As we age, our cells pick up DNA mutations. It was long assumed that these mutations lead to the process of aging, but a growing body of evidence suggests that aging is primarily regulated by “epigenetic” modifications, changes to regulation of genes rather than changes to genes themselves. A new study in the roundworm C. elegans supports this theory.

Researchers at the Max Delbrueck Center for Molecular Medicine found that worms without the gene lin-53 lived shorter than normal lives. They also displayed muscle deterioration and difficulty moving, which is characteristic of old age. lin-53 encodes for a so-called “histone chaperone”, a protein that regulates the activity of DNA by changing the way it’s folded. This change in DNA activity had profound changes to the worms’ metabolism. Of particular interest, worms without lin-53 produced less trehalose, a sugar that had previously been shown to increase lifespan in worms. As a result, feeding the worms additional trehalose was enough to increase the lifespan of these mutant worms.

Much of the research on aging is done in C. elegans because it has a very short lifespan of about two weeks, meaning researchers can study aging in the lab without waiting years to see results. Of course, worms are very distantly related to humans, so what leads to longevity in C. elegans may not necessarily apply to us, despite humans having a version of lin-53. More broadly, the idea that aging is largely driven by epigenetics seems to be true in humans.


Managing Correspondent: Julian Segert

Press article: Epigenetic mechanism appears to strongly influence healthy aging

Original article: The conserved histone chaperone LIN‐53 is required for normal lifespan and maintenance of muscle integrity in Caenorhabditis elegans Aging Cell

Image credit: Wikimedia Commons

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