The Ras/MAP kinase signaling pathway promotes cell divisions during the development of many multicellular organisms. Study of this signaling pathway is significant since mutation of the ras gene in humans is an important step in the generation of cancerous tumors. Many proteins are involved in the regulation and transmission of the Ras/MAP kinase signal, and we have initiated a study of a novel target of this signaling pathway during Caenorhabditis elegans development. The C. elegans predicted open-reading-frame, T08D10.1, codes for member of the CCAAT-box family of DNA-binding proteins and possesses multiple phosphoacceptor sites and docking sites for extracellular regulated kinase (ERK) MAP kinase. In isolation, loss of
tag-295 function through RNAi or deletion does not result in a vulval phenotype, however, RNAi experiments have demonstrated that loss of
tag-295 function can enhance the multivulval phenotype of
let-60(
n1046) animals. We have purified the
tag-295/T08D10.1 protein and biochemically characterized its interactions with purified ERK MAP kinase using in vitro kinase assays. K<sub>m</sub> values of wild-type T08D10.1 are similar to other characterized ERK substrates such as myelin basic protein and LIN-1, therefore, the T08D10.1 transcription factor likely acts as an novel inhibitor of vulval cell divisions that is directly regulated by Ras/MAP kinase mediated signaling.