ArticleCell reports2024
Activity-assembled nBAF complex mediates rapid immediate early gene transcription by regulating RNA polymerase II productive elongation.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Epigenetic regulators polyphenols in neurodegenerative diseases: a promising intervention strategy.Annals of medicine · 2026Review
- An Adnp frameshift variant disrupts Wnt signalling inducing chromatocytoskeletal defects and autism-related behaviour in male mice.EBioMedicine · 2026Article
- Chromatin remodelling subunit SMARCB1 is implicated in dendrite development and complex brain functions.Acta neuropathologica communications · 2026Article
- Neurogenesis and the Epigenetic Landscape: Role of Histone Modifications and Chromatin Remodeling.Brain and behavior · 2026Review
- Mapping the secondary response to traumatic brain injury using spatial transcriptomics shows acute 4-aminopyridine treatment mitigates axonal and molecular pathology.Acta neuropathologica communications · 2026Article
- Co-condensation between transcription factor and cBAF selectively modulates chromatin remodeling and gene expression.Nature communications · 2025Article
- Genome-wide analysis of brain age identifies 59 associated loci and unveils relationships with mental and physical health.Nature aging · 2025Article
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Abstract
Signal-dependent RNA polymerase II (RNA Pol II) productive elongation is an integral component of gene transcription, including that of immediate early genes (IEGs) induced by neuronal activity. However, it remains unclear how productively elongating RNA Pol II overcomes nucleosomal barriers. Using RNAi, three degraders, and several small-molecule inhibitors, we show that the mammalian switch/sucrose non-fermentable (SWI/SNF) complex of neurons (neuronal BRG1/BRM-associated factor or nBAF) is required for activity-induced transcription of neuronal IEGs, including Arc. The nBAF complex facilitates promoter-proximal RNA Pol II pausing and signal-dependent RNA Pol II recruitment (loading) and, importantly, mediates productive elongation in the gene body via interaction with the elongation complex and elongation-competent RNA Pol II. Mechanistically, RNA Pol II elongation is mediated by activity-induced nBAF assembly (especially ARID1A recruitment) and its ATPase activity. Together, our data demonstrate that the nBAF complex regulates several aspects of RNA Pol II transcription and reveal mechanisms underlying activity-induced RNA Pol II elongation. These findings may offer insights into human maladies etiologically associated with mutational interdiction of BAF functions.
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