We isolated the
me98 mutant in a genetic screen for C. elegans mutants with an altered number of GFP::COSA-1 foci, which mark the sites of crossovers in wild-type C. elegans germ cells (ROSU et al. 2013). After multiple rounds of outcrossing, we confirmed that the
me98 mutant is defective in meiotic prophase as i) chromosomes in diakinesis oocytes appear partially decondensed and structurally compromised (Fig. 1A), ii)
me98 fails to form the six GFP::COSA-1 foci observed in wild-type late pachytene meiocytes (Fig. 1B) and iii)
me98 accumulates RAD-51 foci during the course of meiotic prophase (Fig. 1C). Further, 100% of eggs laid by
me98 mutant hermaphrodites are inviable. These defects are reminiscent of those caused by the previously-described
rad-54(
ok615) mutation (METS AND MEYER 2009), and sequencing of the
rad-54 locus in
me98 mutants revealed the presence of a 13bp deletion in the second exon of the annotated transcript (I:9065652 to I:9065664 of WS269). This lesion creates a frameshift that would result in premature termination of translation in the third exon (of seventeen) of the predicted transcript (Fig. 1D), suggesting that it is likely a null allele. Of note, the previously described
rad-54 loss-of-function allele,
ok615, is an insertion/deletion that also affects the neighboring gene
snx-3 (Fig 1E). As gonads of
rad-54(
me98) mutants appear overall healthier than those in the
ok615 mutant,
me98 could be a valuable tool to analyze the specific function of
rad-54.