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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE235309 | GEO | 2023/10/01

REPOSITORIES: GEO

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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.

2023-10-01 | GSE235303 | GEO

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

2023-10-01 | GSE235301 | GEO

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

| PRJNA985668 | ENA

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

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

| PRJNA985679 | ENA

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

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

| PRJNA985672 | ENA

Chromatin accessibility promotes hematopoietic and leukemia stem cell activity.

Project description:Chromatin organization is a highly orchestrated process that influences gene expression, in part by modulating access of regulatory factors to DNA and nucleosomes. Here, we report that the chromatin accessibility regulator HMGN1, a target of recurrent DNA copy gains in leukemia, controls myeloid differentiation. HMGN1 amplification is associated with increased accessibility, expression, and histone H3K27 acetylation of loci important for hematopoietic stem cells (HSCs) and leukemia, such as HoxA cluster genes. In vivo, HMGN1 overexpression is linked to decreased quiescence and increased HSC activity in bone marrow transplantation. HMGN1 overexpression also cooperates with the AML-ETO9a fusion oncoprotein to impair myeloid differentiation and enhance leukemia stem cell (LSC) activity. Inhibition of histone acetyltransferases CBP/p300 relieves the HMGN1-associated differentiation block. These data nominate factors that modulate chromatin accessibility as regulators of HSCs and LSCs, and suggest that targeting HMGN1 or its downstream effects on histone acetylation could be therapeutically active in AML.

| S-EPMC7076002 | biostudies-literature

EBF2 transcriptionally regulates brown adipogenesis via the histone reader DPF3 and the BAF chromatin remodeling complex.

Project description:The transcription factor early B-cell factor 2 (EBF2) is an essential mediator of brown adipocyte commitment and terminal differentiation. However, the mechanisms by which EBF2 regulates chromatin to activate brown fat-specific genes in adipocytes were unknown. ChIP-seq (chromatin immunoprecipitation [ChIP] followed by deep sequencing) analyses in brown adipose tissue showed that EBF2 binds and regulates the activity of lineage-specific enhancers. Mechanistically, EBF2 physically interacts with the chromatin remodeler BRG1 and the BAF chromatin remodeling complex in brown adipocytes. We identified the histone reader protein DPF3 as a brown fat-selective component of the BAF complex that was required for brown fat gene programming and mitochondrial function. Loss of DPF3 in brown adipocytes reduced chromatin accessibility at EBF2-bound enhancers and led to a decrease in basal and catecholamine-stimulated expression of brown fat-selective genes. Notably, Dpf3 is a direct transcriptional target of EBF2 in brown adipocytes, thereby establishing a regulatory module through which EBF2 activates and also recruits DPF3-anchored BAF complexes to chromatin. Together, these results reveal a novel mechanism by which EBF2 cooperates with a tissue-specific chromatin remodeling complex to activate brown fat identity genes.

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Acute BAF perturbation causes immediate changes in chromatin accessibility.

Project description:Cancer-associated, loss-of-function mutations in genes encoding subunits of the BRG1/BRM-associated factor (BAF) chromatin-remodeling complexes1-8 often cause drastic chromatin accessibility changes, especially in important regulatory regions9-19. However, it remains unknown how these changes are established over time (for example, immediate consequences or long-term adaptations), and whether they are causative for intracomplex synthetic lethalities, abrogating the formation or activity of BAF complexes9,20-24. In the present study, we use the dTAG system to induce acute degradation of BAF subunits and show that chromatin alterations are established faster than the duration of one cell cycle. Using a pharmacological inhibitor and a chemical degrader of the BAF complex ATPase subunits25,26, we show 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 an almost complete loss of chromatin accessibility at BAF-controlled sites, especially also at superenhancers, providing a mechanism for intracomplex synthetic lethalities.

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