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ABSTRACT: Mechanism of action of Bv-ZM in alleviating cadmium stress in wheat

PROVIDER: PRJNA1143153 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30174033_1.fastq.gz	Fastqsanger.gz
	SRR30174033_2.fastq.gz	Fastqsanger.gz
	SRR30174034_1.fastq.gz	Fastqsanger.gz
	SRR30174034_2.fastq.gz	Fastqsanger.gz
	SRR30174035_1.fastq.gz	Fastqsanger.gz

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Project description:The recurring t(10;17)(p15;q21) chromosomal translocation as detected in a subset of human acute myeloid leukemia (AML) patients produces an aberrant fusion gene ZMYND11-MBTD1 (ZM), the biological consequence of which, however, remains elusive. Here we show that ZM chimera confers primary murine hematopoietic stem/progenitor cells (HSPCs) an indefinite self-renewal capability ex vivo and causes AML in vivo. Genomics analyses revealed that ZM directly binds to and maintains high expression of pro-leukemic transcription factor (TF) genes such as Hox, Meis1, Myc, Myb, and Sox4. Mechanistically, ZM interacts with and recruits the Tip60 acetyltransferase complex, both of which occupy promoter-proximal genomic regions that are enriched with histone acetylation and devoid of H3K27me3. Furthermore, systematic mutagenesis of ZM revealed an essential requirement of Tip60 association and an H3K36me3-binding PWWP domain for leukemic transformation and proto-oncogene activation. Finally, inhibitor of histone acetylation-‘reading’ bromodomain proteins is efficacious in treating ZM-induced AML. Collectively, this study demonstrated the AML-causing effect of ZM chimera with relevant animal models, examined into its gene-regulatory functions and protein interactome, and reports a promising mechanism-based therapeutic strategy.

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