Yeast defective in the checkpoint kinase Rad53 fail to recover from transie
nt DNA replication blocks and synthesize intact chromosomes. The effecters
of Rad53 relevant to this recovery process are unknown. Here we report that
overproduction of the chromatin assembly factor Asf1 can suppress the Ts p
henotype of mrc1rad53 double mutants and the HU sensitivity of rad53 mutant
s. Eliminating silencing also suppresses this lethality, further implicatin
g chromatin structure in checkpoint function. We find that Asf1 and Rad53 e
xist in a dynamic complex that dissociates in response to replication block
s and DNA damage. Thus, checkpoint pathways directly regulate chromatin ass
embly to promote survival in response to DNA damage and replication blocks.