Washington, Nov 27 : Researchers from Harvard Medical School claim to have identified what can be called as potentially universal mechanism of aging.
They found that DNA damage decreases a cell's ability to regulate which genes are turned on and off in particular settings. This mechanism might explain the process of aging.
"This is the first potentially fundamental, root cause of aging that we've found," said Harvard Medical School professor of pathology David Sinclair.
"There may very well be others, but our finding that aging in a simple yeast cell is directly relevant to aging in mammals comes as a surprise," he added.
It is already known that a group of genes called sirtuins are involved in the aging process.
Earlier, a research team led by Sinclair in the Massachusetts Institute of Technology lab of Leonard Guarente found that a particular sirtuin in yeast affected the aging process in two specific ways-it helped regulate gene activity in cells and repair breaks in DNA.
As DNA damage accumulated over time, however, the sirtuin became too distracted to properly regulate gene activity, and as a result, characteristics of aging set in.
In the new study, Philipp Oberdoerffer, a postdoctoral scientist in Sinclair's Harvard Medical School lab, used a sophisticated microarray platform to probe the mammalian version of the yeast sirtuin gene in mouse cells.
Oberdoerffer found that a primary function of sirtuin in the mammalian system was to oversee patterns of gene expression (which genes are switch on and which are switch off).
If the wrong genes are switched on, this can harm the cell.
The sirtuins guard genes that should be off and ensure that they remain silent. To do this, they help preserve the molecular packaging-called chromatin-that shrink-wraps these genes tight and keeps them idle.
When DNA is damaged by UV light or free radicals, sirtuins leave their genomic guardian posts and aid the DNA repair mechanism at the site of damage.
As a result the chromatin wrapping may start to unravel, and the genes that are meant to stay silent may in fact come to life.
Many of these haplessly activated genes are directly linked with aging phenotypes.
In the study conducted using mouse models, the researchers found that a number of such unregulated genes were persistently active in older mice.
"It is remarkable that an aging mechanism found in yeast a decade ago, in which sirtuins redistribute with damage or aging, is also applicable to mammals," says Leonard Guarente, Novartis Professor of Biology at MIT, who is not an author on the paper.
"This should lead to new approaches to protect cells against the ravages of aging by finding drugs that can stabilize this redistribution of sirtuins over time," he added.
These findings appear in the journal Cell.