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Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (RNA-seq)

ABSTRACT: We examine the epigenetic role of the SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) in the epithelial response to RSV infection. Wild type and SMARCA4 silenced cells were subjected to short read illumina RNA Seq in the absence or presence of RSV infection. Cells were infected for 0, 16 h or 24 h prior to RNA seq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE161846 | GEO | 2021/01/01

REPOSITORIES: GEO

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Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (ATAC-seq)

Project description:We examine the epigenetic role of the SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) in the epithelial response to RSV infection. Wild type and SMARCA4 silenced cells were subjected to ATAC-seq in the absence or presence of RSV infection. Cells were infected for 0 or 24 h prior to RNA seq.

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Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-01-01 | GSE161849 | GEO

Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response

Project description:Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response

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SMARCA4 regulates BRD4 nuclear distribution in cellular plasticity

Project description:Inducible cell stress programs in basal epithelial cells shape repair and host defense pathways in mucosal surfaces. Previously, we discovered that expression of the core SWI/SNF complex ATPase, SMARCA4/Brg1, is required for genomic organization supporting a fully differentiated epithelial state, regulating cellular plasticity, paracrine mesenchymal signaling and anti-viral response. Here, we observe that SMARCA4 expression is intrinsically engaged with IFN response genes and dynamically engages the atypical histone acetyltransferase, BRD4, upon RSV infection, an association required for intrinsic immunity. To investigate the mechanisms how the SMARCA4 BRD4 complex functions in intrinsic immunity, we performed Cleavage Under Targets and Release Using Nuclease (CUT&RUN) of BRD4 binding in wild type (WT) and SMARCA4 knockdown (KD) small airway epithelial cells in mock- or RSV-infected states. In mock-infected cells, 4,017 high confidence BRD4 peaks are identified that localize to the gene bodies controlling motility programs. By contrast, RSV replication repositions BRD4 to 2,339 regions, upstream of transcription start sites in genes controlling inducible cytokine, cell adherence and anti-viral programs. RSV redistributes BRD4 into super enhancers regulating immune response-associated long noncoding RNAs. BRD4 binding is not affected by SMARCA4 KD in mock-infected cells, but BRD4 recruitment is reduced on 739 peaks after RSV infection, including superenhancers. These data extend the complex interrelationship between the SWI/SNF ATPases and that of the BRD4 bromodomain epithelial progenitors linking cell state and innate immunity.

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Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (RNA-seq)

Project description:Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (RNA-seq)

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Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (ATAC-seq)

Project description:Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (ATAC-seq)

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Project description:Epigenetics plays an important role in the priming the dynamic response of airway epithelial cells to infectious and environmental stressors. Here, we examine the epigenetic role of the SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) in the epithelial response to RSV infection. Depletion of SMARCA4 destabilized the abundance of the SMARCE1/ARID1A SWI/SNF subunits, disrupting the innate response and triggering a hybrid epithelial/mesenchymal (E/M) state. Assaying SMARCA4 complex-regulated open chromatin domains by transposase cleavage -next generation sequencing (ATAC-Seq), we observed that the majority of cleavage sites in uninfected cells have reduced chromatin accessibility. Paradoxically, SMARCA4 complex-depleted cells showed enhanced RSV-inducible chromatin opening and gene expression in the EMT pathway genes, MMP9, SNAI1/2, VIM, and CDH2. Focusing on the key MMP9, we observed that SMARCA4 complex depletion reduced basal BRD4 and RNA Polymerase II binding, but enhanced BRD4/Pol II binding in response to RSV infection. In addition, we observed that MMP9 secretion in SMARCA4 complex deficient cells contributes to mesenchymal transition, cellular fusion (syncytia) and subepithelial myofibroblast transition. We conclude the SMARCA4 complex is a transcriptional repressor of epithelial plasticity, whose depletion triggers a hybrid E/M state that affects the dynamic response of the small airway epithelial cell in mucosal remodeling via paracrine MMP9 activity.

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Project description:Alterations in chromatin structure caused by deregulated epigenetic mechanisms collaborate with underlying genetic lesions to promote cancer. SMARCA4/BRG1, a core component of the SWI/SNF ATP-dependent chromatin-remodelling complex, has been implicated by its mutational spectrum as exerting a tumour-suppressor function in many solid tumours; recently however, it has been reported to sustain leukaemogenic transformation in MLL-rearranged leukaemia in mice. Here we further explore the role of SMARCA4 and the two SWI/SNF subunits SMARCD2/BAF60B and DPF2/BAF45D in leukaemia. We observed the selective requirement for these proteins for leukaemic cell expansion and self-renewal in-vitro as well as in leukaemia. Gene expression profiling in human cells of each of these three factors suggests that they have overlapping functions in leukaemia. The gene expression changes induced by loss of the three proteins demonstrate that they are required for the expression of haematopoietic stem cell associated genes but in contrast to previous results obtained in mouse cells, the three proteins are not required for the expression of c-MYC regulated genes.

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siRNA Knockdown of SWI/SNF complex proteins in prostate cancer cell lines

Project description:Here we performed transcriptional profiling of the prostate cancer cell lines LNCaP and 22Rv1 comparing non-targeting siRNA treatment versus siRNAs targeting SWI/SNF complex proteins (SMARCA2, SMARCA4, and SMARCB1). Goal was to determine the effect of SWI/SNF knockdown on gene expression in prostate cancer. Two-condition experiment: non-targeting siRNA versus SWI/SNF-siRNA treated cells. Three SWI/SNF proteins were targeted: SMARCA2, SMARCA4, and SMARB1. Biological replicates: 1 control replicate, 2 treatment replicates per SWI/SNF protein. Technical replicates: 1 replicate per SWI/SNF protein. Cell lines: 22Rv1 and LNCaP.

2013-07-20 | E-GEOD-40384 | biostudies-arrayexpress

Binding specificity and function of the SWI/SNF subunit SMARCA4 bromodomain interaction with acetylated histone H3K14.

Project description:Bromodomains (BD) are conserved reader modules that bind acetylated lysine residues on histones. Although much has been learned regarding the in vitro properties of these domains, less is known about their function within chromatin complexes. SWI/SNF chromatin-remodeling complexes modulate transcription and contribute to DNA damage repair. Mutations in SWI/SNF subunits have been implicated in many cancers. Here we demonstrate that the BD of Caenorhabditis elegans SMARCA4/BRG1, a core SWI/SNF subunit, recognizes acetylated lysine 14 of histone H3 (H3K14ac), similar to its Homo sapiens ortholog. We identify the interactions of SMARCA4 with the acetylated histone peptide from a 1.29 Å-resolution crystal structure of the CeSMARCA4 BD-H3K14ac complex. Significantly, most of the SMARCA4 BD residues in contact with the histone peptide are conserved with other proteins containing family VIII bromodomains. Based on the premise that binding specificity is conserved among bromodomain orthologs, we propose that loop residues outside of the binding pocket position contact residues to recognize the H3K14ac sequence. CRISPR-Cas9-mediated mutations in the SMARCA4 BD that abolish H3K14ac binding in vitro had little or no effect on C. elegans viability or physiological function in vivo. However, combining SMARCA4 BD mutations with knockdown of the SWI/SNF accessory subunit PBRM-1 resulted in severe developmental defects in animals. In conclusion, we demonstrated an essential function for the SWI/SNF bromodomain in vivo and detected potential redundancy in epigenetic readers in regulating chromatin remodeling. These findings have implications for the development of small-molecule BD inhibitors to treat cancers and other diseases.

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