The Drosophila empty spiracles (ems) and the vertebrate Emx1 and Emx2 genes define brain regions in a way that brain parts expressing these genes are largely missing in loss-of function mutants. Additionally, ems is involved in tracheal development, and Emx2 knockout mice completely lack a urogenital system. Burglin et al. (1989) first identified
ceh-2 in a screen for C. elegans homeobox genes. With the ems/Emx genes
ceh-2 shares a hexapeptide, 80% identity in the homeodomain and flanking regions as well as an intron at a conserved position. However, the function of
ceh-2 does not seem to be comparable to ems/Emx: Anti-peptide antibody staining and expression of gfp/lacZ reporter constructs are restricted to a subset of cells in the pharynx, muscle
m2, epithelial
e2, and the neurons I3, M3 l/r, and NSM l/r. In an EMS mutagenesis screen we isolated
ceh-2(
ch4), a 2.5 kb deletion that covers the hexapeptide and homeodomain. The mutant is perfectly viable and fertile and shows no obvious phenotype. What might
ceh-2 do? Among the
ceh-2 expressing cells, M3 and NSM have been described in more detail. M3 l/r are inhibitory glutamatergic neurons that controls pharynx muscle relaxation. Laser ablation of M3 causes the pharynx muscle to relax more slowly after contraction, a pump cycle is about 10% longer and the electropharyngeogram lacks several inhibitory post-synaptic potentials (Avery, 1993; Raizen and Avery, 1994). Although
ceh-2(
ch4) mutants do not look starved as M3 ablated animals do, it may be useful to test for M3 activity in
ceh-2(
ch4). NSM l/r contain serotonine and stimulate pumping; we will test
ceh-2(
ch4) for corresponding defects. In addition we will express
ceh-2 in Drosophila ems mutants to test whether
ceh-2 can rescue some of the fly phenotypes. References: Avery (1993) J. Exp. Biol. 175:283-297 (and many WBG abstracts) Burglin et al. (1989) Nature 341:239-243 Raizen and Avery (1994) Neuron 12:483-495