Catalina Pereira, Gerardo A Arroyo-Martinez, Matthew Z Guo, Michael S Downey, Emma R Kelly, Kathryn J Grive, Shantha K Mahadevaiah, Jennie R Sims, Vitor M Faca, Charlton Tsai, Carl J Schiltz, Niek Wit, Heinz Jacobs, Nathan L Clark, Raimundo Freire, James Turner, Amy M Lyndaker, Miguel A Brieno-Enriquez, Paula E Cohen, Marcus B Smolka, Robert S Weiss
DNA damage response mechanisms have meiotic roles that ensure successful gamete formation. While completion of meiotic double-strand break (DSB) repair requires the canonical RAD9A-RAD1-HUS1 (9A-1-1) complex, mammalian meiocytes also express RAD9A and HUS1 paralogs, RAD9B and HUS1B, predicted to form alternative 9-1-1 complexes. The RAD1 subunit is shared by all predicted 9-1-1 complexes and localizes to meiotic chromosomes even in the absence of HUS1 and RAD9A. Here, we report that testis-specific disruption of RAD1 in mice resulted in impaired DSB repair, germ cell depletion, and infertility...
February 8, 2022: ELife