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CD4+ T cells From Children With Active Juvenile Idiopathic Arthritis Show Altered Chromatin Features Associated With Transcriptional Abnormalities (RNA-seq)

ABSTRACT: We used a multi-omics approach in an attempt to identify mechanisms driving the transcriptional abnormalities in peripheral blood CD4+ T cells of children with active JIA. We demonstrate that active JIA is associated with distinct alterations in CD4+ T cell chromatin, as assessed by ATAC-seq studies. However, 3D chromatin architecture, assessed by HiChIP and simultaneous mapping of CTCF anchors of chromatin loops, reveals that normal 3D chromatin architecture is largely preserved in JIA CD4+ T cells. However, overlapping CTCF binding, ATACseq, and RNAseq data with known JIA genetic risk loci demonstrated the presence of genetic influences on the observed transcriptional abnormalities and identified candidate target genes. These studies demonstrate the utility of multi-omics approaches for unraveling some of the most vexing questions regarding the pathobiology of autoimmune diseases.

ORGANISM(S): Homo sapiens

PROVIDER: GSE164213 | GEO | 2021/01/05

REPOSITORIES: GEO

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CD4+ T cells From Children With Active Juvenile Idiopathic Arthritis Show Altered Chromatin Features Associated With Transcriptional Abnormalities (ATAC-seq)

Project description:We used a multi-omics approach in an attempt to identify mechanisms driving the transcriptional abnormalities in peripheral blood CD4+ T cells of children with active JIA. We demonstrate that active JIA is associated with distinct alterations in CD4+ T cell chromatin, as assessed by ATAC-seq studies. However, 3D chromatin architecture, assessed by HiChIP and simultaneous mapping of CTCF anchors of chromatin loops, reveals that normal 3D chromatin architecture is largely preserved in JIA CD4+ T cells. However, overlapping CTCF binding, ATACseq, and RNAseq data with known JIA genetic risk loci demonstrated the presence of genetic influences on the observed transcriptional abnormalities and identified candidate target genes. These studies demonstrate the utility of multi-omics approaches for unraveling some of the most vexing questions regarding the pathobiology of autoimmune diseases.

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CD4+ T cells From Children With Active Juvenile Idiopathic Arthritis Show Altered Chromatin Features Associated With Transcriptional Abnormalities (ChIP-seq)

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Project description:The transcription factor CTCF appears indispensable in defining topologically associated domain boundaries and maintaining chromatin loop structures within these domains, supported by numerous functional studies. However, acute depletion of CTCF globally reduces chromatin interactions but does not significantly alter transcription. Here we systematically integrated multi-omics data including ATAC-seq, RNA-seq, WGBS, Hi-C, Cut&Run, CRISPR-Cas9 survival dropout screening, time-solved deep proteomic and phosphoproteomic analyses in cells carrying auxin-induced degron at endogenous CTCF locus. Acute CTCF protein degradation markedly rewired genome-wide chromatin accessibility. Increased accessible chromatin regions were largely located adjacent to CTCF-binding sites at promoter regions and insulator sites and were associated with enhanced transcription of nearby genes. In addition, we used CTCF-associated multi-omics data to establish a combinatorial data analysis pipeline to discover CTCF co-regulatory partners in regulating downstream gene expression. We successfully identified 40 candidates, including multiple established partners (i.e., MYC) supported by all layers of evidence. Interestingly, many CTCF co-regulators (e.g., YY1, ZBTB7A) that have evident alterations of respective downstream gene expression do not show changes at their expression levels across the multi-omics measurements upon acute CTCF loss, highlighting the strength of our system to discover hidden co-regulatory partners associated with CTCF-mediated transcription. This study highlights CTCF loss rewires genome-wide chromatin accessibility, which plays a critical role in transcriptional regulation

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Project description:CTCF plays a critical role in maintaining the three-dimensional (3D) chromatin organization, which is important for gene regulation, as it allows distal regulatory elements to come into proximity with one another. However, the detailed mechanism responsible for establishing and maintaining the recruitment of CTCF remains elusive. Here, we use in situ Hi-C to show that the ATP-dependent chromatin remodeler, Chd4, regulates intra-chromatin looping by controlling chromatin accessibility to conceal aberrant CTCF-binding sites in mouse embryonic stem cells (mESCs). These aberrant CTCF-binding sites are embedded in B2 SINEs and are localized within the interior of chromatin loops. In the absence of Chd4, the aberrant CTCF-binding sites become accessible and improper CTCF recruitment occurs, resulting in disorganization of the 3D chromatin architecture and subsequent disruption of enhancer-promoter interactions and the transcription of the corresponding genes. These results indicate that Chd4 regulates adequate transcription of mESCs by securing the proper 3D chromatin organization.

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