Homologous recombination is carefully orchestrated to maintain genome integrity. RAD51D has been previously shown to be essential for double‐strand break repair in mammalian somatic cells. However, the function of RAD51D during meiosis is largely unknown.

 

Here, through detailed analyses of Osrad51d single and double mutants, we pinpoint the specific function of OsRAD51D in coordinating homologous pairing and recombination by preventing nonhomologous interactions during meiosis.

 

OsRAD51D is associated with telomeres in both meiocytes and somatic cells. Loss of OsRAD51D leads to significant induction of nonhomologous pairing and chromosome entanglements, suggesting its role in suppressing nonhomologous interactions. The failed localization of OsRAD51 and OsDMC1 in Osrad51d , together with the genetic analysis of Osrad51d Osdmc1a Osdmc1b , indicates that OsRAD51D acts at a very early stage of homologous recombination. Observations from the Osrad51d pair1 and Osrad51d ku70 double mutants further demonstrate that nonhomologous interactions require double‐strand break formation but do not depend on the KU70‐mediated repair pathway. Moreover, the interplay between OsRAD51D and OsRAD51C indicates both conservation and divergence of their functions in meiosis.

 

Altogether, this work reveals that OsRAD51D plays an essential role in the inhibition of nonhomologous connections, thus guaranteeing faithful pairing and recombination during meiosis.