The maternal-effect-lethal gene
aph-1 is essential for early embryonic development. Mutations in
aph-1 were isolated in the Priess lab and found to cause an embryonically arrested phenotype that is remarkably similar to that of
glp-1 mutant embryos. The phenotype of
aph-1 mutants suggests that the
aph-1 gene product might be involved in the same specific cell induction events that are mediated by the GLP-1 receptor. As a way of learning more about the specific role of
aph-1 in these cell communication events, we have carried out a screen for suppressors of the weak
aph-1(
zu147) allele. We have identified 6 independent mutations that suppress the partial maternal-effect lethality caused by
aph-1(
zu147). One of these mutations appears to map to the
aph-1 gene locus (or at least very close), and is likely to be a revertant of the
aph-1(
zu147) allele. The other four mutations are unlinked to
aph-1. Complementation and mapping analysis indicates that at least three different genes are represented by these mutations. These suppressor mutations do not appear to have phenotypes of their own other than suppression of
aph-1(
zu147). Allelespecificity and interactions with other genes are currently being tested. Our latest mapping information for these suppressors will also be presented.