PI(4,5)P₂ forms dynamic cortical structures and directs actin distribution as well as polarity in Caenorhabditis elegans embryos Available to Purchase

Asymmetric division is crucial for embryonic development and stem cell lineages. In the one-cell Caenorhabditis elegans 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 (PIP₂) localizes to polarized dynamic structures in C. elegans zygotes, distributing in a PAR-dependent manner along the anterior–posterior (A–P) embryonic axis. PIP₂ 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 PIP₂ and F-actin cortical movements are coupled, with PIP₂ structures moving slightly ahead of F-actin. Importantly, we established that PIP₂ cortical structure formation and movement is actin dependent. Moreover, we found that decreasing or increasing the level of PIP₂ resulted in severe F-actin disorganization, revealing interdependence between these components. Furthermore, we determined that PIP₂ 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, PIP₂, modulates actin organization and cell polarity in C. elegans embryos.