Faithful inheritance of chromosomes during sexual reproduction requires the coordinated action of multiple meiosis-specific chromosome structural components, meiotic recombination proteins, and regulatory factors. Mutagenesis-based genetic screening approaches in C. elegans have proven highly fruitful for identifying key components of this meiotic machinery. Here we report two novel meiosis components identified using such strategies. The
me96 mutant was identified in a cytological screen for meiotic abnormalities visible in oocytes at diakinesis, the last stage of meiotic prophase. Overall,
me96 worms produce 60% dead embryos and 11% male progeny and exhibit a mixture of univalents and bivalents at diakinesis. Notably, the phenotype becomes progressively more severe as the worms get older. Mapping, RNAi and sequencing revealed that the
me96 allele contains an early stop mutation in the F26H11.4 gene, thus defining a novel component of the meiotic machinery. F26H11.4 has three paralogs in C. elegans; interestingly, whereas F26H11.4 exhibits oogenesis-enriched expression, its three paralogs are expressed in spermatogenesis, suggesting sex-specific functional diversification. Immunofluorescence experiments show that loading of the synaptonemal complex appears normal in the
me96 mutant, but RAD-51 foci, which are markers of DNA double strand breaks (DSBs), are reduced. This suggests that F26H11.4 is involved in regulating DSB formation or processing, steps that are critical for meiotic recombination. Further characterization of this mutant will provide new insights into the complex regulation of meiotic recombination. The
tn309 mutant was isolated in a screen for temperature-sensitive embryonic lethal mutants in the Greenstein lab. At 25 degrees, the
tn309 mutant exhibits achiasmate chromosomes in diakinesis-stage oocytes and produces both dead embryos (70-80%) and a high incidence of males (10%), phenotypes indicative of a meiotic defect. The
tn309 mutation has been mapped to a 0.68 cM region on chromosome I containing 34 genes, none of which are previously known meiosis genes. Further genetic mapping, RNAi experiments and sequencing are under way to identify the molecular change responsible for the
tn309 phenotype.