After an initial period of rapid cell proliferation, the C. elegans embryo assumes a bean-shaped morphology with the outermost layer consisting of dorsal, lateral, and ventral rows of hypodermal cells. At this stage, actin reorganizes in the cortex of all hypodermal cells to form an array of parallel filament bundles that run circumferentially around the embryo. These actin filaments subsequently contract to elongate the hypodermal cells, as well as the entire embryo, approximately four-fold in the anteroposterior direction. Circumferential microtubules also form at the bean stage in the cortex of the dorsal and ventral hypodermal cells and persist throughout elongation. These microtubules appear to distribute the force of actin filament contraction uniformly across the surface of the embryo. We are attempting to identify genes that control this restructuring of cytoskeletal elements using separate screens for zygotic lethal and temperature-sensitive mutations. We have isolated a collection of mutants that show arrested elongation (less than two-fold) but terminal differentiation of all tissues. Further analysis revealed that most mutants have an abnormal pattern or number of hypodermal cells at the bean stage which may subsequently result in defective elongation. However, several zygotic lethal mutations in a gene named hmp-1
(humpback) arrest elongation at about 1.25-fold and generate ectopic lumps in the hypodermis without altering the pattern of hypodermal cells. hmp-1
mutant embryos show many circumferential actin filament bundles and microtubules, and we are now examining the pattern of cytoskeletal elements for subtle defects. We have recently obtained transgenic rescue of the hmp-1
mutant phenotype and will present a molecular analysis of the gene.