Asymmetric cell divisions, where cells divide with respect to a polarized axis and give rise to daughter cells with different fates, are critically important during 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 has been a paradigm for understanding mechanisms of PAR polarization, but much less is known about polarity reestablishment during subsequent divisions. Here, we investigate the polarization of the P1 cell of the two-cell embryo. A posterior PAR-2 domain forms in the first four minutes of the birth of P1, and polarization becomes stronger over time. Initial polarization depends on the PKC-3 and PAR-1 kinases. However, in par-1 mutants, delayed polarization can occur, at a time when centrosome-associated AIR-1 is near the posterior cortex and myosin flows towards the anterior. Loss of myosin and par-1 function together results in more severe polarity defects. Based on these and other results, we propose that PAR polarity in the P1 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 myosin flow and PKC-3.

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