The C. elegans PAR proteins regulates cell polarity and asymmetric divisions during early embryogenesis. As for other par genes,
par-4 mutations induce polarity defects in the embryo, including synchronous divisions at the two-cell stage and lack of P-granule segregation, resulting in embryonic lethality. However, the mechanism by which PAR-4 regulates cell polarity is still unclear and information is missing about potential members of the PAR-4 signaling pathway in C. elegans. As actomyosin contractility regulation is a critical process for polarity establishment and maintenance in the first steps of embryo development, we investigated whether actomyosin function was affected in
par-4 embryos. We used confocal videomicroscopy to monitor actomyosin dynamics in control and
par-4(
it57ts) embryos expressing NMY-2::GFP. We measured several contractility defects during the early polarisation phase and the first division of the zygote for
par-4(
it57ts) when compared to control embryos. We found that the velocity of NMY-2 patches that move toward the anterior pole during polarity establishment is reduced in
par-4(
it57ts) embryos. Furthermore, we observed multiple furrow ingressions at the time of cytokinesis during the division of
par-4(
it57ts) 1-cell embryos. These furrowing defects were associated with increased nuclear movements and membrane engulfment at the site of furrowing and led to a delay in cytokinesis completion in
par-4(
it57ts) mutants compared to control embryos. Interestingly we identified
ani-2, one of the C. elegans homologues of the actin-binding protein anillin, as a suppressor of
par-4(
it57ts) embryonic lethality. We hypothesized that PAR-4 and ANI-2 function antagonistically in a common actin-regulation pathway in the early embryo. Our results show that ANI-2 depletion by RNAi can indeed partially revert the actomyosin defects of
par-4(
it57ts) embryos, indicating that an increase of ANI-2 function is responsible for contractility defects observed in
par-4(
it57ts) embryos. Furthermore, immunolocalisation experiments showed that the loss of PAR-4 activity favors membranous ANI-2 localization in early embryos. Taken together, these results suggest a model in which PAR-4 regulates actomyosin contractility by inhibiting ANI-2 localization at the plasma membrane during the first steps of embryonic development.