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β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [RNA-seq LSK]

ABSTRACT: β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [RNA-seq LSK]

PROVIDER: PRJNA987676 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25029384_1.fastq.gz	Fastqsanger.gz
	SRR25029384_2.fastq.gz	Fastqsanger.gz
	SRR25029385_1.fastq.gz	Fastqsanger.gz
	SRR25029385_2.fastq.gz	Fastqsanger.gz
	SRR25029386_1.fastq.gz	Fastqsanger.gz

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β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [RNA-seq LSK]

Project description:Replication stress is a main driver of functional decline of hematopoietic stem cells (HSCs), which carry the highest burden of maintaining genomic integrity and functionality within the hematopoietic system. Here, we identify a novel signaling axis in which β-catenin and Hoxa9 function in a compensatory manner to preserve HSC functionality by protecting DNA replication dynamics and genomic integrity, in part via regulation of Prmt1 activity. Co-inactivation of β-catenin and Hoxa9 induces severe hematopoietic defects accompanied by accumulating replication stress and DNA damage resulting in functional HSC decline. Furthermore, we illustrate how β-catenin and Hoxa9 pathways converge on the pivotal downstream target, Prmt1, which functions to maintain an adequate supply of DNA replication and repair factors. Prmt1 aids in alleviating replication stress and DNA damage accumulation thereby preserving HSC integrity and functionality.

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β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [ATAC-Seq]

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β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [CUT&RUN]

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β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [RNA-seq dKO_HSPCs]

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β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner

Project description:β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner

| PRJNA987671 | ENA

β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [ATAC-Seq]

Project description:β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [ATAC-Seq]

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β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [CUT&RUN]

Project description:β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [CUT&RUN]

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β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [RNA-seq dKO_HSPCs]

Project description:β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [RNA-seq dKO_HSPCs]

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Genes differentially expressed in MLL-AF9-transduced versus HOXA9/MEIS1-transduced LSK cells

Project description:HOXA9 and MEIS1 are essential downstream effectors of the MLL-AF9 oncoprotein during leukaemia induction. Leukaemia derived from MLL-AF9-transduced LSK cells has a more aggressive phenotype than that derived from HOXA9/MEIS1-transduced LSK cells. To determine differential gene expression that contributes to increased aggressiveness in MLL-AF9-induced leukaemia, microarray was performed on LSK cells transduced with MLL-AF9 versus HOXA/MEIS1 oncogenes.

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miRNAs differentially expressed in MLL-AF9-transduced versus HOXA9/MEIS1-transduced LSK cells

Project description:HOXA9 and MEIS1 are essential downstream effectors of the MLL-AF9 oncoprotein during leukemia induction. Leukemia derived from MLL-AF9-transduced LSK cells has a more aggressive phenotype than that derived from HOXA9/MEIS1-transduced LSK cells. To determine differential miRNA expression that contributes to increased aggressiveness in MLL-AF9-induced leukemia, miRCURY LNA microRNA Array was performed on LSK cells transduced with MLL-AF9 versus HOXA/MEIS1 oncogenes.

2019-07-03 | E-MTAB-7356 | biostudies-arrayexpress

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