Synaptic plasticity: Adding a piece to the LTP jigsaw.

摘要

Telomere capping affords protection against checkpoint mechanisms that would normally sense and respond to the presence of DNA double-stranded breaks (DSBs). Ribeyre and Shore now find that the telomere-interacting factors RAPl-interacting factor 1 (Rifl) and Rif2 each use distinct mechanisms to prevent checkpoint activation at short telomeres and that they can exert this effect in trans to block a response at neighbouring telomeres.Telomere capping complexes protect telomeres from resection throughout the cell cycle. Rifl and Rif2 also inhibit resection of telomeres and alter checkpoint protein binding. However, as they also influence telomere elongation, their direct role in protecting telomeres has been unclear. Ribeyre and Shore therefore set out to address how Rifl and Rif2 act at de novo telomeres, using an established single cell assay in which telomeric sequences of defined length are placed on either side of an induced DSB.