Linking the Rb and Polycomb Pathways

Abstract

Polycomb group (PcG) proteins associate to form complexes that repress Hox genes, thereby imposing the patterning of Hox expression required for development. However, these proteins have a second Hox-independent role in regulating cell proliferation. Our results suggest that association between Rb and PcG proteins forms a repressor complex that blocks entry of cells into mitosis. Also, we provide evidence that Rb colocalizes with nuclear PcG complexes and is important for association of PcG complexes with nuclear targets. The Rb-PcG complex may provide a means to link cell cycle arrest to differentiation events leading to embryonic pattern formation.

Pocket proteins and cell cycle control

“…In another study, p16 was used to induce pocket protein activity in osteosarcoma cells (Dahiya et al, 2001). Here, the repression of cyclin A was associated with recruitment of Brm to the promoter, consistent with a role for chromatin remodeling in this setting as well.…”

“…In addition, however, cyclin A repression required the polycomb group protein HPC2, and was accompanied by HPC2 binding to the cyclin A promoter. Overexpression experiments suggested that HPC2 might bind the promoter through a complex of E2F, pRB, and a corepressor called CtBP (Dahiya et al, 2001(Dahiya et al, , 2003, although it is unclear whether the endogenous HPC2 is recruited to the promoter in this way.…”

Cell cycle control and beyond: emerging roles for the retinoblastoma gene family

“…Previous studies have suggested that SWI-SNF activity may be important for Rb-related growth suppression, and this is dependent on Rb binding to BRG1 at the core of the SWI-SNF complex (Dunaief et al, 1994). Furthermore, the role of SWI-SNF in Rb growth suppression appears linked, at least in part, to the ability of Rb to efficiently recruit HDAC-1 and -3 (Dahiya et al, 2001).…”

Recent lessons in gene expression, cell cycle control, and cell biology from adenovirus

“…CtBPs inhibit transcription in part by binding to several distinct histone deacetylases (HDACs) (Chinnadurai, 2002). However, repression at some promoters occurs by HDAC-independent mechanisms since it is not affected by the general HDAC inhibitor trichostatin A. HDAC-independent mechanisms include recruitment of histone methylating Polycomb complex proteins (Meloni et al, 1999;Sewalt et al, 1999;Dahiya et al, 2001;Nielsen et al, 2001;Trimarchi et al, 2001;Vandel et al, 2001;Ogawa et al, 2002;Attwooll et al, 2005) and the subsequent binding of HP1 and other heterochromatin-associated proteins that probably repress transcription by inhibiting promoter access to general transcription factors (Cao and Zhang, 2004;Levine et al, 2004;Lund and van Lohuizen, 2004;Ringrose and Paro, 2004).…”