Can you disprove this secular argument against evolution?

That paper deals with non-random nature of mutations and not with differences between various life forms. You are the one grasping at straws. Transposon was placed in an intron of the cortex gene. And guess what?https://www.sciencenewsforstudents.org/...oth-went-dark-side

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The teams have evidence that the cortex gene helps determine when certain wing scales grow. And in butterflies and moths, the timing of wing-scale development affects their colors, says Reed. You see colors popping up almost like a paint-by-numbers.

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As we can see, besides being uneducated about evolution, biology, mathematics, logic and linguistic you've also shown yourself to be a lier. Transposons have nothing to do with neither randomness nor evolution. Barbara McClintock who was awarded with the Nobel Prize for her discovery of transposable elements said that transposable elements are controlling elements. Control and randomness are opposite concepts.Gifts of Speech - Barbara McClintock"... These proved to be transposable elements that could regulate gene expressions in precise ways. Because of this I called them " controlling elements ". Their origins and their actions were a focus of my research for many years thereafter. It is their origin that is important for this discussion, and it is extraordinary."Edited by forexhr, : No reason given.

So now you're behaving like a typical disingenuous creationist cherry picker. The paper actually tells you that.....

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....it may not be practical to extrapolate very much from an asexually reproducing species such as E. coli to organisms that reproduce sexually.

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And Stumpf warns that because bacteria live in such large populations, their evolution in aggregate may be more predictable than that of larger, more dispersed species.

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It was a mutation in the cortex that changed the colour of the moth period. It's just too bad that you find it incovenient. And the mutation was random and affected the evolution of the moth. Weird huh?

Read up on your molecular biology. Transposable elements can regulate nearby genes by virtue of methylation properties, etc., but transposons that "jump" into gene sequences are a form of mutation and are not regulating elements. There's often a happy medium between control and randomness in genomics, and they are both exploited by selection to "drive" the evolution of species. Why do you feel the need to insult people here?Edited by Genomicus, : No reason given.

Entire? If you agree with my post in its entirety, then you are disagreeing with your own O.P. Right in everything except the numbers. In terms of the repressor function, there are probably far more "favourable outcomes". There could well be ~10^108 (Szostak). That's because the paper looks at function in a "family" of proteins derived from the one that's actually there, but not at the sequentially "unrelated" proteins that also might perform that specific function. The 10^57 would be identifiable as "family" by sequence similarity - they would all have at least 20 identical positions (there were 8 that they considered unchangeable in the sample of 33). That's one of your technical errors. I don't know why you made it, because you must know that there are "super-families" identifiable by function but not by sequence, and the paper doesn't actually claim that their 1 in 10^63 figure covers all proteins that could give a minimal selectable function in that context. As I said in my previous post, the first paper in your O.P. covers the highly degenerate "spellings" of the protein that's there, but not its "synonyms" and their multiple spellings. Why not just skip to an entire complex organism, like Homo Sapiens. If you "critically examine the logical consequences" of the paper, the implications are that ~18*10^14 protein search resources would be required for our 18,000 proteins. I'm sure you won't make the mistake of multiplying that for all complex species, as they share many proteins. If our life system currently uses 1 billion proteins, then that would require 10^20 search resources. Or any new functional protein in any context. Getting an added step in an already complex system with existing proteins is no more difficult than getting the first proteins in life from random assemblies. Probably easier. Really? By how much? Are you suggesting, say, ten times, so it would take 10^21 to get 1 billion proteins? Organisms do their protein searching "experiments" in vivo.I'm glad you agree with me so far. So, you can now see that there's no case "against evolution" in your O.P. to be "disproved". There's just a sharpshooter fallacy and technical mistakes.Still, thanks to you for an O.P. that actually links to some interesting papers, and I think you might thank me for reading the papers and helping you through all this.

Yes, landing inside a gene can affect its potential protein-coding capacity, but from that it does not follow that the "jump" in the genome of the peppered moth was not pre-programmed, especially if we take into account that it resulted in a phenotypic effect and is located in intronic region of the cortex gene. Control and randomness have nothing to do with evolution. Control is an instance of functional living systems, while randomness is the lack of predictability in events, which is the general characteristic of natural processes. Evolution on the other hand is concerned with the origin of higher life forms. Higher life forms are characterized by organs, organ systems, de novo molecular machines, metabolic pathways,... none of which can be produced by evolution due to lack of resources, as I already explained. Not people, but only one intellectually dishonest individual.

