let-502 rho-binding kinase and
mel-11 myosin phosphatase regulate Caenorhabditis elegans embryonic morphogenesis. Genetic analysis presented here establishes the following modes of
let-502 action: (i) loss of only maternal
let-502 results in abnormal early cleavages, (ii) loss of both zygotic and maternal
let-502 causes elongation defects, and (iii) loss of only zygotic
let-502 results in sterility. The morphogenetic function of
let-502 and
mel-11 is apparently redundant with another pathway since elimination of these two genes resulted in progeny that underwent near-normal elongation. Triple mutant analysis indicated that
unc-73 (Rho/Rac guanine exchange factor) and
mlc-4 (myosin light chain) act in parallel to or downstream of
let-502/mel-11. In contrast
mig-2 (Rho/Rac),
daf-2 (insulin receptor), and
age-1 (PI3 kinase) act within the
let-502/mel-11 pathway. Mutations in the sex-determination gene
fem-2, which encodes a PP2c phosphatase (unrelated to the MEL-11 phosphatase), enhanced mutations of
let-502 and suppressed those of
mel-11.
fem-2's elongation function appears to be independent of its role in sexual identity since the sex-determination genes
fem-1,
fem-3,
tra-1, and
tra-3 had no effect on
mel-11 or
let-502. By itself,
fem-2 affects morphogenesis with low penetrance.
fem-2 blocked the near-normal elongation of
let-502;
mel-11 indicating that
fem-2 acts in a parallel elongation pathway. The action of two redundant pathways likely ensures accurate elongation of the C. elegans embryo.