[
European Worm Meeting,
2004]
In a videorecording screen of chromosome I embryonic lethals identified by RNAi, we found that the first division of B0511.9(RNAi) embryos was sometimes symmetric instead of asymmetric, similar to that seen in par mutants, suggesting a defect in embryonic polarity (Zipperlen, et al, 2001). After further analyses of B0511.9(RNAi) embryos we found that the phenotypes mimic those seen after mutation of APC complex components (e.g., mat mutants). Under strong RNAi conditions, B0511.9(RNAi) embryos arrest in meiosis I with a persistent meiotic metaphase spindle. Mutation or RNAi depletion of APC components causes an identical phenotype because of their necessity in cell cycle progression (Wallenfang and Seydoux, 2000; Golden et al, 2000; Furuta et al, 2000). Under weak RNAi conditions, B0511.9(RNAi) embryos progress through meiosis. However, nucleocentrosomal rotation in P0 fails, PAR-3 is found around the whole cortex of P0, and PAR-2 is cytoplasmic. The first division is symmetric in these embryos. In some cases, embryos arrest with persistent mitotic metaphase spindles. These weak B0511.9(RNAi) phenotypes are very similar to those seen in some alleles of mutants in APC components (Rappleye, et al 2002; Shakes et al, 2003). The phenotypic similarities of B0511.9(RNAi) embryos and APC mutants suggests that B0511.9 functions with the APC. B0511.9 encodes a novel protein with no detectable similarities in the database. To strengthen the link with the APC, we are currently testing whether B0511.9 protein associates with APC components in vivo.