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Higher mutation rates in non-double helix DNA create intriguing alternative to common ancestry


Researchers report that DNA sequences that can fold into shapes other than the classic double helix tend to have “higher mutation rates” than other regions in the human genome

“Most of the time we think about DNA as the classic double helix; this basic form is referred to as ‘B-DNA,'” said Wilfried Guiblet, co-first author of the paper, a graduate student at Penn State at the time of research and now a postdoctoral scholar at the National Cancer Institute. “But, as much as 13% of the human genome can fold into different conformations called ‘non-B DNA.’ We wanted to explore what role, if any, this non-B DNA played in variation that we see in mutation rates among different regions of the genome.” …

“When we look at all the known factors that influence regional variation in mutation rates across the genome, non-B DNA is the largest contributor,” said Francesca Chiaromonte, Huck Chair in Statistics for the Life Sciences at Penn State and one of the leaders of the research team. “We’ve been studying regional variation in mutation rates for a long time from a lot of different angles. The fact that non-B DNA is such a major contributor to this variation is an important discovery.”

Penn State, “ Unusual DNA folding increases the rates of mutations” at ScienceDaily

Then we learn something else that’s interesting:

“Mutations are usually thought to be so rare, that when we see the same mutation in different individuals, the assumption is that those individuals shared an ancestor who passed the mutation to them both,” said Makova, a Penn State Cancer Institute researcher. “But it’s possible that the mutation rate is so high in some of these non-B DNA regions that the same mutation could occur independently in several different individuals. If this is true, it would change how we think about evolution.”

Penn State, “ Unusual DNA folding increases the rates of mutations” at ScienceDaily

The paper is open access.

By all means change how you think about evolution. It’s a complex world out there.

(I can post again! Gave up there for a while...) This is reminiscent of the question of whether endogenous retroviruses enter a species and then end up in a descendant species (the evolutionist view), or whether the viruses show a preference for particular spots in DNA, and therefore end up in (nearly) the same places in different species independently. EDTA
Penn State: "... that the same mutation could occur independently in several different individuals. If this is true, it would change how we think about evolution.”" FINALLY! Doubting common descent and shared errors ... i would never expect to hear something like that from Darwinists :)))) martin_r
Different forms of DNA: https://microbenotes.com/different-forms-of-dna-b-form-a-form-z-form/ from the Different-forms-of-DNA-article, i like this part: "There is simply not enough room for the DNA to be stretched out in a perfect, linear B-DNA conformation. In nearly all cells, from simple bacteria through complex eukaryotes, the DNA must be compacted by more than a thousand fold in order even to fit inside the cell or nucleus." :)))))) "there is not enough room ... must be compacted ...." typical Darwinian fluff.... so why after billions of years, 'Nature' did not make MORE ROOM ? Instead of it, 'Nature' did it AS COMPLICATED AD POSSIBLE - compacting the DNA molecule ... Compacting DNA makes everything more complicated in respect to DNA transcription, DNA replication, DNA repair, and so on ... martin_r
Let me add another example of 'common ancestry' and 'shared DNA errors': from my blog at www.StuffHappens.info quoting a mainstream paper: Same pseudogenes evolved independently in human and non-human primate lineages A pseudogene is defined to be a gene that has lost its function, especially it has lost the ability of coding protein. In general, a pseudogene is generated by gain of premature stop codons due to point mutations or flame-shift mutations. The acceptance of premature stop codons in a gene depends strongly on a functional constraint or functional importance of the gene product. In most cases, premature stop codons are accepted only when a gene is functionally compensated by duplicates. However, pseudogenization of single copy genes (a single-copy pseudogene) has been sometimes found in humans and non-human primate genomes. Furthermore, in some cases, deterioration of a gene has taken place independently in different primate lineages. This might be “convergent [repeated] evolution in pseudogenization.” For example, urate oxidase gene, of which product converts purine to allantoin in a purine catabolic pathway, was deteriorated independently in grate-apes/humans and gibbons. Further, a search of human specific pseudogenes reveals 14 cases of independent loss of function in single-copy genes in human and non-human primate lineages. These single-copy pseudogenes might reflect changes in functional significance in biosystems by some particular reasons. These reasons could be related to species-specific traits in morphology and physiology. In this introduction, I review these single-copy pseudogenes and the convergent evolution of pseudogenization in humans and non-human primates and argue the biological significance of psuedogenizations. source: http://primate-society.com/ips/public/ips_program/IPS10-534.pdf PS: WHAT? repeated independent evolution of pseudogenes ???? no way, Darwinists said, that pseudogenes are shared among primates - AN ULTIMATE EVIDENCE OF APE TO HUMAN EVOLUTION ... martin_r
the whole common ancestry idea (despite it looked convincing) is just another example of how Darwinists misinterpreted reality and misled lay public ... they did it so many times ... a misinterpretation after a misinterpretation after a misinterpretation ... (not to mention darwinians' deliberate frauds) martin_r

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