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Gene expression change after inactivation of MEF2D or PU.1 by CRISPR-Cas9

ABSTRACT: Gene expression change after inactivation of MEF2D or PU.1 by CRISPR-Cas9

PROVIDER: PRJNA772713 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16481575.fastq.gz	Fastqsanger.gz
	SRR16481576.fastq.gz	Fastqsanger.gz
	SRR16481577.fastq.gz	Fastqsanger.gz
	SRR16481578.fastq.gz	Fastqsanger.gz
	SRR16481579.fastq.gz	Fastqsanger.gz

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Gene expression change after inactivation of MEF2D or PU.1 by CRISPR-Cas9

Project description:Transcriptional dysregulation is a prominent feature in leukemia. Here, we systematically surveyed the transcription factor (TF) vulnerabilities in leukemia, and uncovered TF clusters that exhibit context-specific addictions within and between different subtypes of leukemia. We focused on and validated MEF2D as a requirement exclusively in AML with high IRF8 expression. Transcriptomic and chromatin-binding profiling revealed a key TF circuit composed of MEF2D-IRF8 vital for AML maintenance. AML can acquire dependence on this circuit through various mechanisms, including enhancer activation of the circuit via MLL-rearrangement. IRF8 cooperates with PU.1 to control PU.1/MEIS1 co-regulated transcriptional outputs, meanwhile coordinating with MEF2D to directly regulate genes in a non-redundant manner. Collectively, our study nominates a TF circuit in support of the pathogenesis of AML.

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Project description:Cancer cell type-selective addiction of transcription-chromatin regulatory program provides opportunities for therapeutic interventions. Here, we uncovered an IRF8-MEF2D transcription factor (TF) regulatory circuit as an acute myeloid leukemia (AML)-biased dependency. Combining CRISPR-based genetic screens, transcriptional analysis, and chromatin profiling, we demonstrated that a chromatin regulator, ZMYND8, directly regulates IRF8 and MYC expression through occupying AML-specific enhancer regions. ZMYND8 was essential for AML proliferation both in vitro and in vivo. The ZMYND8-occupied IRF8 enhancer was further characterized using Circular Chromosome Conformation Capture and CRISPRi-based perturbation assays and was observed in primary patient cells. Importantly, mutagenesis experiments revealed that the PHD/Bromodomain/PWWP reader module is required for ZMYND8 tethering to leukemia-essential co-activator BRD4 for enhancer-mediated gene regulation. Our results rationalize ZMYND8 as a potential selective therapeutic target for modulating the IRF8/MYC transcriptional networks in AML.

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