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May 01, 2001;15 (9): 1061-6.

Asf1 links Rad53 to control of chromatin assembly.

F Hu, A A Alcasabas, S J Elledge
Author Information
  1. F Hu: Verna and Mars McLean Department of Biochemistry and Molecular Biology, Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas 77030, USA.
PMID: 11331602 DOI: 10.1101/gad.873201

Abstract

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.

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Grants

  1. R01 GM044664/NIGMS NIH HHS
  2. R37 GM044664/NIGMS NIH HHS
  3. GM44664/NIGMS NIH HHS

MeSH Term

Cell Cycle Proteins
Checkpoint Kinase 2
Chromatin
DNA Damage
DNA Replication
Fungal Proteins
Gene Expression Regulation, Fungal
Gene Silencing
Genes, Lethal
Genes, Suppressor
Intracellular Signaling Peptides and Proteins
Molecular Chaperones
Mutation
Nucleosomes
Protein Kinases
Protein Serine-Threonine Kinases
Saccharomyces cerevisiae Proteins
Temperature
Yeasts

Chemicals

ASF1 protein, S cerevisiae
Cell Cycle Proteins
Chromatin
Fungal Proteins
Intracellular Signaling Peptides and Proteins
Molecular Chaperones
Nucleosomes
Saccharomyces cerevisiae Proteins
Protein Kinases
Checkpoint Kinase 2
MEC1 protein, S cerevisiae
Protein Serine-Threonine Kinases
RAD53 protein, S cerevisiae
Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Word Cloud

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