s The demise of a TUDOR under stress opens a chromatin link to 53BP1

The mechanisms that localise 53BP1 to sites of DNA double-strand breaks (DSBs) have remained elusive, despite this protein's key roles in DNA damage response signalling and repair processes. Recent studies, including the work by Mallette et al (2012) in this issue of The EMBO Journal, now provide crucial insights into the roles of ubiquitin-dependent signalling cascades at DNA damage sites required for chromatin-mediated 53BP1 recruitment