The retinoblastoma-susceptibility gene product binds directly to the human TATA-binding protein-associated factor TAF11250 (transcription factor TFIID/protein-protein interaction)

RB, the protein product of the retinoblas- toma tumor-suppressor gene, regulates the activity of specific transcription factors. This regulation appears to be mediated either directly through interactions with specific transcrip- tion factors or through an alternative mechanism. Here we report that stimulation of Spl-mediated transcription by RB is partially abrogated at the nonpermissive temperature in ts13 cells. These cells contain a temperature-sensitive muta- tion in the TATA-binding protein-associated factor TAF11250, first identified as the cell cycle regulatory protein CCG1. The stimulation of Spl-mediated transcription by RB in ts13 cells at the nonpermissive temperature could be restored by the introduction of wild-type human TAF11250. Furthermore, we demonstrate that RB binds directly to hTAF11250 in vitro and in vivo. These results suggest that RB can confer transcrip- tional regulation and possibly cell cycle control and tumor suppression through an interaction with TFIID, in particular with TAF11250. In this study, we sought to identify the mechanism through which RB stimulates Spl-mediated transcription. We mapped the domain(s) in Spl important for conferring the effect of RB in vivo, using GAL4-Spl fusions. A region in Spl similar to the