Asymmetric division is crucial for embryonic development and stem cell lineages. In the one-cell embryo, a contractile cortical actomyosin network contributes to asymmetric division by segregating partitioning-defective (PAR) proteins to discrete cortical domains. In the current study, we found that the plasma membrane lipid phosphatidylinositol 4,5-bisphosphate (PIP) localizes to polarized dynamic structures in zygotes, distributing in a PAR-dependent manner along the anterior-posterior (A-P) embryonic axis. PIP cortical structures overlap with F-actin, and coincide with the actin regulators RHO-1 and CDC-42, as well as ECT-2. Particle image velocimetry analysis revealed that PIP and F-actin cortical movements are coupled, with PIP structures moving slightly ahead of F-actin. Importantly, we established that PIP cortical structure formation and movement is actin dependent. Moreover, we found that decreasing or increasing the level of PIP resulted in severe F-actin disorganization, revealing interdependence between these components. Furthermore, we determined that PIP and F-actin regulate the sizing of PAR cortical domains, including during the maintenance phase of polarization. Overall, our work establishes that a lipid membrane component, PIP, modulates actin organization and cell polarity in embryos.

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