Baku, September 24 (AZERTAC). Researchers at the Salk Institute have discovered a toggle switch for aging cells. By controlling the growth of telomeres, it may eventually be possible to coax healthy cells to keep dividing and generating even in old age.

The cells in our bodies are constantly dividing, replenishing our lungs, skin, liver, and other organs. Regrettably, most human cells can't keep on dividing forever. Each time a cell divides, a cellular "timekeeper" at the ends of the chromosomes shortens. These timekeepers, called telomeres, are like the aglets at the end of your shoelaces — those important bits of plastic that prevent the lace ends from fraying. But in the case of shortened telomeres, cells are no longer able to divide, resulting in a host of aging-related complications, including organ and tissue degeneration.

Back in 1973, Soviet biologist Alexey Olovnikov predicted the existence of a "fix" or compensatory mechanism for this process. Scientists Carol Greider and Elizabeth Blackburn were awarded the Nobel Prize in 1984 by proving him right. Their team discovered that some cells produce an enzyme called telomerase, which rebuilds telomeres and allows cells to divide indefinitely. This enzyme — which carries its own template (in the form of an RNA molecule) to elongate the telomeres — adds DNA sequence repeats to the end of DNA strands in the telomere regions. Think of them as disposable buffers that block the ends of chromosomes.

Aging, therefore, was thought to arise from a lack of telomerase — but it now appears that telomerase activity is a bit more complicated than that.

The new research shows that telomerase has a kind of toggle switch, and if the switch happens to be flipped to the "off" position, merely having adequate levels of telomerase in our cells may simply not be enough. The research team of Vicki Lundblad and Timothy Tucey discovered that telomerase — even when present — can be turned off, or disassembled. That's a huge deal because an understanding of how this "off" switch can be manipulated — thereby slowing down the telomere shortening process — could eventually lead to treatments for an assortment of aging-related diseases. For example, the regeneration of vital organs later in life.

Lundblad and Tucey made the discovery while working with the yeast Saccharomyces cerevisiae, the same yeast used to make wine and bread. The team developed a strategy that allowed them to observe each component during cell growth and division at very high resolution. This led to an unexpected series of discoveries into how — and when — the telomerase complex puts itself together.