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.

减数分裂重组对于确保减数分裂I期间忠实的染色体分离的基因交换和Chiasmata的产生至关重要。减数分裂重组是由DNA双链断裂（DSB）引发，随后是DNA修复的多个过程。重组酶如何定位于DSB的确切机制仍不清楚。在这里，我们显示C19orf57 / 4930432K21Rik / BRME1是小鼠减数分裂重组的参与者。C19orf57 / 4930432K21Rik / BRME1与单链DNA（ssDNA）结合蛋白BRCA2和MEILB2 / HSF2BP结合，它们是重组酶在DSB位点上的关键募集者。C19orf57 / 4930432K21Rik / BRME1的破坏显示出对DSB修复和男性生育能力的严重影响。值得注意的是，从DSB位点去除ssDNA结合蛋白的过程被延迟，并且相应地，RAD51和DMC1在切除的ssDNA上的装载受到损害。Brme1敲除（KO）精母细胞。我们提出，C19orf57 / 4930432K21Rik / BRME1通过减数分裂重组过程中与BRCA2-MEILB2 / HSF2BP复合体的相互作用来调节重组酶对减数分裂DSB位点的定位。