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Background  The  retinoblastoma  tumor suppressor (Rb) acts in a conserved pathway that is deregulated in most human cancers. Inactivation of the single Rb-related gene in  Caenorhabditis elegans, lin-35 , has only limited effects on viability and fertility, yet causes changes in cell-fate and cell-cycle regulation when combined with inactivation of specific other genes. For instance,  lin-35  Rb is a synthetic multivulva (synMuv) class B gene, which causes a multivulva phenotype when inactivated simultaneously with a class A or C synMuv gene.    Results  We used the ORFeome RNAi library to identify genes that interact with  C. elegans lin-35  Rb and identified 57 genes that showed synthetic or enhanced RNAi phenotypes in  lin-35  mutants as compared to  rrf-3  and  eri-1  RNAi hypersensitive mutants. Based on characterizations of a deletion allele, the synthetic  lin-35  interactor  zfp-2  was found to suppress RNAi and to cooperate with  lin-35  Rb in somatic gonad development. Interestingly, ten splicing-related genes were found to function similar to  lin-35  Rb, as synMuv B genes that prevent inappropriate vulval induction. Partial inactivation of specific spliceosome components revealed further similarities with  lin-35  Rb functions in cell-cycle control, transgene expression and restricted expression of germline granules.    Conclusion  We identified an extensive series of candidate  lin-35  Rb interacting genes and validated  zfp-2  as a novel  lin-35  synthetic lethal gene. In addition, we observed a novel role for a subset of splicing components in  lin-35  Rb-controlled processes. Our data support novel hypotheses about possibilities for anti-cancer therapies and multilevel regulation of gene expression.

bmc developmental biology

Large-scale RNAi screens identify novel genes that interact with the C. elegans retinoblastoma pathway as well as splicing-related components with synMuv B activity