So, you are an expert at every single level of biology?
Didn't say I was. What I am suggesting, and will continue to emphasize, is that your lack of knowledge of the
relevant biological disciplines shows itself repeatedly. There's a certain suspicious arrogance on your part wherein you have the audacity to critique well-evidenced theory without deeply understanding really anything about the relevant biology -- whether it's genomics, molecular biology, biochemistry, or population genetics.
There is no quote, you need to read her papers.
I was familiar with the discoveries and experimental approaches of Barbara McClintock's research when I was a sophomore in high school. I have rather extensively read her notable publications, probably more so than you have or ever will. But, idk, maybe you could cite which paper in particular supports your assertion that the transposition mechanism is pre-programmed in such a way that insertions shouldn't count as beneficial mutations.
It's only non-random insofar as the inverted repeats in the transposon sequence restricts the reposition of that transposon to genomic locations with complementary sequences; but given that the inverted repeat regions of transposons consist of only a small number of nucleotides, there are many, many regions in the genome which would have complementary sequences.
This is non sequitur. We're talking about the causes of the jumps, and not about the characteristics of transposable elements.
Then you don't know how to think experimentally. To understand the causes of the jumps, it is immensely useful to examine the characteristics of transposable elements. The above observations, coupled to reams of experimental research on transposons, indicate that transopson insertions are mutations which are just as stochastic and just as forceful a driver of evolution as substitution mutations (e.g., consider that the transposition rate in bacteria is similar to the spontaneous mutation rate).
Blargh. It gets frustrating when the people who claim to be refuting a theory held by the vast majority of molecular biologists don't take the time to, like, actually study molecular biology.
WOW. What an ignorance. Using an authority as evidence against an argument belongs to the category of logical fallacies.
And an incapacity for verbal comprehension belongs in a number of categories, as well. I am not making an appeal to authority in the above quote; I'm stressing, again, the absurdity of someone trying to argue about molecular biology while having only a rudimentary-at-best understanding of that field.
Also, the ToE has nothing to do with biology, but it is a concept, a human mental construct about unseen past events that is contradicted by every instance of observation in biology.
...says the individual who doesn't understand much about, like, any of the relevant scientific disciplines.
I already said why I think so: "given the fact that most mutations are neutral or harmful, while mutation in British peppered moths resulted in a phenotypic effect(non-neutreal) and it didn't negatively affect the protein-coding capacity of the cortex gene(non-harmful) that indicates that this mutation was pre-programmed in the genome." Hence, simple probability.
Yeah, reading that made me almost spit out my coffee on my computer screen. There is absolutely not a shred of evidence that this mutation was pre-programmed in the genome any more than substitution mutations are. There is, however, a large amount of experimental research which shows that transposon insertions are stochastic, and so the peppered moth example is an excellent example of a beneficial mutation. I bet if BLASTed the peppered moth's transposon insertion sequence, I'd find a ton of homologs in the moth's genome -- and the distribution of these homologs would be random and non-predictable. What do you think?
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