High copy number suppression of the meiotic arrest caused by a <i>dmc1</i> mutation: <i>REC114</i> imposes an early recombination block and <i>RAD54 </i>promotes a <i>DMC1</i>‐independent DSB repair pathway

Abstract

Over-expression of REC114 suppresses meiotic arrest by preventing formation of DSBs. High copy numbers of RAD54 activate a DMC1-independent mechanism that promotes repair of DSBs by homology-mediated recombination. The ability of RAD54 to promote DMC1-independent recombination is proposed to involve suppression of a constraint that normally promotes recombination between homologous chromatids rather than sisters.