ΔNp73β puts the brakes on DNA repair

Abstract

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. Copyright © 2010 by Cold Spring Harbor Laboratory Press.