The Saccharomyces cerevisiae MUM2 Gene Interacts With the DNA Replication Machinery and Is Required for Meiotic Levels of Double Strand Breaks

Author:

Davis Luther1,Barbera Maria1,McDonnell Amanda1,McIntyre Katherine2,Sternglanz Rolf2,Jin Quan-wen3,Loidl Josef3,Engebrecht JoAnne1

Affiliation:

1. Department of Pharmacological Sciences, Graduate Program in Genetics

2. Department of Biochemistry and Cell Biology, State University of New York, Stony Brook, New York 11794-8651

3. Department of Cytology and Genetics, Institute of Botany, University of Vienna, Vienna, Austria A-1030

Abstract

Abstract The Saccharomyces cerevisiae MUM2 gene is essential for meiotic, but not mitotic, DNA replication and thus sporulation. Genetic interactions between MUM2 and a component of the origin recognition complex and polymerase α-primase suggest that MUM2 influences the function of the DNA replication machinery. Early meiotic gene expression is induced to a much greater extent in mum2 cells than in meiotic cells treated with the DNA synthesis inhibitor hydroxyurea. This result indicates that the mum2 meiotic arrest is downstream of the arrest induced by hydroxyurea and suggests that DNA synthesis is initiated in the mutant. Genetic analyses indicate that the recombination that occurs in mum2 mutants is dependent on the normal recombination machinery and on synaptonemal complex components and therefore is not a consequence of lesions created by incompletely replicated DNA. Both meiotic ectopic and allelic recombination are similarly reduced in the mum2 mutant, and the levels are consistent with the levels of meiosis-specific DSBs that are generated. Cytological analyses of mum2 mutants show that chromosome pairing and synapsis occur, although at reduced levels compared to wild type. Given the near-wild-type levels of meiotic gene expression, pairing, and synapsis, we suggest that the reduction in DNA replication is directly responsible for the reduced level of DSBs and meiotic recombination.

Publisher

Oxford University Press (OUP)

Subject

Genetics

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