A recent study published in Nature reveals an interaction between SWI/SNF subunits and mitotic chromatin,which is essential for establishing gene bookmarks and preserving cell identity.1 The findings deepen our unders...A recent study published in Nature reveals an interaction between SWI/SNF subunits and mitotic chromatin,which is essential for establishing gene bookmarks and preserving cell identity.1 The findings deepen our understanding of how SWI/SNF complexes regulate transcriptional memory heritability for cell fate commitment(Fig.1),thus validating the indispensability of SWI/SNF complexes in development and association of their perturbance with tumorigenesis and neurodevelopment disorders.展开更多
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-dependen...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).展开更多
文摘A recent study published in Nature reveals an interaction between SWI/SNF subunits and mitotic chromatin,which is essential for establishing gene bookmarks and preserving cell identity.1 The findings deepen our understanding of how SWI/SNF complexes regulate transcriptional memory heritability for cell fate commitment(Fig.1),thus validating the indispensability of SWI/SNF complexes in development and association of their perturbance with tumorigenesis and neurodevelopment disorders.
基金Open Access funding enabled and organized by Projekt DEAL.
文摘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).
