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. Author manuscript; available in PMC: 2018 Aug 12.
Published in final edited form as: Crit Rev Oncog. 2015;20(3-4):199–216. doi: 10.1615/critrevoncog.2015013566

FIG. 4:

FIG. 4:

Regulation of gene expression by SWI/SNF and Polycomb repressive complex 2 (PRC2) complexes. During lineage-specific differentiation, the SWI/SNF complex, which includes SMARCB1, interacts with transcription factors, histone acetyltransferases, and transcriptional regulators to activate expression of target genes. Acetylation of histone H3K27 is present at transcriptionally active genes. Opposing the SWI/SNF complex is the PRC2 complex, which contains EZH2. PRC2 interacts with DNA methyltransferases and histone deacetylases to silence gene expression. The transcriptionally inactive genes are marked by methylation at histone H3K27. In rhabdoid tumors the loss of SMARCB1 expression prohibits the normal functions of the SWI/SNF complex, resulting in altered gene expression.