Loss of Rap1 Induces Telomere Recombination in the Absence of NHEJ or a DNA Damage Signal

Abstract

Shelterin the Ends The ends of linear chromosomes suffer two problems: They cannot be replicated to their termini, resulting in loss of terminal sequences; and they can be mistakenly sensed as DNA double-strand breaks, activating DNA repair pathways that can result in serious genome derangement. These problems are solved by the addition of telomeres, repeat sequences at the ends of chromosomes, which are shielded by a protein complex called shelterin. Sfeir et al. (p. 1657 ) show that the mouse Rap1 protein, which is part of the shelterin complex and which binds to a second shelterin protein called TRF2, helps prevent telomeres undergoing unscheduled homologous recombination. Such recombination could threaten telomere integrity by generating sequence exchanges between sister telomeres resulting in critically shortened telomeres.