Interaction of Excision Repair Gene Products and Mitotic Recombination Functions in Yeast

Overview

Journal Curr Genet

Specialty Genetics

Date 1993 Dec 1

PMID 8299167

Citations 3

Authors

B A Montelone

Affiliations

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Abstract

We have tested the ability of mutants of three additional genes in the excision repair pathway of Saccharomyces cerevisiae to suppress the hyper-recombination and rad52 double-mutant lethality phenotypes of the rad3-102 (formerly rem1-2) mutation. Such suppression has previously been observed with mutant alleles of RAD1 and RAD4. We had hypothesized that the rad3-102 mutation created elevated levels of DNA lesions which could be processed by the products of the RAD1 and RAD4 genes into recombinogenic double-strand breaks requiring the RAD52 product for repair. In this report, we show that the RAD2, RAD7, and RAD10 genes are also necessary for this processing. We discuss our observations of varying levels of mitotic crossing-over in Rem- rad double-mutant strains.

Citing Articles

A mutant allele of the transcription factor IIH helicase gene, RAD3, promotes loss of heterozygosity in response to a DNA replication defect in Saccharomyces cerevisiae.

Navarro M, Bi L, Bailis A Genetics. 2007; 176(3):1391-402.

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ELG1, a yeast gene required for genome stability, forms a complex related to replication factor C.

Ben-Aroya S, Koren A, Liefshitz B, Steinlauf R, Kupiec M Proc Natl Acad Sci U S A. 2003; 100(17):9906-11.

PMID: 12909721 PMC: 187881. DOI: 10.1073/pnas.1633757100.

Interactions among mutations affecting spontaneous mutation, mitotic recombination, and DNA repair in yeast.

Montelone B, Koelliker K Curr Genet. 1995; 27(2):102-9.

PMID: 7788712 DOI: 10.1007/BF00313423.

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