論文

査読有り 最終著者 責任著者 本文へのリンクあり 国際誌
2020年5月26日

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

31
8
開始ページ
107686
終了ページ
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.celrep.2020.107686
出版者・発行元
Cell Press

Summary
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.

リンク情報
DOI
https://doi.org/10.1016/j.celrep.2020.107686
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32460033
共同研究・競争的資金等の研究課題
減数分裂における高次クロマチン構造の確立機構の解明
共同研究・競争的資金等の研究課題
体細胞分裂と減数分裂の違いを生み出す分子機構の解明
共同研究・競争的資金等の研究課題
体細胞型から減数分裂型の細胞周期調節への切替え機構
ID情報
  • DOI : 10.1016/j.celrep.2020.107686
  • PubMed ID : 32460033

エクスポート
BibTeX RIS