Relief of YY1-induced transcriptional repression by protein-protein interaction with the nucleolar phosphoprotein B23.

Previous studies have shown that the transcription factor YY1 can both activate and repress transcription of many mammalian genes (reviewed by Hahn (Hahn, S. (1992) Curr. Biol. 2, 152-154)). Given the diverse effects of the YY1 protein, it seems likely that its function depends on interaction with other cellular factors. We have used the yeast two-hybrid system to isolate mouse cDNAs encoding proteins capable of directly binding to YY1. Sequence analysis of one clone revealed it had an open reading frame with the potential to code for a protein nearly identical to the previously published mouse nucleolar phosphoprotein B23. The YY1.B23 complex is specific, and occurs in vivo and in vitro. Overexpression of the B23 protein can reverse the transcriptional repression exerted by YY1. These results suggest a role for a nucleolar protein as a component in transcription and provide a possible mechanism for transcriptional regulation by YY1.