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Science 16 January 1998:
Vol. 279. no. 5349, pp. 349 - 352
DOI: 10.1126/science.279.5349.349
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Research Articles

Extension of Life-Span by Introduction of Telomerase into Normal Human Cells

Andrea G. Bodnar, * Michel Ouellette, * Maria Frolkis, Shawn E. Holt, Choy-Pik Chiu, Gregg B. Morin, Calvin B. Harley, Jerry W. Shay, Serge Lichtsteiner, dagger Woodring E. Wright dagger

Normal human cells undergo a finite number of cell divisions and ultimately enter a nondividing state called replicative senescence. It has been proposed that telomere shortening is the molecular clock that triggers senescence. To test this hypothesis, two telomerase-negative normal human cell types, retinal pigment epithelial cells and foreskin fibroblasts, were transfected with vectors encoding the human telomerase catalytic subunit. In contrast to telomerase-negative control clones, which exhibited telomere shortening and senescence, telomerase-expressing clones had elongated telomeres, divided vigorously, and showed reduced staining for beta -galactosidase, a biomarker for senescence. Notably, the telomerase-expressing clones have a normal karyotype and have already exceeded their normal life-span by at least 20 doublings, thus establishing a causal relationship between telomere shortening and in vitro cellular senescence. The ability to maintain normal human cells in a phenotypically youthful state could have important applications in research and medicine.

A. G. Bodnar, M. Frolkis, C.-P. Chiu, G. B. Morin, C. B. Harley, and S. Lichtsteiner are at Geron Corporation, 230 Constitution Drive, Menlo Park, CA 94025, USA. M. Ouellette, S. E. Holt, J. W. Shay, and W. E. Wright are in the Department of Cell Biology and Neuroscience, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9039, USA.
*   These authors contributed equally to this work.

dagger    To whom correspondence should be addressed. E-mail: slichtste{at}geron.com; wright{at}utsw.swmed.edu

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Science. ISSN 0036-8075 (print), 1095-9203 (online)