In screens for maternal-effect lethal mutants defective in specifying early cell fates, we isolated one allele each of genes we call
mex-2 and
mex-4 . The
mex-2 and
mex-4 mutants have very similar early embryonic phenotypes. In both
mex-2 and
mex-4 mutant embryos, the AB blastomere produces tissues similar to those normally generated by the EMS blastomere. In wild-type embryos, an isolated AB produces neurons and hypodermal cells. In contrast, an isolated AB from a
mex-4 embryo produces body wall muscle (90%), pharyngeal (90%) and intestine (10%) cells. Such a phenotype is suggestive of misregulation of SKN-1, a protein important for specifying these three tissue types. Indeed both
mex-2 and
mex-4 embryos have a higher than wild-type level of SKN-1 protein in AB and its daughters. This result suggests that mutations in these genes affect expression of maternal transcripts. The
mex-4 gene encodes a homologue of the vertebrate DP-1 protein. DP-1 is a member of a transcription heterodimer complex and its dimerization partner is E2F. Multiple E2F homologues are encoded in the C. elegans genome; one of these genes is very close to the genetic position of the
mex-2 gene. I have found that the
mex-2 mutant has a missense mutation in the E2F gene. How do E2F and DP-1 affect early cell fate in the embryo? In other organisms, DP-1 and E2F-1 cooperate to link cell cycle progression with transcription. We have not observed any cell cycle defects in
mex-4 mutant embryos, and the gonad of a
mex-4 hermaphrodite appears normal. Thus, we think that these genes are not affecting cell fates by influencing the cell cycle. Both
mex-2 and
mex-4 genes have roles in postembryonic development. These genes were independently isolated by the Horvitz lab based on their role in the synthetic multivulva pathway. Since ras mutations can suppress the synMuv phenotype, I tested whether ras mutations could also suppress the embryonic defect of
mex-4 mutants. Preliminary experiments indicate that suppression occurs. This result suggests that parallels exist between vulva induction and embryogenesis.