mbk-2 : oma-2

"MBK-2 phosphorylates OMA-1 and OMA-2 in vitro."

oma-1 : oma-2 : zif-1

ZIF-1 activity and GFP::H2Bzif-1 expression are repressed in oocytes and germline blastomeres and both are present in somatic blastomeres. A high level of GFP::H2Bzif-1 was observed in animals homozygous for oma-1(te33);oma- 2(te51) or depleted of oma-1 and oma-2 by RNAi (100%, n=19 and 20, respectively). Similarly, GFP::H2Bzif-1 was detected in oocytes of oma-1(te21);oma-2(RNAi) and oma-1(RNAi);oma-2(te50) animals (100%, n=10 and 15, respectively).

gsk-3 : oma-1

"GSK-3 phosphorylates OMA-1 primarily at T339 and is required for OMA-1 degradation."; "GSK-3 phosphorylation of OMA-1 in vitro is affected by the phosphorylation state at T239."

oma-1 : oma-2 : pie-1

In worms homozygous for oma-1(te33);oma-2(te51) (both loss-of-function mutations), or worms that have been strongly depleted of oma-1 and oma-2 by RNAi, no, or a dramatically reduced level of, PIE-1 in the gonad was detected. Expression of a reporter GFP protein carrying only the first zinc finger of PIE-1 (GFP::PIE-1 ZF1) is dramatically reduced in the oocytes of oma-1(-);oma-2(-) animals.

mbk-2 : oma-1

OMA-1 is phosphorylated by MBK-2.

mbk-2 : oma-1

"Furthermore, consistent with the idea that the cell-fate defects in these mutants result from OMA-1 (and to some extent OMA-2) stabilization, we found that each mutant was suppressed by loss-of-function oma-1 (or oma-2) mutations (Table 1, and data not shown). In the case of the cdk-1(ne2257) and gsk-3(nr2047) mutants, substantial suppression was observed in oma-1(te33) mutants (Table 1). The mbk-2(ne3442) mutant was only weakly suppressed by oma-1(te33) (Table 1)."

mom-2 : oma-1 : oma-2

High levels of GFP::H2Bmom-2 were observed in oocytes following simultaneous depletion of oma-1 and oma-2 by RNAi. Furthermore, ectopic OMA-1 appears to be sufficient to repress GFP::H2Bmom-2 expression in embryos.

gsk-3 : oma-1

"Furthermore, consistent with the idea that the cell-fate defects in these mutants result from OMA-1 (and to some extent OMA-2) stabilization, we found that each mutant was suppressed by loss-of-function oma-1 (or oma-2) mutations (Table 1, and data not shown). In the case of the cdk-1(ne2257) and gsk-3(nr2047) mutants, substantial suppression was observed in oma-1(te33) mutants (Table 1). The mbk-2(ne3442) mutant was only weakly suppressed by oma-1(te33) (Table 1)."

gsk-3 : oma-1

"Furthermore, consistent with the idea that the cell-fate defects in these mutants result from OMA-1 (and to some extent OMA-2) stabilization, we found that each mutant was suppressed by loss-of-function oma-1 (or oma-2) mutations (Table 1, and data not shown). In the case of the cdk-1(ne2257) and gsk-3(nr2047) mutants, substantial suppression was observed in oma-1(te33) mutants (Table 1). The mbk-2(ne3442) mutant was only weakly suppressed by oma-1(te33) (Table 1)."

mbk-2 : oma-1

"Furthermore, consistent with the idea that the cell-fate defects in these mutants result from OMA-1 (and to some extent OMA-2) stabilization, we found that each mutant was suppressed by loss-of-function oma-1 (or oma-2) mutations (Table 1, and data not shown). In the case of the cdk-1(ne2257) and gsk-3(nr2047) mutants, substantial suppression was observed in oma-1(te33) mutants (Table 1). The mbk-2(ne3442) mutant was only weakly suppressed by oma-1(te33) (Table 1)."