Previously, we described two independent screens to identify genes involved in either vulval development or sex myoblast (SM) migration. We have found that mutations in one gene,
sem-5 (sex muscle abnormal), perturb both vulval formation and SM migration, indicating that sem-S is required for both of these processes. The gene
egl-15 is involved in controlling the migration of the SMs in hermaphrodites and interacts with clr-l . This interaction is deduced from the ability of mutations in clr-l to suppress the scrawny phenotype caused by non-null alleles of
egl-15 as well as the ability of
egl-15 mutations to suppress the Clr phenotype caused by mutations in clr-l. We mapped
egl-15 to the
lin-14 contig and rescued the egg- laying defect of
egl-15 mutants using genomic DNA from this region. Interestingly, the genomic fragments that rescue the egg-laying defect of
egl-15 mutants also cause some rescued animals to show the Clr phenotype typical of clr-l mutants. This result suggests that the animal is sensitive to too much as well as too little
egl-15 activity: overexpression results in the Clr phenotype and underexpression results in an egg-laying defect, scrawniness, and lethality. Supp; essors of clr-l define four genes that include
egl-15 and sem-S. In a clr-l (+) background, mutations in sem-S also affect the migrations of the SMs. We have also identified three alleles of sem-S as suppressors of the multivulva phenotype of
lin-15 mutants. sem-S and four other genes (
let-23 n
let-60 IV,
let-341 V, and let
(n2018) IV) found as
lin-15 suppressors affect vulval induction and share other phenotypes (see abstract by Clark and Horvitz). We have identified a 6 kb genomic subclone that rescues both the vulval defect and the Clr suppression phenotypes of sem-S mutants. We are currently sequencing the rescuing genomic DNA and isolating cDNAs to understand the molecular role of sem-S. While SM migration and vulval induction superficially appear to be quite different processes, in fact both involve cell-cell communication between somatic gonadal cells and a set of responding cells, either the SMs or the vulval precursor cells. The genes
let-23 and
let-60 encode proteins similar to either the EGF receptor (Aroian et aL, Nature 348:693, 1990) or ras (Han & Sternberg, Cell 63:921, 1990). These proteins are known to mediate signal transduction in mammals and yeast, which implicates the involvement of sem-S and the other genes of this gene network in the signal transduction processes that control vulval induction and SM migration. It will be interesting to understand both the common and divergent features of these two communication systems.