OMA-1 and OMA-2 are Tis-11 (CCCH) zinc-finger proteins similar to regulators of embryogenesis such as PIE-1, MEX-1, MEX-5/6 and POS-1. OMA proteins are expressed exclusively in developing oocytes and 1-cell embryos, and are rapidly degraded after the 1-cell stage. We have shown that OMA-1 and OMA-2 are redundantly required for oocyte maturation (1). However, analyzing their potential role in the 1-cell embryo has been problematic since
oma-1/2 loss-of-function mutants do not produce embryos. A potential embryonic function for OMA proteins came from characterization of embryos derived from animals with reduction-of-function mutations in both genes.
oma-1(
te21);
oma-2(
te50) animals have an impenetrant defect in oocyte maturation and produce dead embryos. These embryos exhibit primarily defects in the division or development of the P1 blastomere, the germline precursor of the 2-cell stage(2).
Degradation of OMA proteins after the 1-cell stage is important for embryogenesis. The
zu405 mutation causes OMA-1 persistence past the 1-cell stage and embryonic lethality at a non-permissive temperature (3), which can be rescued by depletion of
oma-1. We show that depletion of
oma-2 exacerbates the
zu405 phenotype, resulting in lethality at 15°C, a permissive temperature for
zu405 embryos. Characterization of various molecular markers in early
oma-1(
zu405);
oma-2(RNAi) embryos suggests that somatic cells acquire properties that are normally associated with germline precursors. First, expression of PAR-2 at the apical cortex, usually observed only in germline precursors, is seen in some somatic cells. Second, similar to germline precursors, most somatic cells in
oma-1(
zu405);
oma-2(RNAi) embryos do not express the ubiquitous zygotic gene,
pes-10. Third, degradation of MEX-5 and PIE-1, which normally occurs only in the somatic sisters of germline precursors, is completely prevented in
oma-1(
zu405);
oma-2(RNAi) embryos. A less severe but similar phenotype was seen in the
oma-1(
zu405) single mutant for each marker. Consistent with the model that persisting OMA-1 protein in early embryos represses zygotic transcription, we show that
zu405 rescues the germline desilencing defect of
pie-1 mutant embryos. We propose that OMA proteins function to maintain germline character in 1-cell embryos.