Shelterin fends off six repair pathways

Abstract

Telomeres have to be protected from being recognized as DNA damage by the repair machinery (the so-called 'end-protection problem'). This is mediated by the shelterin complex, and deletion of individual shelterin subunits has revealed that end-protection involves repression of signalling by ataxia telangiectasia mutated (ATM) and ATR, as well as inhibition of repair mediated by the non-homologous end-joining (NHEJ) and homology-directed repair (HDR) pathways.