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Identity crisis when telomeres left unprotected Free
Yun Wu * and Virginia A. Zakian*
Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA *Correspondence to:Yun Wu, E-mail: yunwu@princeton.edu; Virginia A. Zakian, E-mail: vzakian@princeton.edu
J Mol Cell Biol, Volume 2, Issue 1, February 2010, 14-16,  https://doi.org/10.1093/jmcb/mjp031

Loss of shelterin components TRF2 or POT1a–TPP1 complex from the chromosome end triggers DNA damage response (DDR) and aberrant DNA repair events. In a recent Nature paper, Chang and colleagues reported that the DNA repair protein Mre11 contributes to multiple events at the uncapped telomere, including ataxia telangiectasia-mutated (ATM)-dependent signaling, processing of the telomeric G-tail and homologous recombination (HR).