Human telomeres maintain their overhang length at senescence

Weihang Chai, Jerry W. Shay, Woodring E. Wright

Research output: Contribution to journalArticlepeer-review

55 Scopus citations


Normal human cells in culture enter replicative senescence after a finite number of population doublings. The exact molecular mechanisms triggering the growth arrest are poorly understood. A recent report on the disappearance of the G-rich 3′ telomeric overhang in senescent cells led to the hypothesis that loss of the 3′ G-rich overhang is the molecular signal that triggers senescence. Here, we describe a quantitative assay to measure the length of the G-rich 3′ telomeric overhangs from cultured cells. Using both this assay and the conventional nondenaturing hybridization assay for measuring G-rich overhangs, we show that normal human fibroblasts can maintain their overhangs at senescence. Furthermore, cells do not lose their overhangs when they bypass senescence after the inactivation of p53 and Rb. We thus conclude that a global reduction in overhang length is not the molecular signal that triggers replicative senescence.

Original languageEnglish (US)
Pages (from-to)2158-2168
Number of pages11
JournalMolecular and cellular biology
Issue number6
StatePublished - Mar 2005

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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