Recent phylogenetic evidence suggests that hermaphroditism in C. elegans and C. briggsae evolved independently (1). Accordingly, the molecular mechanisms controlling germline sex determination in these two species appear to differ. In the C. elegans germline, the transitory inhibition of
tra-2 mRNA translation by the GLD-1/FOG-2 complex allows entry in spermatogenesis through activity of the FEM (FEM-1, FEM-2, FEM-3), FOG-1, and FOG-3 proteins. Loss-of-function mutations that disrupt inhibition of
tra-2 mRNA translation or the downstream activity of the FEM and FOG proteins result in female worms whose germline only produce oocytes. Interestingly, C. briggsae lacks a
fog-2 orthologue and
Cb-gld-1 appears to promote female germline fate instead of spermatogenesis (2). Thus, the molecular control that generates a sperm/oocyte-producing germline in C. briggsae remains unknown. In C. elegans, alleles of
fem-1 to
fem-3 were isolated as suppressors of
tra-2 (3), which feminize both XX and XO animals. To search for Fem alleles in C. briggsae, we isolated suppressors of a
Cb-tra-2 allele (see poster by Kelleher et al.). 54 independent sup strains were isolated using two different
tra-2(ts) alleles. The strains showed different degrees of suppression of the somatic masculinization phenotype. Surprisingly, no female worms were ever seen and all
tra-2;sup doubly-mutant strains consist of self-fertile hermaphrodites, suggesting that the C. briggsae orthologues of the Fem genes may not be required for the onset of hermaphrodite spermatogenesis. Complementation experiments revealed the presence of at least three such Fem-like genes in C. briggsae. In addition, double mutant analysis using confirmed or likely C. briggsae alleles of
tra-2,
tra-3, and
fem-2, as well as an unmapped suppressor, indicates that the epistatic relationships in the soma are similar to those in the C. elegans sex determination pathway. Further characterization of the role of Cb-fog genes should help to clarify the mechanism through which C. briggsae XX worms regulate the dual germline fate. 1 Kiontke K, Gavin NP, Raynes Y, Roehrig C, Piano F, Fitch DHA (2004). PNAS 101:9003 2 Nayak S, Goree J, Schedl T (2005) PloS 3: 1 3 Hodgkin J. (1986). Genetics 114:15