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Brg1 restrains the pro-inflammatory properties of ILC3s and modulates intestinal immunity [RNA-seq]

ABSTRACT: Brg1 restrains the pro-inflammatory properties of ILC3s and modulates intestinal immunity [RNA-seq]

PROVIDER: PRJNA552810 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9645783.fastq.gz	Fastqsanger.gz
	SRR9645784.fastq.gz	Fastqsanger.gz
	SRR9645785.fastq.gz	Fastqsanger.gz
	SRR9645786.fastq.gz	Fastqsanger.gz

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Brg1 restrains the pro-inflammatory properties of ILC3s and modulates intestinal immunity [ATAC-seq]

Project description:To determine the molecular regulation of ILC3s by Brg1, small intestinal ILC3s (Lin-Thy1highCD45low) from Brg1-deficient and control ILC3s were subjected to assay for transposase-accessible chromatin with high throughput sequencing (ATAC-seq).

2020-07-01 | GSE148078 | GEO

Brg1 restrains the pro-inflammatory properties of ILC3s and modulates intestinal immunity [RNA-seq]

Project description:In order to search for cell-intrinsic targets for Brg1 in ILC3s, Brg1-deficient and control ILC3s were sorted from bone marrow chimeric mice, generated by transfering mixed bone marrow cells of Thy1.1/Thy1.2Rag1-/-Smarca4f/f and Thy1.2Rag1-/-Smarca4f/fRorc-cre donors at 1:1 ratio to sub-lethally irriadiated Rag2-/-Il2rg-/- recipients.

2020-07-01 | GSE133853 | GEO

Brg1 restrains the pro-inflammatory properties of ILC3s and modulates intestinal immunity [ATAC-seq]

Project description:Brg1 restrains the pro-inflammatory properties of ILC3s and modulates intestinal immunity [ATAC-seq]

| PRJNA623010 | ENA

Brg1 restrains the pro-inflammatory properties of ILC3s and modulates intestinal immunity.

Project description:Group 3 innate lymphoid cells (ILC3s), a subset of the innate lymphoid cells, are abundantly present in the intestine and are crucial regulators of intestinal inflammation. Brg1 (Brahma-related gene 1), a catalytic subunit of the mammalian SWI-SNF-like chromatin-remodeling BAF complex, regulates the development and function of various immune cells. Here, by genetic deletion of Brg1 in ILC3s (Smarca4?ILC3), we prove that Brg1 supports the differentiation of NKp46+ILC3s by promoting the T-bet expression in NKp46-ILC3s, which facilitates the conversion of NKp46-ILC3s to NKp46+ILC3s. Strikingly, Smarca4?ILC3 mice of the Rag1-/- background develop spontaneous colitis accompanied with increased GM-CSF production in ILC3s. By construction of a mixed bone marrow chimeric system, we demonstrate that Brg1 enhances T-bet and inhibits GM-CSF expression in ILC3s through a cell-intrinsic manner. Blockade of GM-CSF ameliorates colitis in Rag1-/-Smarca4?ILC3 mice, suggesting that the suppression of GM-CSF production from ILC3s by Brg1 serves as a critical mechanism for Brg1 to restrain intestinal inflammation. We have further demonstrated that Brg1 binds to the Tbx21 and Csf2 gene locus in ILC3s, and favors the active and repressive histones modifications on gene locus of Tbx21 and Csf2 respectively. Our work reveals the essential role of Brg1 in intestinal immunity by regulating ILC3s.

| S-EPMC7790751 | biostudies-literature

ChIP-seq analysis of BATF in ILC3s sorted from small intestine of Rag1-/- mice [CUT&TAG ChIPseq]

Project description:Group 3 innate lymphoid cells (ILC3s) are crucial for the maintenance of host-microbiota homeostasis in gastrointestinal mucosal tissues. The mechanisms that maintain lineage identity of intestinal ILC3s, and ILC3s-mediated orchestration of microbiota and mucosal T cell immunity are elusive. Here, we identified BATF as a gatekeeper of ILC3s homeostasis in the gut. Depletion of BATF in ILC3s resulted in excessive interferon-γ production, dysbiosis, aberrant T cell immune responses and spontaneous inflammatory bowel disease (IBD), which was considerably ameliorated by removal of adaptive immunity or antibiotic treatment. Mechanistically, BATF directly regulates ILC3s identity by globally shapes chromatin landscape of ILC3s. BATF directly binds to the cis-regulatory elements of type 1 effector genes, restrains their chromatin accessibility and inhibits their expression. Conversely, BATF promotes chromatin accessibility of genes involved in MHCII antigen processing and presentation pathways. Collectively, our findings reveal BATF is a promising candidate to maintain ILC3s stability and coordinate ILC3s–mediated control of intestinal homeostasis.

2022-08-31 | GSE168079 | GEO

Chromatin accessibility landscapes of WT (Rag1-/-) and BATF KO (Rag1-/-Batf-/-) ILC3s sorted from small intestine [ATAC-seq]

2022-08-31 | GSE168078 | GEO

Chromatin accessibility landscapes of intestinal WT Nkp46-CC6- ILC3 (Double Negative, DN ILC3) and BATF-deficient cKO DN ILC3s sorted from intestine

2022-09-08 | GSE212590 | GEO

Bulk RNA sequencing of WT (Batf fl/fl) and Batf-/- (Batf fl/fl PLZFcre+) ILC3s sorted from small intestine [bulk RNA-seq]

2022-08-31 | GSE168076 | GEO

Protein-protein interactions of BRG1 or BRG1-HSA in SW13 cells

Project description:The SWI/SNF complex remodels chromatin in an ATP-dependent manner through the ATPase subunits BRG1 and BRM. Chromatin remodeling alters nucleosome structure to change gene expression, however aberrant remodeling and gene expression can result in cancer. The function and localization on chromatin of the SWI/SNF complex depends on the protein makeup of the complex. Here we report the protein-protein interactions of wild-type BRG1 or mutant BRG1 in which the HSA domain has been deleted (BRG1-HSA). We demonstrate the interaction of BRG1 with most SWI/SNF complex members and a failure of a number of these members to interact with BRG1-HSA. These results demonstrate that the HSA domain of BRG1 is a critical interaction platform for the correct formation of SWI/SNF remodeling complexes.

2023-02-15 | PXD029647 | Pride

Comparison of transcriptional profiles of (1) intestinal ILC3s isolated from WT and IL-17D-deficient mice; (2) CD93+ILC3s and CD93-ILC3s from WT mice

Project description:IL-17D/CD93 axis was essential for ILC3s hemostasis. In order to further understand how IL-17D-CD93 axis regulate ILC3s function, we conducted RNA-seq analysis of ILC3s.

2021-05-20 | GSE165788 | GEO

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