ΔNp73β puts the brakes on DNA repair: Figure 1.

Mammalian cells are barraged with endogenous metabolic byproducts and environmental insults that can lead to nearly a million genomic lesions per cell per day. Networks of proteins that repair these lesions are essential for genome maintenance, and a compromise in these pathways propagates mutations that can cause aging and cancer. The p53 tumor suppressor plays a central role in repairing the effects of DNA damage, and has therefore earned the title of “guardian of the genome.” In this issue of Genes & Development , Wilhelm and colleagues (pp. 549–560) demonstrate that p73—an older sibling of p53—inhibits pathways that resolve DNA double-strand breaks.