The plasticity of aging can be controlled epigenetically

February 5, 2014

The plasticity of aging can be controlled epigenetically

Discoveries of proteins closely related to the reproductive system whose inhibition increases longevity. These proteins are involved in epigenetic mechanisms, processes where DNA chemical modifications affect its “packaging” and thus the expression of gene encode proteins.

Studies have been carried out on mice and roundworms by biologists at Stanford University School of Medicine who identified a number of genes that, when inhibited, prolong longevity by 30% in the animal. The gene mainly involved is Ash-2, a gene that produces methyltransferase, a protein that is part of the methyl groups that attach to histones, key elements in the mechanism of DNA twisting and untwisting. The inhibition of Ash-2 reduces the number of methyl groups on histones and somehow lengthens the longevity of the animal.

Additionally, blocking Ash-2 expression only in the germline, but not in the rest of the body, results in an increase of longevity.

 “We do not know exactly how this works mechanistically, but we have shown that the presence of the germline is absolutely essential for this longevity extension to happen,” said Brunet, who concluded, “It makes a sort of sense that the reproductive system would be involved in life span, since it is really the only ‘immortal’ part of an organism. In this context, the body is only a mortal coil,” commented Anne Brunet who led a research team whose study was published in Nature 466, 383-387 (15 July 2010) with the title: Members of the H3K4 trimethylation complex regulate lifespan in a germline-dependent manner in C. elegans.