So you think that DNA microevolutionary adaptation works differently in bacteria than any other replicator? Show us the math, you won't.
You have horrible reading comprehension and look like a sad 1-trick pony. So you think bacterial antibacterial resistance is just like evolutionary changes that result in morphological differences? Go back to the fairy tale forum.
I cited Haldane's paper because he was not modeling DNA microevolution, he is modeling competition. If you understand the physics of biological evolution, you know when Haldane's model is applicable.
I know it basically isn't. You don't.
When I first started studying [sic] Haldane's work, I wondered if there was an exact solution and how it compared to Haldane's approximate solution. I wrote an exact solution and it turns out that Haldane's approximate solution is fairly accurate. But you wouldn't know because you have no idea what Haldane is doing. Actually, his model is quite simple and useful. I used a variation of his model when writing the mathematics for the Lenski experiment.
Looks like an engineer's approach to biology didn't serve you so well.
Here is Ewens, in
an interview in 2004:
A second form of the load concept was introduced by the British biologist-mathematician Haldane who claimed, in 1957, that substitutions in a Darwinian evolutionary process could not proceed at more than a certain comparatively slow rate, because if they were to proceed at a faster rate, there would be an excessive “substitutional load.” Since Haldane was so famous, that concept attracted a lot of attention. In particular, Crow and Kimura made various substitutional load calculations around 1960, that is at about that time that I was becoming interested in genetics.
Perhaps the only disagreement I ever had with Crow concerned the substitutional load, because I never thought that the calculations concerning this load, which he and others carried out, were appropriate. From the very start, my own calculations suggested to me that Haldane’s arguments were misguided and indeed erroneous, and that there is no practical upper limit to the rate at which substitutions can occur under Darwinian natural selection.
And further:
AP: Can I follow that up? Can you, in layman’s terms, explain why you think that there is no upper limit in the way that Haldane suggested?
WE: I can, but it becomes rather mathematical. Let me approach it this way. Suppose that you consider one gene locus only, at which a superior allele is replacing an inferior allele through natural selection. In broad terms, what this requires is that individuals carrying the superior allele have on average somewhat more offspring than the mean number of offspring per parent, otherwise the frequency of the superior allele would not increase. This introduces a concept of a “one-locus substitutional load,” and a formal numerical value for this load is fairly easily calculated. However, the crux of the problem arises when one considers the many, perhaps hundreds or even thousands, substitution processes that are being carried out at any one time. In his mathematical treatment of this “multi-locus” situation, Kimura, for example, in effect simply multiplied the loads at the various individual substituting loci to arrive at an overall total load. The load so calculated was enormous. This uses a reductionist approach to the load question, and to me, this reductionist approach is not the right way of doing things. Further, the multiplicative assumption is, to me, unjustified. It is the selectively favored individuals, carrying a variety of different genes at different loci, who are reproducing and being required to contribute more offspring than the average. If you consider load arguments from that individual-based, non-reductionist basis, the mathematical edifice which Kimura built up just evaporates, and in my view the very severe load calculations which he obtained by his approach became irrelevant and misleading. The individual-based calculations that I made indicated to me that there is no unbearable substitutional load.
So, where is the macroevolutionists' mathematical explanation of the Kishony and Lenski evolutionary experiments? If you want to see that mathematical explanation, you need to expand your reading list beyond your so-called "on topic" journals.
Math is nice, but when the models fail, I look at the actual evidence.
One-trick ponies eventually need to be put out to pasture.
And don't worry about citations to my papers, there are ones you have missed and there will be more by authors that actually want to understand the evolution of drug resistance.
Right - you're the expert at math and drug resistance - so, in your amazingly un-read yet somehow groundbreaking papers, did you first ask where the bacterial genes undergoing selection came from in the first place?
Or do you just do that when you have no clue despite claiming expertise?
What is the probability that an ACCORD transposon inserted into the p450 allele in drosophila that provided them with DDT resistance?
Show your mathemagic.
2002 Sep 27;297(5590):2253-6.
doi: 10.1126/science.1074170.
A single p450 allele associated with insecticide resistance in Drosophila
Abstract
Insecticide resistance is one of the most widespread genetic changes caused by human activity, but we still understand little about the origins and spread of resistant alleles in global populations of insects. Here, via microarray analysis of all P450s in Drosophila melanogaster, we show that DDT-R, a gene conferring resistance to DDT, is associated with over-transcription of a single cytochrome P450 gene, Cyp6g1. Transgenic analysis of Cyp6g1 shows that over-transcription of this gene alone is both necessary and sufficient for resistance. Resistance and up-regulation in Drosophila populations are associated with a single Cyp6g1 allele that has spread globally.
This allele is characterized by the insertion of an Accord transposable element into the 5' end of the Cyp6g1 gene.
