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Different animal species drink from different fountains of youth, which flow with waters of different potency. That’s the gist of a new study of the SIRT6 protein, which is encoded by the so-called longevity gene. In some species, SIRT6 variants repair damaged DNA more efficiently, better preserving health and youthfulness.

By identifying the stronger SIRT6 variants, scientists based at the University of Rochester have determined that DNA repair and longevity coevolve. The scientists also analyzed the molecular differences between the weaker and stronger versions of SIRT found in various rodent species. Even stronger versions of SIRT6 may be found in especially long-lived organisms, the scientists speculate. The strongest SIRT6 proteins may even help researchers find new targets for anti-aging interventions.

As humans and other mammals grow older, their DNA is increasingly prone to breaks, which can lead to gene rearrangements and mutations—hallmarks of cancer and aging. For that reason, researchers have long hypothesized that DNA repair plays an important role in determining an organism’s lifespan. While behaviors like smoking can exacerbate double-strand breaks (DSBs) in DNA, the breaks themselves are unavoidable.

“They are always going to be there, even if you’re super healthy,” said Dirk Bohmann, PhD, professor of biomedical genetics at the University of Rochester. “One of the main causes of DSBs is oxidative damage and, since we need oxygen to breathe, the breaks are inevitable.”

Bohmann is the coauthor of a study a paper (“SIRT6 Is Responsible for More Efficient DNA Double-Strand Break Repair in Long-Lived Species”) that appeared April 18 in the journal Cell. This paper reports that DSB repair, but not nucleotide excision repair (NER), coevolves with maximum lifespan in rodents. (The evolution of NER, the article notes, is shaped primarily by sunlight exposure.)

The University of Rochester researchers, led by biology professors Vera Gorbunova, PhD, and Andrei Seluanov, PhD, analyzed DNA repair in 18 rodent species with lifespans ranging from 3 years (mice) to 32 years (naked mole rats and beavers). They found that the rodents with longer lifespans also experience more efficient DNA repair because the products of their SIRT6 genes—the SIRT6 proteins—are more potent. That is, SIRT6 is not the same in every species.

“We dissected the molecular differences between a weak (mouse) and a strong (beaver) SIRT6 protein and identified five amino acid residues that are fully responsible for their differential activities,” the article’s authors wrote. “Our findings demonstrate that DSB repair and SIRT6 have been optimized during the evolution of longevity, which provides new targets for anti-aging interventions.”

The capacity of the SIRT6 protein to promote double-strand break (DSB) repair accounts for a major part of the variation in DSB repair efficacy between short- and long-lived species. Five amino acids determine the differential activities of mouse and beaver SIRT6. [Cell]

When the researchers inserted beaver and mouse SIRT6 into human cells, the beaver SIRT6 better reduced stress-induced DNA damage compared to when researchers inserted the mouse SIRT6. The beaver SIRT6 also better increased the lifespan of fruit flies versus fruit flies with mouse SIRT6.

Although it appears that human SIRT6 is already optimized to function, “we have other species that are even longer lived than humans,” Seluanov pointed out. Next steps in the research involve analyzing whether species that have longer lifespans than humans—like the bowhead whale, which can live more than 200 years—have evolved even more robust SIRT6 genes.

The ultimate goal is to prevent age-related diseases in humans, Gorbunova declared. “If diseases happen because of DNA that becomes disorganized with age, we can use research like this to target interventions that can delay cancer and other degenerative diseases.”

The post Some Versions of the Longevity Gene Are Spryer Than Others appeared first on GEN – Genetic Engineering and Biotechnology News.

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