FIGL1 attenuates meiotic interhomolog repair and is counteracted by RAD51 paralog XRCC2 and chromosome axis protein ASY1 during meiosis

Abstract

Two recombinases, RAD51 and DMC1, catalyze meiotic break repair to ensure crossovers (COs) between homologous chromosomes (interhomolog) rather than between sisters (intersister). FIDGETIN-LIKE-1 (FIGL1) downregulates both recombinases. However, the understanding of FIGL1 functions in meiotic repair remains limited. Here, we discover new genetic interactions of Arabidopsis thaliana FIGL1 that are important in vivo determinants of meiotic repair outcome. In figl1, compromising the RAD51-dependent repair by either losing RAD51 paralogs (RAD51B or XRCC2) or RAD54 or inhibiting RAD51s catalytic activity results in either unrepaired breaks or meiotic CO defects. Further, XRCC2 physically interacts with FIGL1 and partially counteracts FIGL1 for RAD51 focus formation. Our data support that RAD51-mediated repair mechanisms compensate for the FIGL1 dysfunction. FIGL1 is dispensable for intersister repair in dmc1 but is essential for meiotic repair completion in mutants with impaired DMC1 functions and interhomolog bias such as asy1. We show that FIGL1 attenuates interhomolog repair, and ASY1 counteracts FIGL1 to promote interhomolog recombination.