Chromosome ends teach unexpected lessons on DNA damage signalling

The ATM/ATR-dependent checkpoint kinases restrain mitotic entry when cells accumulate unrepaired DNA double-strand breaks (DSBs) or when telomeres become uncapped. New work by Thanasoula et al (2012) reveals an intricate network of checkpoint interactions in the wake of telomere uncapping through removal of TRF2 or POT1, providing compelling evidence that the mechanism of G2/M checkpoint activation at chromosome end is distinct from the canonical DNA damage response to ionizing radiation (IRs).