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The transition from quiescent to activated states in human hematopoietic stem cells is governed by dynamic 3D genome reorganization [ChIP-Seq]

ABSTRACT: We profiled chromatin accessibility in sorted hematopoietic populations. We used this to identify signatures of chromatin accessibility which discriminated LT-HSC from other hematopoietic stem and progenitor cell populations, discriminated by CTCF binding sites. We further validated this with RNA-Seq on sorted cord blood populations following shCTCF, and Hi-C and CTCF ChIP-Seq on the OCIAML-2 cell line.

ORGANISM(S): Homo sapiens

PROVIDER: GSE125061 | GEO | 2020/11/23

REPOSITORIES: GEO

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The transition from quiescent to activated states in human hematopoietic stem cells is governed by dynamic 3D genome reorganization [RNA-Seq]

Project description:We profiled chromatin accessibility in sorted hematopoietic populations. We used this to identify signatures of chromatin accessibility which discriminated LT-HSC from other hematopoietic stem and progenitor cell populations, discriminated by CTCF binding sites. We further validated this with RNA-Seq on sorted cord blood populations following shCTCF, and Hi-C and CTCF ChIP-Seq on the OCIAML-2 cell line.

2020-11-23 | GSE125063 | GEO

The transition from quiescent to activated states in human hematopoietic stem cells is governed by dynamic 3D genome reorganization [Hi-C]

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The transition from quiescent to activated states in human hematopoietic stem cells is governed by dynamic 3D genome reorganization [ATAC-Seq]

2020-11-23 | GSE125060 | GEO

The transition from quiescent to activated states in human hematopoietic stem cells is governed by dynamic 3D genome reorganization [Low-C]

Project description:Life-long blood production requires long-term hematopoietic stem cells (LT-HSC) - marked by stemness states involving quiescence and self-renewal - to transition into activated short-term HSC (ST-HSC) with reduced stemness. As few transcriptional changes underlie this transition, we used single-cell and bulk ATAC-seq on human HSC and stem/progenitor subsets (HSPC) to uncover chromatin accessibility signatures, one including LT-HSC (LT/HSPC signature) and another excluding LT-HSC (Act/HSPC signature). These signatures inversely correlated during early hematopoietic commitment and differentiation. The Act/HSPC signature contains CTCF binding sites mediating 351 chromatin interactions, engaged in ST-HSC but not LT-HSC, enclosing multiple stemness pathway genes active in LT-HSC and repressed in ST-HSC. CTCF silencing derepressed stemness genes, restraining quiescent LT-HSC from transitioning to activated ST-HSC. Hence, 3D chromatin interactions centrally mediated by CTCF, endow a gatekeeper function that governs the earliest fate transitions HSC make by coordinating disparate stemness pathways linked to quiescence and self-renewal.

2020-11-23 | GSE159287 | GEO

ea9af326-25e0-42af-a639-732a3bafd94b - samples

Project description:To elucidate the epigenetic changes which occur when human long-term hematopoietic stem cells (LT-HSC) become activated we performed Bulk ATAC-Seq on 13 sorted bulk hematopoietic populations from cord bloodas well as single-cell ATAC-Seq upon CD34+CD38-CD45RA- cells enriched for HSC as well as CD34+/CD38+ progenitor cells both from cord blood. These studies revealed gains of chromatin accessibility around CTCF binding sites during HSPC activation, as such we additionally performed Low-C to directly profile the 3D conformation of human cord-blood derived LT-HSC and Short-term hematopoietic stem cells (ST-HSC), as well as Hi-C , ATAC-Seq and CTCF ChIP-Seq upon the OCIAML-2 cell line in which CTCF sites gained during LT-HSC activation are enriched. Finally we transduced human cord-blood LT-HSC with an shCTCF vector; in-vitro cultured LT-HSC cells harbouring shCTCF were used to perform RNA-Seq, and scATAC-Seq was performed on CD34+/CD38- human CB cells transduced with shCTCF, four weeks post xeno-transplantation into mice. Collectively these studies have helped us demonstrate the role of 3D chromatin conformation changes during human LT-HSC activation.

| EGAD00001006447 | EGA

Development of gene expression signatures of CTCF-expressing vs CTCF-depleted hepatocellular carcinoma cells

Project description:To understand the functional role of CTCF in the oncogenesis of HCC, we constructed lentiviruses expressing control shRNA (shCont) or shRNA agains CTCF (shCTCF) and transduced them into PLC5 cells respectively. After 24 hours, cells were cultered in puromycin containing medium (5 ug) for another 24 hours. Cells were returned to normal medium for another 48 hours before total mRNAs were corrected for whole genome gene expression array analysis. Expression of FoxM1 gene from this signature was quantified in an independent set of RNA samples by real-time PCR, confirming differntial expression of this gene in shCTCF expressing cells.

2017-09-30 | GSE100533 | GEO

mRNA-seq in human 293T HEK cells in the presence (shScr) or absence of HSF1 (shHSF1) or CTCF (shCTCF).

Project description:Profiling the mRNA content in 293T human embryonic kidney (HEK) cells in the presence and absence of HSF1 or CTCF. The mRNA was enriched from total cellular RNA using using polyadenyltion-selection. HSF1 (shHSF1) or CTCF (shCTCF) was downregulated using shRNA for 48hours. Scrambled RNA (shScr) was used as a negative control.

2020-11-17 | GSE155541 | GEO

Systematic assessment of ISWI subunits reveals that NURF creates local accessibility for proper CTCF function

Project description:Catalytic activity of the ISWI family of remodelers is critical for nucleosomal organization and transcription factor binding, including the insulator protein CTCF. To define which subcomplex mediates these diverse functions we phenotyped a panel of isogenic mouse stem cell lines each lacking one of six ISWI accessory subunits. Individual deletions of either CERF, RSF1, ACF, WICH or NoRC subcomplexes only moderately affect the chromatin landscape, while removal of the NURF-specific subunit BPTF leads to drastic reduction in chromatin accessibility and Snf2h ATPase localization around CTCF sites. While this reduces distances to the adjacent nucleosomes it only modestly impacts CTCF binding itself. In absence of accessibility, the insulator function of CTCF is nevertheless impaired resulting in lower occupancy of cohesin and cohesin-loading factors, and reduced insulation at these sites, highlighting the need of NURF-mediated remodeling for open chromatin and proper CTCF function. Our comprehensive analysis reveals a specific role for NURF in mediating Snf2h localization and chromatin opening at bound CTCF sites showing that local accessibility is critical for cohesin binding and insulator function.

2024-03-13 | PXD042945 | Pride

Spatial reorganization of telomeres in long-lived quiescent cells.

Project description: Not available

| S-EPMC4581094 | biostudies-literature

Acute depletion of CTCF rewires genome-wide chromatin accessibility

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

2021-07-04 | PXD026484 | Pride

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