Meiotic homologous recombination (HR) initiates with the programmed generation of DNA double-strand breaks (DSBs), which result in the exchange of genetic information and genome diversity. This process requires the tight cooperation of the MRE11-RAD50-NBS1 (MRN) complex to promote DSB formation and DNA end resection. However, the mechanism regulating MRN complex remains to be explored. In the present study, we report that MRN-interacting protein, MRNIP, is a novel factor for HR and is crucial for the expression of the MRN complex and loading of recombinases DMC1/RAD51. Knockout of Mrnip in mice led to aberrant synapsis, impaired HR, and male subfertility. In conclusion, MRNIP is a novel HR factor that probably promotes meiotic progression through the MRN complex. • Mrnip is predominantly expressed in mouse testis. • MRNIP is required for homologous recombination (HR). • MRNIP is required for meiotic DSB repair and chromosome synapsis. • Knockout of Mrnip in mice leads to male subfertility. [ABSTRACT FROM AUTHOR]