ani-2 : par-4

par-4 mutant embryos had an increased number of cytoplasmic ANI-2 puncta and displayed cortical accumulations of ANI-2, mainly at the membrane between the two blastomeres. Cortical ANI-2 was detectable in less than 10% of wild-type embryos but in 85% of par-4 mutant embryos. We also observed that ANI-2 accumulated in the midbodies formed following abnormal cytokinetic furrows in par-4 mutants). These results indicate that ANI-2 localizes to the cortex when PAR-4 activity is compromised and suggest that PAR-4 acts upstream of ANI-2, regulating acto- myosin contractility by preventing ectopic accumulation of ANI-2 at the cortex.

ani-2 : par-4

ani-2 RNAi partially restored the slow cleavage furrow ingression of par-4 mutants

ani-2 : par-4

ani-2 RNAi partially suppresses the embryonic lethality of the par-4(it57) mutation

ani-2 : par-4

ani-2 RNAi partially suppresses the embryonic lethality of the par-4(it47) mutation

ani-1 : par-4

ani-1 RNAi enhanced the slow cleavage furrow ingression defect of par-4 mutants

ani-2 : par-4

ani-2 RNAi partially suppresses the embryonic lethality of the par-4(it47) mutation

ani-2 : par-4

ani-2 RNAi partially suppresses the embryonic lethality of the par-4(it57) mutation

ani-2 : par-4

ani-2 RNAi partially suppreses the slow movement of NMY-2 caused by the par-4(it57) mutation

ani-2 : par-4

ani-2 RNAi partially suppreses the slow movement of NMY-2 caused by the par-4(it47) mutation

ani-2 : par-4

ani-2(ok1147/+) partially suppresses the embryonic lethality of the par-4 mutants at 18 deg C, but not at higher temperatures.