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.
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.
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.
Yes, many designed objects do not show IC but IMO, every object displaying a level of IC equal or superior to two CCC warrants a design inference. So what I am saying is that this level of IC is a hallmark of design, in the sense that it is a very strong indicator of design. A sign of design if you will.
Well, assuming you are correct that whatever you are describing there is needed to calculate FI (and I am not certain you are), that would suggest the DI are just blowing hot air when they say evolution cannot produce results of a given FI. If they can’t even calculate it how, would they know this? Although it would finally explain why they have never, ever, not even once applied FI to an actual biological situation to show that evolution cannot increase it.
And there goes another irony detector.
Huh? IC and CCC are two completely different concepts in the Behe Universe. One cannot be derived from the other. It seems your understanding of ID is as abysmal as your understanding of evolution.
A claim that was refuted over a century ago.
The Mullerian Two-Step, or Why Behe’s “Irreducible Complexity” is silly
Except as pointed out, evolution can also produced biological structures that meet Behe’s criteria for IC. Therefore it can’t be a sign of design (re: biology), because IC is demonstrably not exclusive to artificially designed and manufactured objects.
If ID proponents really wanted to come up with a means to detect design and manufacture, then best way is to start with a hypothesis about how a designer would go about creating or modifying biological organisms. Then determine the hallmarks of that process and see if those hallmarks exist in biology.
The two challenges here seem to be, a) getting past the resistance ID proponents have of asking “how”, and b) risking coming up with hallmarks and hypothesis testing in biology that may reveal organisms does not exhibit design and manufacture.
Please show me a case where it has been demonstrated that unguided, blind evolution produced a biological structure that meet Behe´s criteria for IC.
I gave you the previous link to the Behe interview with Dan Cardinale where they walk through Behe’s criteria and then Dan gives examples of biological structures that meet those criteria: https://www.youtube.com/watch?v=nsErbfaq5mc
I understand it’s an hour long video, but if you have a real interest in trying to defend IC here I highly recommend watching it.
edited to add:
Digging through past threads on this forum, it looks like you have previously been engaged on this exact subject in this thread: Creation Myths with Dr. Michael Behe on "The Edge of Evolution"
It interesting to note that presented with examples of evolved structures that demonstrate IC (per Behe’s basic criteria) you, like Behe, appear to then change the criteria.
Which reinforces that IC is a poorly defined and nebulous concept to begin with.
Does your unsupported opinion count for anything? And “CCC” is something Behe made up, something that seems not to actually exist even for chloroquine resistance in Plasmodium.
Pick a lane.
Said humility befitting a scientist lies in the recognition of one’s own fallibility, the acknowledgement of the possibility of one’s own incorrectness. A scientist has spent enough of their life surrounded by people far more educated than themselves in all manner of areas, and internalized through that experience, that – much though they may have studied – there is for almost every question somebody more knowledgeable, and for almost every guess they’ll make there is a chance it is dead wrong.
The height of arrogance is the idea that watching half a dozen hours’ worth of YouTube sermons, or sitting down in an arm chair for three minutes is all it takes to come up with all manner of gotchas and what-abouts all of the people who spend their lives studying the subject never considered. The idea that confident delivery and flowery jargon is all it takes to get into position to question, let alone undermine, literal centuries’ worth of research, that is arrogance. The idea that having seen next to none of the data, and understood none of the maths, one is still anywhere near adequately equipped not only to meaningfully partake in the conversation, but that there cannot be anything one might have overlooked, that is arrogance. If to the question “How come the entirety of the community of qualified professionals disagrees with basically everything I say?” one’s answer is “They must not have seen all or thought through the facts in such depth as I”, then, respectfully, one has no business lecturing anybody on matters of humility.