Ino80 and Swr1 are ATP-dependent chromatin remodeling enzymes that have been 
implicated in DNA repair. Here we show that Ino80 is required for cell cycle 
checkpoint adaptation in response to a persistent DNA double-strand break (DSB). 
The failure of cells lacking Ino80 to escape checkpoint arrest correlates with 
an inability to maintain high levels of histone H2AX phosphorylation and an 
increased incorporation of the Htz1p histone variant into chromatin surrounding 
the DSB. Inactivation of Swr1 eliminates this DNA damage-induced Htz1p 
incorporation and restores H2AX phosphorylation and checkpoint adaptation. We 
propose that Ino80 and Swr1 function antagonistically at chromatin surrounding a 
DSB, and that they regulate the incorporation of different histone H2A variants 
that can either promote or block cell cycle checkpoint adaptation.