Genetics, Vol. 151, 485-497, February 1999, Copyright © 1999

Role of Saccharomyces cerevisiae Chromatin Assembly Factor-I in Repair of Ultraviolet Radiation Damage in Vivo

John C. Gamea and Paul D. Kaufmana,b
a Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720
b Department of Molecular and Cell Biology, University of California, Berkeley, California 94720

Corresponding author: Paul D. Kaufman, 351 Donner Laboratory, Lawrence Berkeley National Laboratory, Berkeley, CA 94720., pdkaufman{at}lbl.gov (E-mail)

Communicating editor: F. WINSTON

In vitro, the protein complex Chromatin Assembly Factor-I (CAF-I) from human or yeast cells deposits histones onto DNA templates after replication. In Saccharomyces cerevisiae, the CAC1, CAC2, and CAC3 genes encode the three CAF-I subunits. Deletion of any of the three CAC genes reduces telomeric gene silencing and confers an increase in sensitivity to killing by ultraviolet (UV) radiation. We used double and triple mutants involving cac1{Delta} and yeast repair gene mutations to show that deletion of the CAC1 gene increases the UV sensitivity of cells mutant in genes from each of the known DNA repair epistasis groups. For example, double mutants involving cac1{Delta} and excision repair gene deletions rad1{Delta} or rad14{Delta} showed increased UV sensitivity, as did double mutants involving cac1{Delta} and deletions of members of the RAD51 recombinational repair group. cac1{Delta} also increased the UV sensitivity of strains with defects in either the error-prone (rev3{Delta}) or error-free (pol30-46) branches of RAD6-mediated postreplicative DNA repair but did not substantially increase the sensitivity of strains carrying null mutations in the RAD6 or RAD18 genes. Deletion of CAC1 also increased the UV sensitivity and rate of UV-induced mutagenesis in rad5{Delta} mutants, as has been observed for mutants defective in error-free postreplicative repair. Together, these data suggest that CAF-I has a role in error-free postreplicative damage repair and may also have an auxiliary role in other repair mechanisms. Like the CAC genes, RAD6 is also required for gene silencing at telomeres. We find an increased loss of telomeric gene silencing in rad6{Delta} cac1{Delta} and rad18{Delta} cac1{Delta} double mutants, suggesting that CAF-I and multiple factors in the postreplicative repair pathway influence chromosome structure.




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