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The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia (ChIP-seq_human)

ABSTRACT: The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia (ChIP-seq_human)

PROVIDER: PRJNA1043208 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26894458.fastq.gz	Fastqsanger.gz
	SRR32807501.fastq.gz	Fastqsanger.gz
	SRR32807502.fastq.gz	Fastqsanger.gz
	SRR32807503.fastq.gz	Fastqsanger.gz
	SRR32807504.fastq.gz	Fastqsanger.gz

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The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia (ChIP-seq_human)

Project description:Histone H3 lysine 4 tri-methylation (H3K4me3) is abundant in MLL-rearranged (MLL-r) acute myeloid leukemia (AML) cells, but the enzymes responsible and their roles remain unclear. In this study, we perform a CRISPR-tiling screen against known H3K4 methylation modifiers in MLL-r AML model. We found the non-redundant roles of H3K4 methyltransferase SETD1B for growth regulation in NrasG12D or FLT3-ITD-expressing AML cells that exhibit cytokine-independent growth. The disruption of SETD1B catalytic SET domain causes cell cycle arrest, apoptosis, cell differentiation and a downregulation of gene expression, especially in the MYC pathway. H3K4me3 and SETD1B are distributed to the gene body of Myc, and the loss of SETD1B SET domain result in a significant decrease in H3K4me3 breadth. Overexpression of MYC significantly restores the growth defect and transcriptional perturbation in SETD1B SET domain mutant cells. In the meantime, the expression of MYC does not rescue the reduced H3K4me3 breadth and RNA polymerase II elongation in SETD1B mutant cells. A disruption of H3K4 demethylase KDM5C enhances global H3K4me3 level and promotes the proliferation of AML cell, and partially rescues the defective cell growth of SETD1B SET domain mutant cells. These data indicate that SETD1B is required for both H3K4me3 breadth and Myc expression to support advanced AML cell proliferation. Thus, a thorough understanding of the SETD1B-mediated H3K4me3 breadth will be critical for the development of markers and therapies for leukemia subtypes that are MYC-dependent.

2025-04-28 | GSE248322 | GEO

The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia (CUT&Tag)

2025-04-28 | GSE248318 | GEO

The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia (RNA-seq)

2025-04-28 | GSE248325 | GEO

The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia (ChIP-seq_mus)

2025-04-28 | GSE248323 | GEO

The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia

Project description:The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia

| PRJNA1043212 | ENA

The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia (CUT&Tag)

Project description:The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia (CUT&Tag)

| PRJNA1043206 | ENA

The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia (ChIP-seq_mus)

Project description:The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia (ChIP-seq_mus)

| PRJNA1043213 | ENA

The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia (RNA-seq)

Project description:The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia (RNA-seq)

| PRJNA1043214 | ENA

The catalytic domain of SETD1B regulates H3K4me3 breadth and Myc expression in MLL-r leukemia

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-04-28 | GSE248326 | GEO

Comparative gene expression analysis in OCI-LY19 isogenic cell lines with SETD1B mutation or KMT2D+SETD1B double mutants.

Project description:The translocation t(14;18) activates BCL2 and is considered the initiating genetic lesion in most follicular lymphomas (FL). Surprisingly, FL patients fail to respond to the BCL2 inhibitor, Venetoclax. We show that mutations and deletions affecting the histone lysine methyltransferase SETD1B (KMT2G) occur in 7% of FLs and in 16% of diffuse large B cell lymphomas (DLBCL). Deficiency in SETD1B confers striking resistance to Venetoclaxand to an experimental MCL-1 inhibitor. SETD1B also acts as a tumor suppressor andcooperates with loss ofKMT2Din lymphoma development in vivo. Consistently, loss of SETD1B in human lymphomas typically coincides with loss of KMT2D. Mechanistically, SETD1B is required for the expression of several pro-apoptotic BCL2 family proteins. Conversely, inhibitors of the KDM5 histoneH3K4demethylases restore BIM and BIK expression and synergize with Venetoclax inSETD1B-deficient lymphomas.

2024-08-23 | GSE273152 | GEO

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