Repair of DNA broken ends is similar in embryonic fibroblasts with and without telomerase

Radiat Res. 2004 Aug;162(2):136-42. doi: 10.1667/rr3203.

Abstract

Telomeres cap the ends of chromosomes, preventing end-to-end fusions and subsequent chromosome instability. Here we used a telomerase knockout model to investigate whether telomerase participates in the processes of DNA break repair by de novo synthesis of telomere repeats at broken chromosome ends (chromosome healing). Chromosome healing giving rise to new detectable telomeric signals has not been observed in embryonic fibroblasts of telomerase-proficient mice exposed to ionizing radiation. Since the synthesis of telomeric sequences to broken DNA ends would make them refractory to rejoining events, the efficiency of rejoining of broken chromosomes in cell environments with and without telomerase has also been investigated. We conclude that the efficiency of rejoining broken chromosomes is not significantly different in the two cell environments. All together, our results indicate that there is no significant involvement of telomerase in the healing of broken DNA ends by synthesizing new telomeres in mouse embryo fibroblasts after exposure to ionizing radiation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • DNA Damage*
  • DNA Repair*
  • Embryo, Mammalian / cytology
  • Embryo, Mammalian / metabolism*
  • Fibroblasts / metabolism
  • In Situ Hybridization, Fluorescence
  • Mice
  • Mice, Knockout
  • Telomerase / genetics
  • Telomerase / physiology*

Substances

  • Telomerase