The coronin-like protein POD-1 is required for anterior-posterior axis formation and cellular architecture in the nematode Caenorhabditis elegans

Establishment of anterior-posterior (a-p) polarity in the Caenorhabditis el egans embryo depends on filamentous (F-) actin. Previously, we isolated an E-actin-binding protein that was enriched in the anterior cortex of the one -cell embryo and was hypothesized to link developmental polarity to the act in cytoskeleton. Here, we identify this protein, POD-I, as a new member of the coronin family of actin-binding proteins. We have generated a deletion within the pod-1 gene. Elimination of POD-1 from early embryos results in a loss of physical and molecular asymmetries along the a-p axis. For example , PAR-1 and PAR-3, which themselves are polarized and required for a-p pola rity, are delocalized in pod-1 mutant embryos. However, unlike loss of PAR proteins, loss of POD-I gives rise to the formation of abnormal cellular st ructures, namely large vesicles of endocytic origin, membrane protrusions, unstable cell divisions, a defective eggshell, and deposition of extracellu lar material. We conclude that, analogous to coronin, POD-I plays an import ant role in intracellular trafficking and organizing specific aspects of th e actin cytoskeleton. We propose models to explain how the role of POD-1 in basic cellular processes could be linked to the generation of polarity alo ng the embryonic a-p axis.