We are interested in the process of epidermal morphogenesis. Mutations in the Eph receptor tyrosine kinase
vab-1 and the ephrin ligand
mab-26/efn-4 cause variable defects in gastrulation cleft formation and epidermal enclosure. The most striking embryonic phenotype of
efn-4 mutations is the persistence of an aberrant gastrulation cleft due to defective migrations of neuroblasts following gastrulation.
efn-4 mutations are synthetically lethal with all
vab-1 mutations tested suggesting that they do not function in a simple receptor-ligand linear pathway (see abstract by Chin-sang and Chisholm). To identify genes potentially functioning in the
efn-4 pathway we examined mutants with phenotypes similar to those of
efn-4 .
mab-20 mutations cause defects in male tail morphogenesis similar to those of
efn-4 mutants (Baird et al, Development 113: 515).
mab-20 encodes a homologue of the vertebrate semaphorin 2a and is required for the correct formation of P cell contacts during epidermal morphogenesis (Roy et al, Development 127: 755). We have analyzed the early embryonic phenotypes of the null allele
mab-20(
ev574) and a weaker allele
e819 using 4D microscopy. Like
efn-4 mutants,
mab-20 mutants display variable defects during gastrulation cleft formation. 34% of embryos displayed gastrulation clefts that persisted until ventral enclosure, followed by failure of epdiermal enclosure. A small number of animals had disorganized gastrulation clefts, were able to enclose ventrally, then ruptured at the 2 or 3-fold stage or were unable to elongate past 2-fold. 23% of embryos displayed a larger than normal gastrulation cleft but were able to enclose and hatch. Phenotypic analysis of
mab-20;
efn-4 double mutants suggests that the
efn-4 and
mab-20 mutations are additive for later defects. However, defects in gastrulation cleft closure and epidermal enclosure are not additive in the double mutants. Taken together, our data suggest that
mab-20 and
efn-4 might function in a common or antagonistic pathway to regulate neuron migrations during gastrulation cleft closure but that they have different functions later in embryogenesis. The additive effects of
mab-20;
efn-4 double mutants show that the synthetic lethality observed between
efn-4 and
vab-1 mutations is specific. We therefore screened for mutations that synergize with a
vab-1 kinase allele. From a pilot screen we identified a mutation defining a new locus, vab
(ju105) X .
ju105 mutant larvae have posterior morphological defects and are movement impaired.
ju105 mutant embryos have a low penetrance of gastrulation cleft defects and often fail to elongate past 2-fold. The characterization and mapping of vab
(ju105) will be presented.