¹Cancer Research Center, Boston University School of Medicine, Boston, MA, USA

Correspondence: Professor S Wang, Cancer Research Center, R-906, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA. E-mail: sw184@bu.edu

Received 21 December 2006; Revised 23 March 2007; Accepted 1 April 2007; Published online 7 May 2007.

Abstract

The SWI/SNF complex participates as a co-activator in the transcriptional regulation of certain genes. Conversely, we and others have recently established that Brg1 and Brm, the central components of SWI/SNF, act instead as co-repressors for E2F-mediated transcriptional repression, and for the transcription of certain other promoters. We report here that Brg-1 and Brm can switch their mode of function at same promoter between activation and repression by ligand-directed differential coordination with BAF155, BAF170, HDAC1, p300 and prohibitin. This ligand and context-dependent reprogramming of the SWI/SNF complex allows it to differentially serve as either a co-repressor or a co-activator of transcription at the same promoter.