Well, now, some monkeys are apes, but all apes are monkeys. In the cladistic sense of the terms, that is.
I know that, but Gil specified the “ape clade,” not any “monkey clade.”
I suppose that was the wrong term. You made them hallmarks of design by simply asserting that they were. But in fact there are evolutionary routes to IC, and many designed (manufactured) objects do not show IC. As I see @AnEvolvedPrimate has already pointed out.
Yes, that was puzzling.
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How do you define “fixed in the human population”? What entity is fixed? There are 4805 known variants!
Please list the NOTCH2 alleles that you have determined to be fixed and the criterion/criteria by which you did so. Are you even aware that alleles, not genes, are what we are referring to with respect to fixation?
Aren’t most of the 4805 known human variants functional?
Do you see how, even in what may be a good-faith effort on your part, you are ignoring/avoiding most of the evidence in front of you?
You’re right. I was confused.
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The fossil record isn’t great, but evolutionary developmental genetics may have something to say:
https://www.nature.com/articles/s41559-020-01349-0
All the variants are functional to some degree or we would not have the sequence in the data base.
No. That would only be appropriate if your statement was a subjective opinion, rather than a ridiculous falsehood you can’t be bothered to justify.
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What evidence do you believe shows that they appeared “abruptly”? You should realize the fossil record cannot demonstrate this. So what else?
Correct me if I am wrong, but I don’t believe Behe, himself, ever suggested IC was a “hallmark of design.” He only thought it was something evolutionary processes could not produce. That is not quite the same thing as saying it is a “hallmark of design.” Many things designed by humans continue to function after one or more of its components are missing or malfunctioning. I mean, how many planes would be crashing if that wasn’t the case? In that instance, redundancy of function is a hallmark of good design. IC would be a sign of incompetence.
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Completely false, because humans are diploid organisms. Unbelievable.
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How so ?
That’s how I see it too. Also, almost every designed object can be used even if bits of it are missing, especially modern items with lots of functions and unnecessary features, even those that don’t have redundant backup systems.
Aeroplanes are not IC because they continue to be viable even when the lemon-scented paper napkins are absent.
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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