We have begun to investigate the genetic control of embryonic polarity in the early C. elegans embryo. GLP-1, a membrane receptor required for inductive cell interactions, is normally restricted to AB and its descendants by translational repression of maternal
glp-1 mRNA both prior to the 2-cell stage as well as in P1 and its descendants (Evans et al., 1994). Our approach has been to screen mutant embryos with a-GLP-1 antibodies for an altered pattern of GLP-1 expression. We first examined existing mutant embryos. The par genes influence many aspects of embryonic asymmetry, including P-granule segregation and asymmetric cleavage; we find that mutant embryos of four par genes (
par-1, -2, -3, and -4) mislocalize GLP-1, but those of two others (
par-5 and
par-6) do not . Therefore, proper localization of GLP-1 is not necessarily coupled to other asymmetries, such as asymmetric cleavage. The
skn-1,
mex-1 and
pie-1 genes influence blastomere identity, but do not affect GLP-1 localization. Finally, among 17 temperature sensitive emb and zyg maternal effect lethal (Mel) mutants examined to date, only one,
emb-8, mislocalizes GLP-1. We have also screened for new mutants that disrupt GLP-1 expression. We have currently screened nearly 5000 genomes and have identified seven mutants with altered GLP-1. Two are new alleles of
par-4; the other five are being characterized currently. Of these five, three have symmetrical and synchronous early divisions similar to the pars, while the other two appear to be more like wild type. Thus, we may have identified new loci that affect specific steps in the process of localizing GLP-1.