Papers

Peer-reviewed International journal
May 26, 2020

Meiosis-Specific C19orf57/4930432K21Rik/BRME1 Modulates Localization of RAD51 and DMC1 to DSBs in Mouse Meiotic Recombination.

Cell reports
  • Kazumasa Takemoto
  • ,
  • Naoki Tani
  • ,
  • Yuki Takada-Horisawa
  • ,
  • Sayoko Fujimura
  • ,
  • Nobuhiro Tanno
  • ,
  • Mariko Yamane
  • ,
  • Kaho Okamura
  • ,
  • Michihiko Sugimoto
  • ,
  • Kimi Araki
  • ,
  • Kei-Ichiro Ishiguro

Volume
31
Number
8
First page
107686
Last page
107686
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1016/j.celrep.2020.107686

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.

Link information
DOI
https://doi.org/10.1016/j.celrep.2020.107686
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32460033
ID information
  • DOI : 10.1016/j.celrep.2020.107686
  • Pubmed ID : 32460033

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