Key Innovation in Lambda PhageReally? It didn't take much crossing of that vast space to find a new specific function, did it? You should understand by now from the second paper you linked to in the O.P., the Szostak paper and the one linked to above that potentially functional proteins cannot be very rare islands in a huge sea of non-functionality, as you want them to be. It stayed exactly the same while gaining a new function? Why is it amazing? If our ancestors observed some rabbits being born from others, why would it be amazing if they inferred that all rabbits came into existence this way? And why would it be amazing if they were sceptical of an alternative suggestion by conjurers that they could produce new rabbits ex nihilo out of hats?

I think I already addressed this nonsensical point of yours. Resources that are already spent on search for protein A, which is located in a specific location in the genome of a particular species, cannot be spent on search for protein B which is located in other location of the genome or in other species. Let me use an example for illustration.Suppose that each of these two words: "CAT" and "DOG", represents a functional protein fold that needs to be found for adaptation purposes, while the text below represents the genomes of three individual organisms(A, B, C), that all have two duplicated gens, "wdc" and "aii", that are free to explore the above mentioned folds:A) ..............wdc..................................aii
B) ..............wdc..................................aii
C) ..............wdc..................................aiiAfter the reproduction, we have these changes(mutations):A) .....A........wdc...........P........U............Dii
B) .......H......wdc........T.......E................aFi
C) .....T........wdc..........P........Z..............aKiAs we can see, although we have spent 12 mutational resources, we have produced just 3 changes in the "aii" gene, while the "wdc" gene didn't get any change. Since the sequence space of "aii" gene is 17,576(26^3) we need on average 17,576 changes on its locus to produce the "DOG" fold. Once these resources are spent they cannot be spent on search for "CAT" fold on "wdc" loci, or search for any other functional fold. To find the "CAT" fold we need another 17,576 resources.What you did in your nonsensical statement, is put together all the mutations in the history of life that occured in all species of organisms and in all genes, and than you used this number as a separate instance for every new search. This is like writing down every dollar you spent this year and then saying that these, already spent dollars, can now be used for new purchases. All other points in your response are based on misunderstanding of this concept.Given the fact that you cannot comprehend something so simple(that you cannot spend something that has already been spent), it's no wonder that you bought the theory of evolution from the Darwinian evangelists.Edited by forexhr, : No reason given.Edited by forexhr, : No reason given.

Pre-programmed by what? You can't just drop the word "pre-programmed" around and let that take care of your problems. What do you hypothesize pre-programmed this class II transposon to jump specifically into the intron sequence that it did?Introns have a ton of sequences. The inverted repeats of transposable elements consist of very short nucleotide sequences, so there's a huge number of possible intronic sites that the transposon could be ligated to.So where's your evidence that this insertion mutation was pre-programmed in a meaningful way?

I presented my evidences already. 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. But nevertheless, whatever the cause is, this doesn't change the physical impossibility of evolution.Edited by forexhr, : No reason given.Edited by forexhr, : No reason given.

Why does that indicate that this mutation was pre-programmed in the genome? Your logic doesn't add up. And what is the biochemical mechanism of this pre-programming? Describe it to me.Edited by Genomicus, : No reason given.

I am not an expert in this area, but Barbara McClintock, who was, said that the occurrence of the movement and placement of transposable elements is non-random. I believe that these elements are used by cells to regulate specific coding regions of the genome in response to a certain environmental factor. How this happens, exactly, I don’t know.

Ah, great, you came around here pretending to know everything. Now you're backing off.

It shows. So what's her exact quote?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. 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. We're not talking about how transposable elements regulate genes; we're talking about why you think that the act of a transposon jumping into another genomic region is a pre-programmed act. So describe to me the pre-programming mechanism that makes you think that the insertion in this moth's genome doesn't count as a beneficial mutation.Edited by Genomicus, : No reason given.Edited by Genomicus, : No reason given.

Providing arguments for statements is not "pretending to know everything" but appropriate form of discussing or debating. Is this statement of yours some kind of projection, or some kind of reflection of your personality?

So, you are an expert at every single level of biology? There is no quote, you need to read her papers. This is non sequitur. We're talking about the causes of the jumps, and not about the characteristics of transposable elements. WOW. What an ignorance. Using an authority as evidence against an argument belongs to the category of logical fallacies. 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. 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.There is no need for me to describe the exact pre-programming mechanism. Even the most important molecular mechanisms, like those responsible for sperm-egg binding and fusion are largely unknown to science, and yet you are expecting from me to describe the exact mechanisms for something that was largely ignored by geneticists for several decades after Barbara McClintock discovered transposons.