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The lncRNA HERVH negatively regulates chromatin targeting and remodeling mediated by CHD7

ABSTRACT: The lncRNA HERVH negatively regulates chromatin targeting and remodeling mediated by CHD7

PROVIDER: PRJNA718532 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14108000_1.fastq.gz	Fastqsanger.gz
	SRR14108000_2.fastq.gz	Fastqsanger.gz
	SRR14108001_1.fastq.gz	Fastqsanger.gz
	SRR14108001_2.fastq.gz	Fastqsanger.gz
	SRR14108002_1.fastq.gz	Fastqsanger.gz

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The lncRNA HERVH negatively regulates chromatin targeting and remodeling mediated by CHD7 [RNA-seq]

Project description:Chromodomain helicase DNA-binding protein 7 (Chd7) encodes an ATP-dependent chromatin remodeler required for normal human development. De novo mutations in CHD7 are the major cause of CHARGE syndrome which features multiple developmental defects. Previous studies have shown that CHD7 targets to specific genomic loci and alters local transcription potentially by remodeling the chromatin structure in a cell stage and lineage specific manner. We examined whether nuclear RNAs might contribute to its targeting and function. We used PAR-CLIP to identify a lncRNA, HERVH, that is uniquely expressed in pluripotent stem cells and preferentially interacts with CHD7. Knockdown of HERVH using LNAs or knockout of an individual copy of HERVH by CRISPR-Cas9 both resulted in increased binding of CHD7 and increased levels of H3K27ac at a subset of enhancers. Depletion of HERVH led to the activation of multiple genes, several of which might potentially poise cells towards differentiation. CHD7 bound HERVH RNA with high affinity but low specificity and that this interaction decreased the ability of CHD7 to bind and remodel nucleosomes. We present a model in which HERVH acts as a decoy to modulate the dynamics of CHD7 binding to enhancers in pluripotent cells and to prevent the activation of differentiation specific genes.

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HERVH-derived lncRNAs negatively regulate chromatin targeting and remodeling mediated by CHD7.

Project description:Chd7 encodes an ATP-dependent chromatin remodeler which has been shown to target specific genomic loci and alter local transcription potentially by remodeling chromatin structure. De novo mutations in CHD7 are the major cause of CHARGE syndrome which features multiple developmental defects. We examined whether nuclear RNAs might contribute to its targeting and function and identified a preferential interaction between CHD7 and lncRNAs derived from HERVH loci in pluripotent stem cells. Knockdown of HERVH family lncRNAs using LNAs or knockout of an individual copy of HERVH by CRISPR-Cas9 both resulted in increased binding of CHD7 and increased levels of H3K27ac at a subset of enhancers. Depletion of HERVH family RNAs led to the activation of multiple genes. CHD7 bound HERVH RNA with high affinity but low specificity and this interaction decreased the ability of CHD7 to bind and remodel nucleosomes. We present a model in which HERVH lncRNAs act as a decoy to modulate the dynamics of CHD7 binding to enhancers in pluripotent cells and the activation of numerous genes that might impact the differentiation process.

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The lncRNA HERVH negatively regulates chromatin targeting and remodeling mediated by CHD7

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

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