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CUX1 regulates human hematopoietic stem cell chromatin accessibility via the BAF complex [ChIP-seq]

ABSTRACT: CUX1 regulates human hematopoietic stem cell chromatin accessibility via the BAF complex [ChIP-seq]

PROVIDER: PRJNA985672 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24974353.fastq.gz	Fastqsanger.gz
	SRR24974354.fastq.gz	Fastqsanger.gz
	SRR24974355.fastq.gz	Fastqsanger.gz
	SRR24974356.fastq.gz	Fastqsanger.gz
	SRR24974357.fastq.gz	Fastqsanger.gz

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CUX1 regulates human hematopoietic stem cell chromatin accessibility via the BAF complex [CUT&RUN]

Project description:CUX1 is a HOX-family transcription factor that is essential for development and differentiation of multiple tissues. CUX1 is recurrently mutated or deleted in cancer, particularly in myeloid malignancies. However, the mechanism by which CUX1 regulates gene expression and differentiation remains poorly understood, creating a barrier to understanding the tumor suppressive functions of CUX1. Herein, we demonstrate that CUX1 directs the BAF chromatin remodeling complex to DNA to increase chromatin accessibility in hematopoietic cells. CUX1 preferentially regulates lineage-specific enhancers, and CUX1 target genes are predictive of cell fate in vivo. These data indicate that CUX1 functions as a pioneer factor to epigenetically regulate hematopoietic lineage commitment and homeostasis, and CUX1 deficiency disrupts these processes in stem and progenitor cells, facilitating transformation.

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CUX1 regulates human hematopoietic stem cell chromatin accessibility via the BAF complex [ChIP-seq]

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CUX1 regulates human hematopoietic stem cell chromatin accessibility via the BAF complex [ATAC-seq]

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CUX1 regulates human hematopoietic stem cell chromatin accessibility via the BAF complex

Project description:CUX1 regulates human hematopoietic stem cell chromatin accessibility via the BAF complex

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CUX1 regulates human hematopoietic stem cell chromatin accessibility via the BAF complex [CUT&RUN]

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CUX1 regulates human hematopoietic stem cell chromatin accessibility via the BAF complex [ATAC-seq]

Project description:CUX1 regulates human hematopoietic stem cell chromatin accessibility via the BAF complex [ATAC-seq]

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RNA-seq of sorted murine long-term hematopoietic stem cells segmented on CUX1 levels with and without CUX1 knockdown

Project description:Hematopoietic stem cells (HSCs) possess properties of both self-renewal and multipotent differentiation; however, the regulation of these opposing properties remains elusive. Using a novel reporter mouse, we demonstrate the dose-dependent role of the transcription factor, CUX1, in HSC fate. As CUX1 levels naturally rise, HSCs gradually lose repopulating capacity. CUX1 knockdown reverses this process and reverts HSCs to an earlier cell state—restoring the transcriptome, chromatin accessibility, repopulating capacity, and self-renewal ability of HSCs with normally low CUX1 levels. In the absence of CUX1, endogenous retroelements (EREs) are aberrantly expressed, leading to a cell-intrinsic inflammatory response, which contributes to CUX1-dependent HSC activity. Likewise, loss of the transcription factor IRF1 attenuates CUX1-mediated HSC reprogramming. This mechanism could be relevant to leukemogenesis as acute myeloid leukemias with CUX1 deletions upregulate EREs and the interferon response. Our findings attribute CUX1 and innate immune activation to the complex molecular underpinnings of HSC fate decisions.

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Acute BAF perturbation causes immediate changes in chromatin accessibility

Project description:Loss-of-function mutations in genes coding for subunits of the large, multifarious BRG1/BRM associated factor (BAF) chromatin remodeling complexes are frequently causative for cancer or developmental diseases1-5. Cells lacking the most frequently mutated subunits like the ATPase SMARCA4 typically exhibit drastic chromatin accessibility changes, especially of important regulatory regions6-12. However, so far it remains unknown how these changes are established over time, and whether they are causative for intra-complex synthetic lethalities abrogating the formation (SMARCC1-SMARCC2)8,13,14 or activity (SMARCA4-SMARCA2)15-17 of BAF complexes. Here, we utilize the dTAG system18 to induce acute degradation of BAF subunits in wild-type and BAF mutant backgrounds and analyze the resulting chromatin accessibility changes with high kinetic resolution. We observe that chromatin alterations are established faster than the duration of one cell cycle and that maintaining genome accessibility requires constant ATP-dependent remodeling. Completely abolishing BAF complex function by acute degradation of a synthetic lethal subunit in a paralog-deficient background results in a near-complete loss of chromatin accessibility at BAF-controlled sites, especially at super-enhancers, providing a mechanism for intra-complex synthetic lethalities.

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Single-cell RNA-Seq characterization of CUX1 levels in murine hematopoietic stem cells.

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ATAC-Seq of sorted murine LT-HSCs segemented on intial CUX1 levels with and without CUX1 knockdown.

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