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Gene expression and chromatin accessibility of iLSCs vs iBlasts cells

ABSTRACT: Gene expression and chromatin accessibility of iLSCs vs iBlasts cells

PROVIDER: PRJNA514717 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8435080.fastq.gz	Fastqsanger.gz
	SRR8435090.fastq.gz	Fastqsanger.gz
	SRR8435100.fastq.gz	Fastqsanger.gz
	SRR8435081.fastq.gz	Fastqsanger.gz
	SRR8435091.fastq.gz	Fastqsanger.gz

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Gene expression and chromatin accessibility of iLSCs vs iBlasts cells

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Project description:Analysis of nucleosome positioning and chromatin state by using CpG methyltransferase M.SssI to methylate nuclei. Unmethylated regions that gain methylation (low to high beta value) are known to be accessible and nucleosome depleted. Method used to study changes after epigenetic drug treatments identified that majority of demethylation events are not accompanied by chromatin accessibility changes. RNA harvested from cells post epigenetic drug treatment, with 5-Aza-CdR or SAHA

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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. We found that the chromatin accessibility regulator HMGN1, a target of recurrent DNA copy gains in leukemia, controls myeloid differentiation. HMGN1 amplification was associated with increased accessibility, expression, and histone H3K27 acetylation of loci important for hematopoietic stem cell (HSC) function and AML, such as HoxA cluster genes. In vivo, HMGN1 overexpression was linked to decreased quiescence and increased HSC activity in bone marrow transplantation. HMGN1 overexpression also cooperated with the AML-ETO9a fusion oncoprotein to impair myeloid differentiation and enhance leukemia stem cell (LSC) activity. Inhibition of histone acetyltransferases CBP/p300 relieved 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.

2020-02-25 | PXD017054 | Pride

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