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A Three Nucleotide Change by an Unknown Mechanism

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In today’s Phys.Org news page, we hear about a three nucleotide change in the organism “Trypanosoma brucei, a parasite that causes sleeping sickness in Africa and Chagas disease in Latin America.”

Immediately after “transcription”, via a completely unknown mechanism, a three nucleotide portion of the intron associated with …… is replaced by three different nucleotides. Here’s what they say:

“These are changes for which no chemistry is known and has never been described. We don’t know what enzyme is involved and that is the million-dollar question: What mechanism is doing this? We haven’t a clue,” said Juan Alfonzo, professor of microbiology at The Ohio State University and senior author of the study. . . . .

Alfonzo sought to identify the intron, a specific segment of RNA, that needs to be removed before the tRNA can participate in the selection of the right amino acids during protein production. . . . ..

The trouble was, Alfonzo couldn’t locate the intron that he knew was there. After multiple attempts, he found that the intron’s sequence in this organism changed after transcription, the point at which a copy of RNA is made from a DNA sequence as the first step of gene expression.

This edit – hard to find because of its odd nature – consisted of a change to three nucleotides, the molecules that form DNA and RNA. Because of its rarity and unusual nature, it is called a noncanonical edit.
“It’s noncanonical because it is not typical. It is completely not typical,” Alfonzo said. “And for the first time, we show the biological significance. We show that if you don’t edit, you don’t splice. This editing is required for splicing, and splicing is required for functionality. Otherwise, cells die.”

The editing described here is a swap of three nucleotides for three others that, according to the rules of biology, do not belong where they end up. This is why it looks like a mistake.

In order to live, you must ‘splice.’ In order to ‘splice,’ you must edit. But the ‘edit’ must take place immediately—not through Darwinian or Kimurian ways (neutral drift). And the ‘edit’ is ‘noncanonical,’ which means they don’t know how it happens. And, it violates the “rules of biology.” (But, at least they have a ‘word’ for it: noncanonical. You have to have words if you’re going to be a Darwinist, words like, co-option, convergence, exaptation, spandrels, noncanonical, etc, etc.)

The more they look, the more complex life appears. The more they look, the more laughable the Darwinian paradigm becomes. Where (and when) will it all end? Hopefully, soon.

Comments
HoDH: This is simply one more, rather large, conundrum for evolutionary biology. If a three nucleotide change can take place 'immediately after transcription' in a directed and 'targeted' way, then 'random mutations' appear meaningless in comparison. Even if an explanation is proffered (which will tell us that exaptation occurred---gotta love words), then if it is found that this kind of mechanism routinely occurs in organisms (something no one has thought to look for yet), then the usefulness and power of ordinary population genetics---and genetic drift---will pale in significance. And the truth that evolutionary biologists have no real mechanism by which to explain the rise of complexity will lie naked (as it already does) for all to see. As to the expected, typical evolutionary biology explanation: No problem. The organism stumbled onto to a genetic advantage by deleting and replacing this three nucleotide sequence with a sequence that doesn't allow transcription. This change could only occur because there had already been a gene duplication event, and within the duplicated gene, this replacement didn't occur, thus allowing normal transcription in the organism. Then when the mechanism finally 'evolved' allowing this 'on demand' advantageous shift to occur, the duplicated gene---now no longer needed---was deleted. As is typical of Darwinian pseudo-explanations, this entire scenario lies completely beyond experimental verification. Why? Because if you knock out the replacement mechanism (assuming it is found) without the normal acting 'duplicated gene', the organism to die! Now what do you do with your experiment? And, of course, the transitional species having the 'duplicated gene' is nowhere to be found. So what we're left with is no more than another "just-so" story, the kind that Darwinism is absolutely littered with to almost the point of saturation.PaV
October 5, 2013
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This helps evolution. Yes or No? Sounds pretty darned useful. Thoughts and explanations anybody?Ho-De-Ho
October 4, 2013
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This is somewhat off topic but relative to this blog and website I believe: Red Rain In Sri Lanka: http://science.discovery.com/tv-shows/the-unexplained-files/the-unexplained-files-videos/red-rain-in-sri-lanka.htmsmiddyone
October 3, 2013
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Just no faith in the scientismificists' promissory note, have you, eh, PaV? Shame on you.Axel
October 3, 2013
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