In the Caenorhabditis elegans hermaphrodite germ line, sperm and then oocytes are made from a common pool of germ-cell precursors. The decision to differentiate as a sperm or an oocyte is regulated by the sex-determining gene,
fem-3. Expression of
fem-3 in the hermaphrodite germ line directs spermatogenesis and must be negatively regulated to allow the switch to oogenesis. In adult hermaphrodites (which are producing oocytes), most
fem-3 RNA is found in the germ line, consistent with both the requirement for
fem-3 in hermaphrodite spermatogenesis and the maternal effects of
fem-3 on embryonic sex determination. Whereas loss-of-function mutants in
fem-3 produce only oocytes, hermaphrodites carrying any of nine
fem-3 gain-of-function (gf) mutations make none; instead sperm are produced continuously and in vast excess over wild-type amounts. Genetic analyses suggest that
fem-3(gf) mutations have escaped a negative control required for the switch to oogenesis. Here we report that all nine
fem-3(gf) mutants carry sequence alterations in the
fem-3 3' untranslated region (3' UTR). There is no increase in the steady-state level of
fem-3(gf) RNA over wild-type, but there is an increase in the polyadenylation of
fem-3(gf) RNA that is coincident with the unregulated
fem-3 activity. Results of a titration experiment support the hypothesis that a regulatory factor may bind the
fem-3 3' UTR. We speculate that
fem-3 RNA is regulated through its 3' UTR by binding a factor that inhibits translation, and discuss the idea that this control may be part of a more general regulation of maternal RNAs.