The finding, reported in the current issue of Proceedings of the National Academy of Sciences, could bolster efforts aimed at manipulating the enzyme for therapeutic purposes - whether to prompt cell division in order to replenish stocks of healthy cells, as is needed in bone marrow transplants, or to interrupt the excessive cell proliferation that occurs in cancer cells. Telomerase synthesizes telomeres, snippets of DNA on the ends of chromosomes that function in part like the plastic tips on the ends of shoelaces, preventing the gene-bearing, threadlike spindles from unraveling. With each cycle of cell division, the tips of telomeres drop off, until the chemical bookends become so eroded that the chromosomes become unstable, a condition that signals cells to stop dividing. This natural control on cell division is known as the Hayflick limit.
Cancers develop when cells increasingly ignore or override such signals of chromosome impairment.
Until now, evidence has suggested that the ability of telomerase to extend the life span of cells lay in its capacity to lengthen telomeres. In the current study, a collaboration by the laboratories of Elizabeth Blackburn, PhD, chair of the Department of Microbiology and Immunology at UCSF and Nobel laureate J. Michael Bishop, MD, chancellor of UCSF, researchers have determined that telomerase can extend the life span of human fibroblast cells without lengthening telomeres. The telomerase enzyme, they discovered, caps the ends of telomeres and, in so doing, somehow contributes to telomere, and thus, chromosome, stability - regardless of telomere length. Previous evidence has suggested that telomere length is crucial to determining the life span of cells. But in cells in which we activated the telomerase enzyme, we observed cells thriving despite the fact that their telomeres were very short.