Aging affects everybody, so it’s easy to understand why so much scientific attention is focused on studying it. Scientists in Canada now claim to have found that telomeres play a different role in cellular aging than previously thought.

One of the main points of interest in anti-aging biology are what’s known as telomeres. These are sections of “junk” DNA that form caps on the ends of chromosomes, protecting important genetic information from damage when a cell divides. But a piece of the telomere is eroded away with each cell division, and when it gets too short the cell stops dividing entirely, entering a dormant state known as senescence. The build-up of these senescent cells contributes to a range of symptoms we associate with aging, such as frailty and age-related diseases.

The implication of this model is that telomeres take on a pre-emptive protection role – they signal to cells to stop dividing as soon as one telomere wears out. But there is evidence to suggest that cell division can continue with as many as five dysfunctional telomeres.

In a study published in Nucleic Acids Research, the team of cancer researcher Francis Rodier, an Université de Montréal professor, shows for the first time that cellular senescence, which occurs when aging cells stop dividing, is caused by irreversible damage to the genome rather than simply by telomere erosion.

This discovery goes against the scientific model most widely adopted in the last 15 years, which is based on one principle: telomeres, caps located at the ends of chromosomes whose purpose is to protect genetic information, erode with each cell division. When they get too short, they tell the cell to stop dividing, thus preventing damage to its DNA. Made dormant, the cell enters senescence.

For this model to be valid, the inactivation of a single telomere should be sufficient to activate the senescence program. Rodier’s laboratory and many others had already observed that several dysfunctional telomeres were necessary.