used as a basis for claiming therefore no new functional proteins can evolve by any means, then this claim is fallacious. Because any demonstration that a new functional protein can evolve by a mechanism other than de novo by accumulation of point mutations makes the first claim irrelevant.
Well you’ve now certainly asserted as much, and I have explained why that is wrong. Several times.
Oh okay then. They are! Congratulations. And?
The paper is about searching for more pseudogenes of a specific type, in addition to those already known of all types, in a specific data set, using a specific computational approach. The point was to give a reference for the number, not to highlight the specific 160 additional pseudogenes they find in this paper. I can see how that would get you confused, and I should have just cited reference 4 in that paper instead:
By similar logic it also doesn’t matter what the true rate is if novel genes are observed to evolve in a few weeks of experimental evolution. Then they observationally happen frequently enough for innumerable new genes to be easily evolvable in the totality of the history of life on Earth.
ROFL. No, no he isn’t doing any such thing at all. Axe is mutationally degrading an existing sequence in order to try to estimate the fraction of protein sequence space that would result in that particular structure-function relationship. He wants to know what proportion of 153 amino acid protein sequence space corresponds to what we would classify as functional serine beta-lactamases.
Holy shirt batman. You really have NO clue what is going on, do you?
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