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

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

PROVIDER: PRJNA705995 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13827719_1.fastq.gz	Fastqsanger.gz
	SRR13827719_2.fastq.gz	Fastqsanger.gz
	SRR13827720_1.fastq.gz	Fastqsanger.gz
	SRR13827720_2.fastq.gz	Fastqsanger.gz
	SRR13827721_1.fastq.gz	Fastqsanger.gz

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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.

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

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

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

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

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ChIPseq analysis of IRF4 and BATF in immune cells

Project description:Purpose: The purpose of this study is to find the binding partner of IRF4 in the context of Th17- cell differentiation. To this end, we have used ChIPseq analysis followed by de novo motif search around genome-wide binding sites to identify BATF as the binding partner for IRF4 in the context of not only Th17 cells but other immune cell types as well. Naïve T-cells isolated from the spleen of C57BL/6J mice are cultured under Th17, Th2 or Th0 polarizing conditions for 42 hrs and subject to ChIP using IRF4 and/or BATF antibodies followed by high-throughput sequencing. Bone marrow derived dendritic cells (BMDCs) were stimulated with LPS for 6hrs and similrly subjected to ChIPseq analysis with IRF4.

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Transcriptional profiling of rag1 deficient (rag1-/-) and rag1 heterozygous (rag1+/-) zebrafish kidney and intestine

Project description:Four dual hybridizations of rag1 deficient (rag1-/-) and rag1 heterozygous (rag1+/-) zebrafish cRNAs from kidney and intestine. Keywords: Gene knockout

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ChIPseq analysis of IRF4 and BATF in immune cells

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