We have investigated the role of Caenorhabditis elegans RAD-51 during meiotic prophase and embryogenesis, making use of the silencing effect of RNA interference (RNAi).
rad-51 RNAi leads to severe defects in chromosome morphology in diakinesis oocytes. We have explored the effect of
rad-51 RNAi in mutants lacking fundamental components of the recombination machinery. If double-strand breaks are prevented by
spo-11 mutation,
rad-51 RNAi does not affect chromosome appearance. This is consistent with a role for RAD-51 downstream of the initiation of recombination. In the absence of MRE-11, as in the absence of SPO-11, RAD-51 depletion has no effect on the chromosomes, which appear intact, thus indicating a role for MRE-11 in DSB induction. Intriguingly,
rad-51 silencing in oocytes that lack MSH-5 leads to chromosome fragmentation, a novel trait that is distinct from that seen in
msh-5 mutants and in
rad-51 RNAi oocytes, suggesting new potential roles for the
msh-5 gene. Silencing of the
rad-51 gene also causes a reduction in fecundity, which is suppressed by mutation in the DNA damage checkpoint gene
rad-5, but not in the cell death effector gene
ced-3. Finally, RAD-51 depletion is also seen to affect the soma, resulting in hypersensitivity to ionizing radiation in late embryogenesis.