The
fem-1 gene of C. elegans is one of three genes required for all aspects of male development in the nematode. Current models of sex determination propose that the products of the fem genes act in a novel signal-transduction pathway and that their activity is regulated primarily at the post-translational level in somatic tissues. We analyzed the expression of
fem-1 to determine whether it revealed any additional levels of regulation. Both XX hermaphrodites and XO males express
fem-1 at approximately constant levels throughout development. Somatic tissues in hermaphrodites adopt female fates, but they nonetheless express
fem-1 mRNA and FEM-1 protein, suggesting that the regulation of
fem-1 activity is post-transcriptional and probably post-translational. A compact promoter directs functional expression of
fem-1 transgenes, as assayed by their masculinizing activity in
fem-1 mutants. Activity also requires any two or more introns, suggesting that splicing may enhance
fem-1 expression. The minimal noncoding sequences required for activity of
fem-1 transgenes suffice to direct expression of a
fem-1::lacZ reporter gene in all somatic tissues in both sexes. Many
fem-1 transgenes, including those that rescue male somatic development in
fem-1 mutants, paradoxically feminize the germline. We suggest that they do so by interfering with the germline expression of the endogenous
fem-1 gene.