In C. elegans, most hypodermal cells fuse and generate large syncytia. Two rows of lateral seam cells separate the dorsal from the ventral hypodermal cells in the embryo. The homeobox containing transcription factor
ceh-16 plays a central role in the specification of the seam cells (Cassata et al., 2005). Deletion mutants in
ceh-16 display a recessive embryonic lethal phenotype, which can also be obtained by RNA interference (RNAi) against
ceh-16 using microinjection (Cassata et al., 2005). In
ceh-16 mosaic mutant embryos seam cells that lack
ceh-16 can no longer form a compartment boundary separating the hypodermal cells. The epidermal adherens junction marker AJM-1::GFP reveals that seam cells without
ceh-16 fuse with the hypodermal syncytium. In addition, they leave their lateral position and migrate either dorsally or ventrally. CEH-16::GFP is expressed early in cells of the AB lineage (28-56 cell stage), in
hyp5 and seam cells (250 minutes after the first cleavage), in several anterior neurons and in DA1 and DD1 motoneurons (after hatching) (Cassata et al., 2005). We are interested in the identification of downstream targets of
ceh-16.
ceh-16 encodes the ortholog of the Drosophila engrailed protein for which a conserved relationship with the hedgehog signalling pathway was shown. C. elegans lacks a bona fide hedgehog homolog, but a family of genes (warthogs and groundhogs) was identified, which encode a Hint/hog domain with similarity to hedgehog (Aspck et al., 1999). Expression analysis of warthog and groundhog genes suggests that some of these genes might play a role in hypodermal and seam cell specification. We are currently testing the relationship between
ceh-16 and wrt genes. In addition, we are interested in the identification of regulators of
ceh-16 using an automated large scale screen.