The epidermis of C. elegans originates as a patch of six rows of cells on the dorsal side of the embryo. The epidermis then actively migrates ventrally, completely enclosing the embryo. This migration is led by the two outermost rows of cells which eventually meet at the ventral midline (Williams-Masson, Malik and Hardin; in preparation). Once the embryo is enclosed, actin microfilaments in the epidermis contract circumferentially causing the embryo to elongate (Priess and Hirsh 1985); without proper enclosure elongation does not occur normally. We are investigating the
zen-2 locus which is required for enclosure of the embryo by the epidermis.
zen-2 (zygotic enclosure defective) embryos differentiate all cell types, including epidermis, in normal or near normal quantities. Pharynx, intestine and body wall muscle appear to be patterned and positioned normally in mutant embryos. The only observed defect is the failure of the epidermis to migrate around to the ventral side and enclose the embryo.
zen-2 mutants fail to elongate as a result of this absence of enclosure. To determine whether the enclosure defect is because of abnormal epidermal patterning and/or inability of epidermal cells to migrate ventrally, we are staining mutant embryos with the antibody MH27. This antibody recognizes a component of adherens junctions in epithelial cells and allows comparison of the early patterning of cells in mutant and wild-type embryos.
zen-2 was isolated in a general zygotic embryonic lethal screen and maps to the cluster of LGII based on linkage to genetic markers. Complementation tests against various deficiencies place
zen-2 between
rol-6 and
zyg-9 on the genetic map.
zen-2 may be a null allele based on phenotypic similarity to a deficiency which deletes the locus. We are attempting to obtain transformation rescue by injecting
zen-2 heterozygotes with nine overlapping cosmids that span the entire region. Only one allele of
zen-2 currently exists; we have initiated a screen to identify additional alleles.