The cit+ trait in the LTEE is IC.
If the function is fitness(which it is in life), then high FI has already evolved in the LTEE too. Don’t you remember anything? This has been pointed out to you before on this forum.
This appears to be a possible reason function is maintained despite a problematic mutation. I concede that function maybe maintained despite a non functional allele.
Do you agree that many of the variants in uniprot that show no problem may be to due to the fact that humans are diploid organisms?
Not sure at all this is true
In order to establish this, you will need to calculate the increase in FI associated with the LTEE.
You seem to believe that what you or some other participants here assert is performative, as if stating something automatically makes you win a debate. But you are mistaking assertion for achievement.
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Hey, what a great idea! It seems to me this would be an obvious study for ID proponents to do: Measure the FI of the strains in the LTEE over time (the necessary data is all freely available) and show whether it ever increases. That would be a perfect way to falsify one the chief claims of ID.
How odd that, as far as I can tell, no one in the DI has ever done this.
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That’s mighty big of you to concede something many learn in high-school level genetics.
I doubt it because of the way they’d be discovered. But that’s a concept that’s far too advanced for someone who doesn’t understand that null alleles are typically recessive.
Are you aware of all the sources of mutational data contained in uniprot?
The Cit+ trait required the following mutation (technically it required more as it is known this one alone doesn’t suffice, but this will do for showing it is IC):
The citT transporter normally sits downstream of a promoter that is suppressed under aerobic conditions. That means when oxygen is present the cell doesn’t take in citrate.
During the course of the experiment the “segment amplified in Cit+” part was copied and inserted into the rnk gene. That means it was duplicated, and there is now a copy of the citT transporter sitting downstream of the rnk promoter, which is active when oxygen is present. For aerobic cit+ to work, the citT transporter must be present, and the promoter that is active under aerobic conditions must be present. Remover either one of these two parts and cit+ fails to function. Since removal of any one of these parts renders it nonfunctional, the trait is IC.
Btw even Behe agrees the trait is IC, he just responds by saying “simple” IC systems can evolve, and more complex ones can’t because the more parts it has the less probable the outcome. You know, his usual Texas Sharpshooter sh1te.
Do you not recall that I did this? You even agreed.
Okay here we go again:
Depending on what you think the ratio of beneficial to neutral/deleterious mutations are (and if you accept Sanford’s estimation that Lenski’s 1998 paper is the most reliable here), the ratio of beneficial to deleterious mutations in the LTEE is 1 in 106.
Since roughly 25 to 40 beneficial mutations (depending on which of the 12 replicate populations we pick) have by now fixed in each population, we can just calculate the total FI of 25 mutations, each with a probability of 10-6.
-log2((10-6)25) = 498.3 bits.
Wow you win the all time forum gold medal for ironic statement. I’ve literally done that calculation before to you. You semi-agreed (probably didn’t know how to respond because you stopped responding). So you really did repress the memory I see. Hilarious. No, actually, sad.
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Pretty much, as I’m a geneticist.
Are you aware how silly it is for you to be arguing with a geneticist based on assumption that humans and mice are haploid?
Are you aware how silly it is for you to acknowledge something that fundamental and label it as a concession?
You’re projecting.
You’re here trying to debate with people who know and do science from a position of ignorance. You could try to view this as an educational exercise instead of a debate to be won.
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I am not sure what pretty much means.
The question is if the differences in the notch 2 protein sequence in humans and mice are due to design differences or fixed mutations is humans.
I made a mistake in not considering the diploid genome in my answer. You corrected me and I appreciate that. The implications of the diploid genome I agree are important.
Meaning I am aware of the ways in which human variants and alleles are discovered by clinical geneticists over time. It’s not a random sample.
Not just your answer. It’s your premise: your doubting that known mechanisms can account for the difference between the human and murine orthologs was based on the false assumption that humans and mice are haploid.
But will you remember it?
Yet you already ignored them when you repeated:
Understanding that we are diploids demolishes your premise. Given that there are 4500 known variants, you are predictably ignoring my point about fixation.
Whether humans are haploid or diploid the question remains open.
I think it does little to change the premise as other proteins also show variants among humans but have identical consensus sequences between mice and humans.
The other issue is the proteins Jak 1 and 2 that bind to notch 1 and 2 also vary between mice and humans. Independent mutation becoming compatible would potentially be a rare event.
Given that there are 4500 known variants, you are predictably ignoring my point about fixation.
If one has any human compassion for Bill, this is painful to watch. If, that is.
I am not ignoring it and you may very well be right that the difference may be the result of fixation over time but there are still issues with that hypothesis.
You most certainly are.
That wasn’t my point at all, which is why I’m pointing out that you are ignoring it.
What does the existence of 4500 known variants tell us, Bill?
Bill, I think the point is that fixation, as a term, refers to there not being literal thousands of more or less common alleles in the population. Therefore, being most charitable, what ever you mean by “fixed in the human population” must be something other than fixation. So John asked just what you meant, and how one would go about differentiating between “fixed” and non-“fixed” alleles in accord with your proprietary definition of that term.
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I don’t quite understand your calculation, but in any case it has nothing to do with the increase in the FI associated with the LTEE.
You seem to be interested in events whose probability of occurrence varies, according to your calculation, between 10^-150 and 10^-240, depending on the replicates.
Do you realize that such events are extraordinarily unlikely, to the point of being practically impossible in the context of observable phenomena in the universe. And you want us to believe that this type of event happened not only once, but 12 times!!!
In any case, the probability of occurrence of the type of event you are considering is very high since it seems to occur each time an experiment is launched!
I don’t know if you’ve done the calculation before to me, but as I’ve shown above, your calculation is flawed.
This is impossible because there is no way to calculate for a given strain the number of genotypes associated with a given level of fitness. As the French saying goes « a l’impossible, nul n’est tenu», not even the DI folks!
You remind me of Fauci saying that contesting him was akin to contesting science. An attitude somewhat lacking in the humility befitting a scientist.