Multiple pathways for reestablishing PAR polarity in C. elegans embryo.

Asymmetric cell divisions, where cells divide with respect to a polarized axis and give rise to daughter cells with different fates, are critically important for development. In many such divisions, the conserved PAR polarity proteins accumulate in distinct cortical domains in response to a symmetry breaking cue. The one-cell C. elegans embryo is a paradigm for understanding mechanisms of PAR polarization, but much less is known about polarity in subsequent divisions. Here, we investigate the polarization of the P cell of the two-cell embryo. A posterior PAR-2 domain forms in the first 4 ​min, and polarization becomes stronger over time. Initial polarization depends on the PAR-1 and PKC-3 kinases, and the downstream polarity regulators MEX-5 and PLK-1. However, par-1 and plk-1 mutants exhibit delayed polarization. This late polarization correlates with the time of centrosome maturation and actomyosin flow, and loss of centrosome maturation or myosin in par-1 mutant embryos causes an even stronger polarity phenotype. Based on these and other results, we propose that PAR polarity in the P cell is generated by at least two redundant mechanisms: There is a novel early pathway dependent on PAR-1, PKC-3 and cytoplasmic polarity, and a late pathway that resembles symmetry breaking in the one-cell embryo and requires PKC-3, centrosome associated AIR-1 and myosin flow.