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EPIGENOMICS

Chromatin openness requires continuous SWI/SNF activity

Nature Genetics volume 53, pages 263–264 (2021)Cite this article

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Chromatin structure, specifically sites of open or accessible chromatin, regulates transcription-factor binding, thereby determining cell-type-specific gene expression. Two new studies identify a constant requirement for SWI/SNF-complex remodeling to maintain open chromatin. In both studies, acute inhibition or degradation of the BRG1 or BRM ATPase subunits through chemical or genetic methods led to a loss of chromatin accessibility, in some cases affecting transcription-factor binding and altered gene expression.

Mammalian SWI/SNF complexes use ATP that is hydrolyzed by a core ATPase, BRG1 (also known as SMARCA4) or BRM (also known as SMARCA2), to generate chromatin accessibility. Previous studies have used conditional knockout or knockdown to show that BRG1 is required to maintain chromatin accessibility at SWI/SNF-complex target sites1,2,3,4. However, because of the slow decay of BRG1 protein in these systems (~72–96 hours), whether BRG1 is continuously required to generate open chromatin or is required only at defined cellular transitions, such as after DNA replication, was unclear. Acute depletion of yeast SWI2 results in rapid changes in chromatin accessibility5,6, but the dependence on the cell cycle is undetermined. Thus, how dynamic the generation of accessible chromatin is, as well as the effects of this process on transcription-factor binding and gene expression, are not known.

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Fig. 1: SWI/SNF activity is needed to maintain accessible chromatin.

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  1. Molecular and Cell Biology Laboratory, Salk Institute for Biological Studies, La Jolla, CA, USA

    Diana C. Hargreaves

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  1. Diana C. Hargreaves
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Correspondence to Diana C. Hargreaves.

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Hargreaves, D.C. Chromatin openness requires continuous SWI/SNF activity. Nat Genet 53, 263–264 (2021). https://doi.org/10.1038/s41588-021-00781-7

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