Also, as White explained in the paper that started Behe on this whole brainstorm of his, there are many factors other than the mere presence of the resistant strain that will determine whether that strain will become established after use of chloroquine. The goal of the paper Lee was discussing was to determine whether CR in malaria would wane after chloroquine use was stopped. Treating asymptomatic infections with chloroquine is a good way to test that, but it doesnât tell you if the strain has completely disappeared.
Anyway, I continue to be amused at the particular form of creationist thinking @lee_merrill has been demonstrating here. According to him, if a strain gradually declines for eight years, then (as he mistakenly believes) finally disappears completely in the ninth year, this equates to it having instantly disappeared in a single year. How special is that?
I guess I missed that. This certainly seems like an accurate summary of how this discussion has proceeded:
OTOH, I donât really see how that link you provided amounts to an admission that Beheâs calculations were based on a faulty assumption. That said, I donât really know what Lee was trying to say there:
On reviewing âThe Edge of Evolutionâ again, I realized I had gotten Beheâs argument wrong, he does require simultaneous mutations, since he is considering a set of two mutations, where a single mutation in the set is deleterious. Apologies, especially to rogue06.
But I do wonder in the case of chloroquine resistance, whether each of the two required mutations is deleterious by itself. I think not, since the probability of both mutations is the multiplied probability of one mutation singly.
He mentions the cilium and the flagellum and the machinery that builds them, for starters.
Chloroquine resistance arises in about 1 in 10^20 organisms, whereas atovaquone resistance arises in about 1 in 10^12 organisms. This is evidence that 2 individually deleterious mutations (therefore needing to be simultaneous) are required.
And from 13% to apparent absence in 1 year, so that would indicate negative selection.
If the two mutations on each main path are deleterious, it does.
Nope, I havenâtâŚ
He defends his hypothesis versus the critics in A Mousetrap for Darwin.
Yes, but in resistance to penicillin, the organism survives, or it doesnât.
So that would be te forward approach? Axe was aware of such when he wrote his paper:
âA number of studies have suggested that functional sequences are not extraordinarily rare,1., 2., 3., 4., 5. while others have suggested that they are.6., 7., 8., 9. One of two approaches is typically used in these studies. The first, which could be termed the forward approach, involves producing a large collection of sequences with no specified resemblance to known functional sequences and searching either for function or for properties generally associated with functional proteins. If the relevant sort of properties can be found among more or less random sequences, this provides a direct demonstration of their prevalence. The second approach works in reverse from an existing functional sequence. Here, the question is how much randomization a sequence known to have the relevant sort of function can withstand without losing that function.â
That would be one new protein-protein binding site, though, within Beheâs edge.
Thatâs a suggestion, a selectable path for a cilium or a flagellum would serve as a counter-example.
But he tested for penicillin resistance, correct?
Certainly, but function typically depends on structure: âSince tertiary structure is needed for a typical enzyme active site to form, one way to obtain this estimate is to measure the prevalence of sequences supporting a working active site.â
Well, Behe references malaria and HIV as confirming his estimate of the difficulty of producing a new protein-protein binding site: âCould the edge of evolution be as close as a single cellular protein-protein binding site, rather than two? After all, no new such interactions have been uncovered in malaria and HIV.â (The Edge of Evolution, p. 145)
Because I find his arguments convincing, one new protein-protein binding site in HIV is within the edge. And I have not examined his arguments (or @swamidass 's arguments) for common descent, from what I have seen, there are good arguments against it.
I like trying out ideas in internet forums, especially with experts. It helps me understand better, and understand whether the ideas and arguments hold up well.
So then, you might need to be a bit more agnostic about common descent. The RTB article you linked to does not present any challenge to our argument for common descent.
In real science, one tries to falsify oneâs own hypothesis. In pseudoscience, one pretends that rhetoric trumps everything, as you are doing here. Behe literally rejected the scientific method when under oath.
No, that is objectively false. So why not just admit that you donât understand the concept of a continuous function instead of repeating your false claims?
Yes, which is much better than Axeâs.
Yes, but he didnât cite much of the evidence from it.
Thatâs what the cited paper does. Axe is off by a magnitude of 10^69. Thatâs a pretty impressive error.
Which is not an accurate description of what he did, particularly since he didnât measure enzymatic activity.
One of the five that have been described in the primary literature that Behe doesnât bother reading. Going from zero to one is an infinitely large error itself, no?
At only a single concentration. Penicillin resistance is a continuous function too. Thatâs why the paper is so lame.
You arenât understanding at all. Different structures often have the same enzymatic activity.
Heâs wrong. Objectively.
Behe has admitted that the HIV part of that is false, remember?
So why did you quote Beheâs false statement today, as though he is some sort of authority?
Science is about the evidence, which Behe only pretends to examine.
Please show your math.
My, thatâs convenient. What about all the evidence for common descent? Have you ever examined any evidence at all? Why is it all rhetoric?
Do you think any of them are? Has your understanding increased?
I was very interested to find the good arguments against common descent. Imagine my surprise when the only argument mentioned was that modern Homo sapiens has a slightly differently shaped skull than other species of Homo. Now thatâs underwhelming. Itâs more pathetic than any of the arguments @lee_merrill has attempted here. Prior commitment to a belief functions as a very efficient set of blinders.
No, how you sample does matter:
âFor this reason, intragenic recombination effectively explores functional ridges through a protein sequence space that is mostly nonfunctional.â
How did it matter in that specific experiment?
Very good, Lee, very impressive. You were able to find the word ânonfunctionalâ somewhere in that study.
I guess that somehow negates these words (along with every other word in that paper).
The model reveals a recombinational landscape that is highly enriched in functional sequences, with properties dominated by a large-scale additive structure. It also quantifies the relative contributions of parent sequence identity, crossover locations, and protein fold to the tolerance of proteins to recombination. Intragenic recombination explores a unique subset of sequence space that promotes rapid molecular diversification and functional adaptation.
@colewd better watch his back. We have a new contender here.
Their experiment was sampling âfunctional ridgesâ in sequence space. So sequence space has ridges, and it matters how you sample.
Yes.
Axe sampled wrong.
Do you understand what is meant by a "recombinational landscape that is highly enriched in functional sequencesâ'? Do you think it is compatible with âOnly 1 in 1070 sequences is functionalâ?
Hint: The answer is âNo.â
Michael Egnor fires back.A sample:
The quote from Egnor (above) bears strong resemblance to Presuppositional Apologetics; an annoying sort of argument I havenât seen for a while.
An interesting phenomenon I appreciate about Presuppositional Apologetics is that the more popular it gets, the less popular it gets.
Egnorâs reply is a train wreck, but chief among the many problems is that it is reasonable to accept universal laws as designed or teleological while also accepting evolution. Evolution is about biology, not philosophy or theology.
The Rosenhouse book is available and looks interesting:
How was sampling not done correctly in this experiment?
Ohh, he DI is really pulling out the big guns now. A neurosurgeon, of all people?
He sampled randomly, though.
Do you mean this paper? This is about intragenic recombination, like the chimeric genes discussed at Pandaâs Thumb. It would not seem surprising if you get more functionality by fusing gene parts together, also, this would not be typical of evolution.
Then there is this quote: " For comparison, random mutation libraries with the same number of mutations are estimated to contain 10â20 orders of magnitude fewer functional sequences [13]â[15]."