Class A and class B synthetic Multivulva (synMuv) genes function in genetically redundant pathways to inhibit vulval fate specification. While the exact mechanism of inhibition in C. elegans is unknown, many synMuv genes encode proteins that have been implicated in transcriptional repression in other systems, such as the class B synMuv gene
lin-35 Rb (Lu and Horvitz, 1998). The cellular focus of synMuv genes is currently unclear. Originally, synMuv genes were proposed to act non-autonomously to repress vulval fates from within the
hyp7 (Herman and Hedgecock, 1990; Hedgecock and Herman, 1995), but were subsequently proposed to act autonomously within the vulval precursor cells (VPCs) (Lu and Horvitz, 1998; Thomas and Horvitz, 1999). It is also conceivable that synMuv genes, which in general are broadly expressed, may have more than one cellular focus. Determining the cellular focus of synMuv gene activity is critical to understanding their roles during vulval development and the signalling events that lead to the invariant pattern of VPC fates, as models for the role of synMuv genes depend on inferences about their cellular focus. For example, the existence of an inhibitory signal was inferred based on the interpretation that
hyp7 is the focus of
lin-15 (Herman and Hedgecock, 1990); additionally, the view that LIN-35 Rb and transcription factors activated by the Ras-MAP kinase cascade compete with target gene promoters to antagonize vulval induction (Lu and Horvitz, 1998) requires that the focus of
lin-35 activity be the VPCs. Utilizing both mosaic analysis and tissue-specific promoters for rescue experiments, we are currently trying to determine the focus of class B synMuv gene
lin-35. We will report on our progress at the meeting. Hedgecock E.M., and Herman R.K. (1995). Genetics 141, 989-1006; Herman R.K., and Hedgecock E.M. (1990). Nature 348, 169-171; Lu X., and Horvitz, H.R. (1998). Cell 95, 981-991; Thomas, J.H., and Horvitz, H.R. (1999). Development 126, 3449-3459.