| Literature DB >> 32460033 |
Kazumasa Takemoto1, Naoki Tani2, Yuki Takada-Horisawa3, Sayoko Fujimura2, Nobuhiro Tanno3, Mariko Yamane4, Kaho Okamura3, Michihiko Sugimoto5, Kimi Araki6, Kei-Ichiro Ishiguro7.
Abstract
Meiotic recombination is critical for genetic exchange and generation of chiasmata that ensures faithful chromosome segregation during meiosis I. Meiotic recombination is initiated by DNA double-strand break (DSB) followed by multiple processes of DNA repair. The exact mechanisms for how recombinases localize to DSB remain elusive. Here, we show that C19orf57/4930432K21Rik/BRME1 is a player for meiotic recombination in mice. C19orf57/4930432K21Rik/BRME1 associates with single-stranded DNA (ssDNA) binding proteins, BRCA2 and MEILB2/HSF2BP, which are critical recruiters of recombinases onto DSB sites. Disruption of C19orf57/4930432K21Rik/BRME1 shows severe impact on DSB repair and male fertility. Remarkably, removal of ssDNA binding proteins from DSB sites is delayed, and reciprocally, the loading of RAD51 and DMC1 onto resected ssDNA is impaired in Brme1 knockout (KO) spermatocytes. We propose that C19orf57/4930432K21Rik/BRME1 modulates localization of recombinases to meiotic DSB sites through the interaction with the BRCA2-MEILB2/HSF2BP complex during meiotic recombination.Entities:
Keywords: Chromosome; DSB; Meiosis; RAD51; fertility; meiotic recombination; spermatogenesis
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Year: 2020 PMID: 32460033 DOI: 10.1016/j.celrep.2020.107686
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423