Cover image

The structure of XOL-1, the primary determinant of sexual fate in C. elegans. Shown here is a ribbon diagram of the XOL-1 crystal structure (red). XOL-1 is merged with a Nomarski photomicrograph of a C. elegans male and hermaphrodite mating pair (cyan false color). These worms have a defective dpy-28 dosage compensation gene that prevents hermaphrodites from down-regulating their X-linked transcript levels and causes death or a Dumpy phenotype (shown here). The background of the image is the diffraction pattern generated from crystals of the XOL-1 protein. When active, XOL-1 promotes male development by ensuring that dpy-28 and other hermaphrodite-specific dosage compensation and/or sex determination genes are functionally inactive; when inactive, XOL-1 promotes the hermaphrodite fate, including the activation of X-chromosome dosage compensation. The crystal structure unexpectedly showed XOL-1 to be a member of the GHMP kinase family, previously characterized as comprising only small molecule kinases involved in metabolic pathways. (For details, see Luz et al., p. 977.)