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PRMT7 regulated chromatin accesibility in myeloid cells [ATAC-Seq]

ABSTRACT: PRMT7 regulated chromatin accesibility in myeloid cells [ATAC-Seq]

PROVIDER: PRJNA643578 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12130209_1.fastq.gz	Fastqsanger.gz
	SRR12130209_2.fastq.gz	Fastqsanger.gz
	SRR12130210_1.fastq.gz	Fastqsanger.gz
	SRR12130210_2.fastq.gz	Fastqsanger.gz

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PRMT7 regulated chromatin accesibility in myeloid cells [ATAC-Seq]

Project description:Under inflammatory conditions the extravasation of monocytes into tissues through trans-endothelial migration is a fundamental immunological process underlying innate inflammatory responses across multiple organ systems contributing to tissue injury and the progression of autoimmunity, cardiovascular disease and particularly chronic lung disease. Methylation of protein arginine residues via protein arginine methyltransferases (PRMTs) is a post-translational epigenetic modification implicated in inflammatory responses. How PRMTs, particularly PRMT7, epigenetically regulates monocyte-driven inflammatory response in disease remains unclear. Here, we perform ATAC-seq analysis on an MHS macrophage cell line in which PRMT7 has been disrupted by CRISPR/Cas9 to examine chromatin accessibility regulated by PRMT7.

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Chromatin accesibility in mice T-ALL tumors

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Effect of the depletion of RBP33 (Tb927.8.990) on chromatin accesibility in bloodstream Trypanosoma brucei [ATAC-seq]

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Project description:ATAC-seq of 79 primary samples obtained from human acute leukemias, namely AML, T-ALL and mixed myeloid/lymphoid leukemias with CpG Island Methylator Phenotype (CIMP). Moreover, ATAC-seq of CD34+ HSPCs from 3 healthy donors are included. ATAC-seq was performed as described (Buenrostro et al., 2013) with a modification in the lysis buffer to reduce mitochondrial DNA contamination. Due to patient confidentiality considerations, the raw data files for this dataset have been deposited to the EGA controlled-access archive under the accession numbers EGAS00001007094 (study); EGAD00001011050 (dataset).

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YEATS2 O-GlcNAcylation Promotes Chromatin Association of the ATAC complex and Lung Cancer Tumorigenesis

Project description:The intracellular O-linked N-acetylglucosamine (O-GlcNAc) modification is known to be enriched in the nucleus and in particular on chromatin, but many of its chromatin targets remain to be identified. Herein we demonstrate the O-GlcNAcylation of YEATS Domain Containing 2 (YEATS2), a subunit of the chromatin Ada-two-A-containing (ATAC) complex and a reader of histone H3K27ac. We show that YEATS2 interacts with the O-GlcNAc transferase (OGT) and further pinpoint its major O-GlcNAcylation site to be Thr604 using electron transfer dissociation mass spectrometry. O-GlcNAcylation promotes the chromatin association of YEATS2, and the affinity between YEATS2 and other ATAC components on chromatin, such as ZZZ3, GCN5 and PCAF. Downstream, YEATS2-T604A attenuated the ATAC-dependent histone H3K9ac levels and inactivated the expression of essential ribosomal genes as shown in chromatin immunoprecipitation assays. Further, xenograft experiments show that YEATS2 O-GlcNAcylation promotes lung cancer tumorigenesis. Our work reveals the critical role of YEATS2 O-GlcNAcylation in stabilizing the ATAC complex on chromatin and expands the chromatin substrates of OGT.

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