Journal article
Human telomeres maintain their overhang length at senescence
Molecular and cellular biology, Vol.25(6), pp.2158-2168
03/2005
Handle:
https://hdl.handle.net/2376/101857
PMCID: PMC1061618
PMID: 15743814
Abstract
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.
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Details
- Title
- Human telomeres maintain their overhang length at senescence
- Creators
- Weihang Chai - Department of Cell Biology, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9039, USAJerry W ShayWoodring E Wright
- Publication Details
- Molecular and cellular biology, Vol.25(6), pp.2158-2168
- Academic Unit
- UNKNOWN
- Publisher
- United States
- Grant note
- R01 AG001228 / NIA NIH HHS AG01228 / NIA NIH HHS
- Identifiers
- 99900546551001842
- Language
- English
- Resource Type
- Journal article