Cell polarity is critical to the early C. elegans development. The first division of the embryo is asymmetric, giving rise to the large anterior cell AB and the small posterior cell P 1 . Genetic screens identified par mutants (Kemphues et al., 1988) that perturb this anterior-posterior (a-p) polarity. Early experiments indicated that actin also played a role in a-p polarity (Hill and Strome, 1988). To explore this further, we isolated actin-binding proteins (ABPs) present in embryos (Aroian et al., 1997). One of these, CABP11, was polarized to the anterior of 1-cell embryos. Here we characterize CABP11, now called POD-1, with surprising results. POD-1 is an unusual protein that encodes two degenerate copies of the ABP Coronin. POD-1 protein localizes to the anterior cortex of P cells in a cell-cycle dependent manner. We knocked
pod-1 out by generating a deletion allele.
pod-1 is required only maternally, suggesting a specialized role in embryogenesis. Loss of
pod-1 leads to loss of asymmetry similar to par mutants-- the first cleavage is often symmetric, leading to synchronous and parallel second divisions. Germline granules are missegregated, and both PAR-3 and PAR-1 protein lose their asymmetry. Thus,
pod-1 is required for a-p polarity. Reciprocally, some par genes are required for POD-1 asymmetry. These data suggest
pod-1 functions in same pathway as par genes. However, unlike other polarity mutants, loss of
pod-1 leads to dramatic defects in the physical organization of the early embryo, i.e. , formation of blebs, formation of abnormal endocytic compartments, formation of unstable cell divisions, and impaired eggshell function. Cortical actin is not perturbed in the mutant and the cell-cycle progresses normally. To achieve higher resolution, we compared wild-type and mutant embryos at the ultrastructural level. Although the eggshell appeared normal, abnormal plaque material was found on the surface of mutant embryos. These data suggest
pod-1 represent a new class of developmental gene in the early embryo. We believe that
pod-1 influences embryonic polarity via a cellular mechanism also required for cell architecture and that
pod-1 links the generation of embryo polarity to the cytoskeleton. Our results allow us to hypothesize on the mechanism involved in generating polarity.