In screens for Caenorhabditis elegans mutants defective in vulval morphogenesis, we isolated multiple mutants in which the uterus and the vulva fail to make a functional connection, resulting in an egg-laying defective phenotype. Two of these connection of gonad defective (Cog) mutants carry alleles of the
egl-26 gene. We demonstrate that vulval lineages in
egl-26 mutant animals are normal, but one vulval cell,
vu1F, adopts an abnormal morphology. This results in formation of an abnormally thick layer of vulval tissue at the apex of the vulva and a physical blockage of the exit to the vulva from the uterus.
egl-26 was cloned and is predicted to encode a novel protein. Mosaic analysis indicates that
egl-26 activity is required in the primary vulval lineage for
vu1F morphogenesis. Expression of a functional translational fusion of EGL-26 to GFP was observed within the primary vulval lineage only in vulE, which neighbors
vu1F. EGL-26 is localized at the apical edge of the
vu1E cell. It is thus possible that
vu1E acts to instruct morphological changes in the neighboring cell,
vu1F, in an interaction mediated by EGL-26.