A team of scientists from Japan and New Zealand have helped baker’s yeast live 50% longer than usual by artificially stabilising a genetic sequence called ribosomal DNA (rDNA).
The new study is the first to measure the anti-ageing effects of more stable rDNA. Findings have been published in the scientific journal Current Biology.
Massey University geneticist Austen Ganley and his colleagues from the National Institute of Genetics in Japan studied the Sir2 protein. Sir2 was previously found to extend the lifespan of yeast although scientists didn’t know exactly why.
Ganley and his team artificially replicated Sir2’s stabilising effect on rDNA, proving that its anti-ageing effect came exclusively through rDNA stability.
“[The new study] is significant because in humans there are 7 sirtuins [the equivalent of the Sir2 gene] and they all behave very differently to the yeast Sir2 gene,” Ganley said.
“In contrast, the rDNA genes are very similar between yeast and humans, therefore rDNA gene instability may be the common factor in ageing across life.”
Ribosomal DNA is particularly prone to being damaged by radiation and normal chemical reactions in the body. If cells are damaged, they generally stop dividing.
Cell division is how the body grows and repairs itself; cells that stop dividing but remain in the body have been linked to ageing.
The study’s authors say that rDNA is a “hot spot for production of the ageing signal”, and “a major lifespan-determining factor that acts to maintain genome integrity”.
In a statement last week, Massey University described the findings as a step towards anti-ageing drugs, but Ganley said the role of rDNA in human ageing had yet to be clarified.
“We know human rDNA is unstable like yeast,” he told Business Insider.
“The first step is to see whether this rDNA instability is associated with ageing, as no one has ever checked this, and its technically difficult to do.
“If this is true, then the next step would be to find what gene(s) stabilise the rDNA in humans. Sir2 does this job in yeast, but it doesn’t seem to do it in humans, so there must be some other gene responsible.
“Once we’ve found this gene, the final thing is to find some way to artificially activate it, and thus stabilise the rDNA.”
The study builds on previous research by lead researcher Takehiko Kobayashi from the National Institute of Genetics.
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