The "SynMuv" genes appear to be involved in providing a signal that inhibits vulval precursor cells from adopting vulval fates in C. elegans. These genes are called "SynMuv" genes because a Multivulva phenotype is only visible if mutations in two different genes, one from Class A and one from Class B, are combined (a "Synthetic Multivulva phenotype) (see Ferguson and Horvitz 1989). Class B includes a gene encoding a protein related to the tumor suppressor Rb. Class A includes certain components of the nucleosome remodelling and histone deacetylase (NURD) complex (Solari and Ahringer 2000). Other genes related to Rb and NURD have both Class A dna Class B activity (Solari and Ahringer 2000). The
lin-13 gene has genetic properties consistent with function as a SynMuv gene. We have found that null alleles of
lin-13 are temperature-sensitive and maternally rescued, resulting in phenotypes ranging in severity from L2 arrest (when both maternal and zygotic activities are removed at 25o), to sterile Multivulva (when only zygotic activity is removed at 25o), to sterile non-Multivulva (when both maternal and zygotic activities are removed at 15o), to wild-type/Class B SynMuv (when only zygotic activity is removed at 15o). The predicted LIN-13 protein contains multiple zinc fingers and a motif (LXCXE) that has been implicated in Rb binding. In addition, LIN-13 is a nuclear protein and is consistently expressed in many cell types, including
hyp7, at the time of VPC specification. Our results are consistent with a role for LIN-13 in Rb-mediated and NURD-mediated transcriptional control processes that lead to repression of vulval fates. We have begun a genetic mosaic analysis to determine the cellular focus of
lin-13 in vulval development. We will report on our progress and we will also speculate about the connection between
lin-13 and the class B synMuv gene lin-35Rb. Ferguson, E.L. and Horvitz, H.R. (1989) Genetics 123, 109-121 Solari, F. and Ahringer, J. (2000) Current Biology 10, 223-226.