Rb and p130 regulate RNA polymerase I transcription: Rb disrupts the interaction between UBF and SL-1

We have previously demonstrated that the protein encoded by the retinoblast oma susceptibility gene (Rb) functions as a regulator of transcription by R NA polymerase I (rDNA transcription) by inhibiting UBF-mediated transcripti on. In the present study, we have examined the mechanism by which Rb repres ses UBF-dependent rDNA transcription and determined if other Rb-like protei ns have similar effects. We demonstrate that authentic or recombinant UBF a nd Rb interact directly and this requires a functional A/B pocket. DNase fo otprinting and band-shift assays demonstrated that the interaction between Rb and UBF does not inhibit the binding of UBF to DNA, However, the formati on of an UBF/Rb complex does block the interaction of UBF with SL-1, as ind icated by using the 48 kDa subunit as a marker for SL-1, Additional evidenc e is presented that another pocket protein, p130 but not p107, can be found in a complex with UBF, Interestingly, the cellular content of p130 inverse ly correlated with the rate of rDNA transcription in two physiological syst ems, and overexpression of p130 inhibited rDNA transcription. These results suggest that p130 may regulate rDNA transcription in a similar manner to R b.