DOI: 10.1101/518035Jan 11, 2019Paper

Srs2 helicase prevents the formation of toxic DNA damage during late prophase I of yeast meiosis

BioRxiv : the Preprint Server for Biology
Hiroyuki SasanumaAkira Shinohara

Abstract

Proper repair of double-strand breaks (DSBs) is key to ensure proper chromosome segregation. In this study, we found that the deletion of the SRS2 gene, which encodes a DNA helicase necessary for the control of homologous recombination, induces aberrant chromosome segregation during budding yeast meiosis. This abnormal chromosome segregation in srs2 cells accompanies the formation of a novel DNA damage induced during late meiotic prophase-I. The damage may contain long stretches of single-stranded DNAs (ssDNAs), which lead to aggregate formation of a ssDNA binding protein, RPA, and a RecA homolog, Rad51, as well as other recombination proteins inside of the nuclei. The Rad51 aggregate formation in the srs2 mutant depends on the initiation of meiotic recombination and occurs in the absence of chromosome segregation. Importantly, as an early recombination intermediate, we detected a thin bridge of Rad51 between two Rad51 foci or among the foci in the srs2 mutant, which is rarely seen in wild type. These might be cytological manifestation of the connection of two DSB ends and multi-invasion. The DNA damage with Rad51 aggregates in the srs2 mutant is passed through anaphase-I and -II, suggesting the absence of DNA damage-induced ce...Continue Reading

Related Concepts

Cell Nucleus
Chromosomes
Tissue Damage
DNA
DNA Damage
DNA, Single-Stranded
Gene Deletion
Meiosis
Recombinant Proteins
Recombination, Genetic

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