Morphogenesis of the embryo starts at mid-embryogenesis. The hypodermis is known to play a crucial role during this process (Priess and Hirsh, Dev. Biol. 117: 156-173). We are interested in identifying genes that control morphogenesis of the embryo (see abstract by Bosher et al., this meeting). We have performed a pilot Nomarski screen of about 3600 chromosomes for embryonic lethal mutants that would fail to elongate beyond the comma stage. Among mutations that we recovered, the mutation
mc13 (LGX) causes a very strong elongation defect. Three lines of evidence indicate that
mc13, which defines the gene
eld-1 (elongation defective), affects only elongation: 1)
eld-1(
mc13) embryos arrest at the comma stage but do not explode; 2) they have a normal number and arrangement of hypodermal cells as judged by staining with anti-LIN-26 antibodies; 3) they show normal enclosure by hypodermal cells as judged by staining with the mAb MH27. Interestingly, terminal-stage
mc13 embryos develop a large vacuole at the position of the excretory cell, which we interpret as resulting from defective outgrowth of the excretory canal. In addition, the pharynx of
mc13 embryos is short and not connected to the outside, although its overall structure and the number of pharyngeal muscles seem to be normal as judged by staining with the mAbs MH27 and 3NB12; possibly epithelial cells of the pharynx fail to grow out and reach the outside. We suggest that
eld-1 is involved in modifying the shape of epithelial cells during elongation of the embryo, outgrowth of the excretory canal and morphogenesis of the pharynx. Progress in cloning
eld-1 and further characterization of the phenotype will be reported.