The plexin family transmembrane proteins are putative receptors for semaphorins, which are implicated in the morphogenesis of animal embryos including the axonal guidance. We have generated and characterized putative null mutants of the
plx-1 gene encoding C. elegans plexinA. PLX-1 interacts with transmembrane semaphorin Ce-Sema1a and 1b, and
plx-1 mutants exhibited morphological defects in several organs of epidermal origin including the vulva.
plx-1 adult hermaphrodites sometimes had a deformed vulva or extra vulva-like structures. A
plx-1::gfp transgene was expressed in the vulval primordial cells throughout the vulval development. The epidermal cells of the vulval primordium visualized with
ajm-1::gfp were aberrantly arranged in
plx-1 mutants: the rotation-symmetric configuration of the primordum was often disrupted, and cells were sometimes not in contact with each other. Some cells failed to participate in the formation of the main vulva and formed an extra vulva-like structure. A mutation in
smp-1, the gene encoding Ce-Sema1a, also caused the similar defects. At the early stage of the vulval development, the separate vulval precursor cells (VPCs) elongate aniterior-posteriorly and form a continuous single row of cells along the ventral midline in wild type animals. In
plx-1 and
smp-1 mutants, VPCs often made contact with each other along their lateral sides rather than at their tips, and were sometimes separated by
hyp7. Continuous observation of single
plx-1 animals revealed that some VPCs failed to stop elongation after making contact with each other, leading to the overlaps between cells. This observation suggests that PLX-1 and SMP-1 mediates a cell contact-dependent stop signal in elongating vulval precursor cells. It is known that cell fate specifications of VPCs are critically dependent on the positions. In
plx-1 mutants, the arrangement of vulval precursor cells was disrupted sometimes so severely that the proxial-distal order of the cells was sometimes reversed. Analyses using cell-type specific markers revealed that cell fate specifications were sometime affected in
plx-1 mutants. The frequency of defects in the cell fate specification, however, did not appear sufficiently high to fully account for the arrangements defects in later stages, suggesting that PLX-1 may be also involved in the regulation of arrangements and migrations of cells in the later phases of vulva morphogenesis.