Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA675384 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13009089_1.fastq.gz	Fastqsanger.gz
	SRR13009089_2.fastq.gz	Fastqsanger.gz
	SRR13009090_1.fastq.gz	Fastqsanger.gz
	SRR13009090_2.fastq.gz	Fastqsanger.gz
	SRR13009091_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

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

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

| PRJNA675381 | ENA

Genome-wide changes in chromatin accessibility in myoblasts lacking Hira [ATAC-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 | GSE161053 | GEO

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

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

| PRJNA675385 | ENA

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

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

| PRJNA675386 | ENA

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

2021-05-03 | GSE161054 | GEO

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

2021-05-03 | GSE161055 | GEO

Transcription profiling of hip1::ura4+ and slm9::ura4+ S. pombe to investigate the role of the HIRA histone chaperone complex

Project description:The assembly of nucleosomes by histone chaperones is an important component of transcriptional regulation. Here we have assessed the global roles of the S. pombe HIRA histone chaperone complex. Microarray analysis indicates that inactivation of the HIRA complex results in increased expression of at least 4% of fission yeast genes. HIRA-regulated genes overlap with those which are normally repressed in vegetatively growing cells, such as targets of the Clr6 histone deacetylase and silenced genes located in subtelomeric regions. HIRA is also required for silencing of all 13 intact copies of the Tf2 long terminal repeat (LTR) retrotransposon. However, the role of HIRA is not restricted to bona fide promoters, because it also suppresses non-coding transcripts from solo LTR elements and spurious antisense transcripts from cryptic promoters associated with transcribed regions. Furthermore, the HIRA complex is essential in the absence of the quality control provided by nuclear exosome-mediated degradation of illegitimate transcripts. This suggests that HIRA restricts genomic accessibility, and, consistent with this, the chromosomes of cells lacking HIRA are more susceptible to genotoxic agents that cause double strand breaks. Thus the HIRA histone chaperone is required to maintain the protective functions of chromatin.

2009-07-22 | E-MTAB-130 | biostudies-arrayexpress

HIRA protects telomeres against R-loop-induced instability in ALT cancer cells [ATAC-seq]

Project description:Alterations to chromatin modifiers, such as the inactivating mutations in the ATRX-DAXX chromatin remodeling/histone H3.3 deposition complex, are implicated as drivers of the cancer-specific Alternative Lengthening of Telomeres (ALT) pathway. Prior studies revealed that HIRA adapts to compensate for ATRX-DAXX loss to sustain ALT cancer cell survival. However, the specific mechanisms underlying HIRA’s ability to rescue telomeres from the consequences of ATRX-DAXX loss remain unclear. Here, using ATAC-seq and CUT&RUN, we demonstrate that HIRA-mediated deposition of new H3.3 is essential to maintain chromatin accessibility and to prevent the detrimental accumulation of nucleosome-free single-stranded DNA (ssDNA) at telomeres in ATRX-deficient ALT cancer cells. We provide evidence that the timely deposition of new H3.3 by HIRA and interacting partners UBN1 and UBN2 is crucial to prevent unwarranted TERRA R-loop formation and transcription-replication conflicts (TRCs) at telomeres. Furthermore, we determined that the delivery of H3.3 to telomeric chromatin by HIRA may link the phosphorylation of an H3.3-specific amino acid, serine 31, by Chk1 with mechanisms that promote productive ALT. Therefore, these studies identify a role for HIRA-mediated histone H3.3 deposition in TERRA R-loop homeostasis that we propose is essential for ensuring the survival of ALT cancer cells where the ATRX-DAXX complex is activated.

2024-10-21 | GSE269268 | 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

| PRJNA705487 | ENA