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ATAC-seq, ChIP-seq and RNA-seq studies in myoblasts lacking Hira

ABSTRACT: ATAC-seq, ChIP-seq and RNA-seq studies in myoblasts lacking Hira

PROVIDER: PRJNA675381 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13009100_1.fastq.gz	Fastqsanger.gz
	SRR13009100_2.fastq.gz	Fastqsanger.gz
	SRR13009101_1.fastq.gz	Fastqsanger.gz
	SRR13009101_2.fastq.gz	Fastqsanger.gz
	SRR13009102_1.fastq.gz	Fastqsanger.gz

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Genome-wide chromatin state in myoblasts lacking Hira [ChIP-seq]

Project description:Genome-wide chromatin state in myoblasts lacking Hira [ChIP-seq]

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Analysis of the transcriptomic changes of myoblasts lacking Hira [RNA-seq]

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Genome-wide changes in chromatin accessibility in myoblasts lacking Hira [ATAC-seq]

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Genome-wide chromatin state in myoblasts lacking Hira [ChIP-seq]

Project description:The epigenetic mechanisms coordinating the maintenance of adult cellular lineages and the inhibition of alternative cell fates are poorly understood. Here we show that targeted ablation of the histone chaperone HIRA in myogenic cells leads to extensive transcriptional modifications consistent with a major role in maintaining skeletal muscle cellular identity. Conditional ablation of HIRA in muscle stem cells of adult mice compromised their capacity to regenerate and self-renew, leading to tissue repair failure. Epigenetic analysis of Hira-deficient cells showed a drastic reduction of histone variant H3.3 deposition and H3K27ac modification at regulatory regions of muscle genes. By contrast, genes from alternative lineages were ectopically expressed in Hira-mutant cells via MLL1/MLL2-mediated increase of H3K4me3 mark at silent promoter regions. Therefore, HIRA sustains the epigenetic landscape governing muscle cell lineage identity via incorporation of H3.3 at muscle gene regulatory regions, while preventing the expression of alternative lineage genes.

2021-05-03 | GSE161054 | GEO

Analysis of the transcriptomic changes of myoblasts lacking Hira [RNA-seq]

2021-05-03 | GSE161055 | GEO

Genome-wide changes in chromatin accessibility in myoblasts lacking Hira [ATAC-seq]

2021-05-03 | GSE161053 | GEO

ATAC-seq, ChIP-seq and RNA-seq studies in myoblasts lacking Hira

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

2021-05-03 | GSE161056 | GEO

Analysis of the transcriptomic changes of activated satellite cells lacking Hira

2021-05-03 | GSE167911 | GEO

Analysis of the transcriptomic changes of activated satellite cells lacking Hira

Project description:Analysis of the transcriptomic changes of activated satellite cells lacking Hira

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Expression data from Control and HIRA knockdown cells

Project description:The HIRA chaperone complex, comprised of HIRA, UBN1 and CABIN1, collaborates with histone-binding protein ASF1a to incorporate histone variant H3.3 into chromatin in a DNA replication-independent manner. To better understand its function and mechanism, we integrated HIRA, UBN1, ASF1a and histone H3.3 ChIP-seq and gene expression analyses. Most HIRA-binding sites co-localize with UBN1, ASF1a and H3.3 at active promoters and active and weak/poised enhancers. At promoters, binding of HIRA/UBN1/ASF1a correlates with the level of gene expression. HIRA is required for deposition of histone H3.3 at its binding sites. There are marked differences in nucleosome and co-regulator composition at different classes of HIRA-bound regulatory site. Underscoring this, we report novel physical interactions between the HIRA complex and transcription factors, a chromatin insulator and an ATP-dependent chromatin-remodelling complex. Our results map the distribution of the HIRA chaperone across the chromatin landscape and point to different interacting partners at functionally distinct regulatory sites. We used microarrays to detail the global programme of gene expression after knockdown of HIRA HeLa cells were nucleofacted with Dharmacon control siRNA and siRNA to HIRA and RNA was isolated 72 hours after transfection in four biological replicates

2013-04-18 | E-GEOD-45022 | biostudies-arrayexpress

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