All fundamental cellular processes, such as cell shape changes, division, and migration, depend on their polarization into regions with distinctive structural and molecular arrangements. In the C. elegans zygote (one of the best-studied models for cell polarization), embryonic development starts with the establishment of anterior-posterior (front-back) polarity in cells. However, the finer details underlying this subcellular process were largely uncharacterized.
This study proposes a mechanically-driven cell polarization process: the tension generated from the contraction of the actomyosin cortex facilitates the clustering of the polarity proteins PAR3 and PKC3 into high-intensity clusters at the cortex. The clustered PAR proteins have low turn-over rates, and are subsequently passively transported by cortical flows to one end of the cell. This asymmetrical distribution of proteins in cells marks the beginning of cell polarization.
The study also highlights the role of the Rho GTPase family member, CDC42, in PAR protein clustering. Active forms of CDC42 were shown to restrict the incorporation of PKC3 and another PAR protein PAR6 into these clusters.