摘要
A recent article published in Science reveals how the mammalian SWI/SNF (mSWI/SNF) complexes utilize epigenetic cues in the chromatin landscape for differential chromatin remodeling.1 The heteromultimeric ATP-dependent SWI/SNF complexes can alter chromatin architecture leading to gene expression modulation (Fig. 1). Combinatorial and modular assembly of mSWI/SNF complex subunits2 partly underscore their heterogeneity and tissue-specific downstream effects. Given their implication in numerous diseases, including cancers3 and neurodevelopmental disorders,4 the mSWI/SNF or BAF complexes have attracted interest in elucidating their precise action to lend therapeutic ideas. The work of Mashtalir et al.1 has deepened our understanding by decoding the signals which instruct the assembly, localization, and activity of mSWI/SNF complexes. They provide experimental confirmation that the mSWI/SNF complexes depend on single and/or summative histone/nucleosome signatures and subunit modules to determine their activity (Fig. 1).
基金
Open Access funding enabled and organized by Projekt DEAL.