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Vol. 15, No. 9, pp. 1061-1066, May 1, 2001
Verna and Mars McLean Department of Biochemistry and Molecular
Biology, Howard Hughes Medical Institute, Baylor College of Medicine,
Houston, Texas 77030, USA
Yeast defective in the checkpoint kinase Rad53 fail to recover
from transient DNA replication blocks and synthesize intact chromosomes. The effectors of Rad53 relevant to this recovery process
are unknown. Here we report that overproduction of the chromatin
assembly factor Asf1 can suppress the Ts phenotype of mrc1rad53
double mutants and the HU sensitivity of rad53 mutants. Eliminating silencing also suppresses this lethality, further implicating chromatin structure in checkpoint function. We find that
Asf1 and Rad53 exist in a dynamic complex that dissociates in response
to replication blocks and DNA damage. Thus, checkpoint pathways
directly regulate chromatin assembly to promote survival in response to
DNA damage and replication blocks.
[Key Words: Asf1; Rad53; checkpoint kinases; chromatin assembly]
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