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HIRA-mediated loading of histone variant H3.3 controls androgen-induced transcription by regulation of AR/BRD4 complex assembly at enhancers [Dex RNA-seq]

ABSTRACT: HIRA-mediated loading of histone variant H3.3 controls androgen-induced transcription by regulation of AR/BRD4 complex assembly at enhancers [Dex RNA-seq]

PROVIDER: PRJNA996638 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25345132_1.fastq.gz	Fastqsanger.gz
	SRR25345132_2.fastq.gz	Fastqsanger.gz
	SRR25345133_1.fastq.gz	Fastqsanger.gz
	SRR25345133_2.fastq.gz	Fastqsanger.gz
	SRR25345134_1.fastq.gz	Fastqsanger.gz

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HIRA-mediated loading of histone variant H3.3 controls androgen-induced transcription by regulation of AR/BRD4 complex assembly at enhancers [ChIP-Seq]

Project description:To study the function of histone variant H3.3 pathway in androgen receptor-driven transcription in prostate cancer (PCa) we knocked out androgen receptor (AR) and H3.3 chaperones HIRA and DAXX in R1-AD1 (wild type AR) and R1-D567 (deltaLBD AR) cell lines. Integrative analysis with RNA-seq, ChIP-seq and ATAC-seq revealed that HIRA KO deregulates androgen-induced gene expression in PCa by reducing H3.3 incorporation, diminishing H3.3S31Ph and H3K27Ac, thus modifying recruitment of BRD4 and altering AR binding within enhancers of target genes.

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HIRA-mediated loading of histone variant H3.3 controls androgen-induced transcription by regulation of AR/BRD4 complex assembly at enhancers [RNA-Seq]

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HIRA-mediated loading of histone variant H3.3 controls androgen-induced transcription by regulation of AR/BRD4 complex assembly at enhancers [ATAC-Seq]

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HIRA-mediated loading of histone variant H3.3 controls androgen-induced transcription by regulation of AR/BRD4 complex assembly at enhancers [Dex RNA-seq]

Project description:To study the function of histone variant H3.3 pathway in prostate cancer (PCa) we knocked out androgen receptor (AR) and H3.3 chaperones HIRA and DAXX in R1-AD1 FLAG-HA-H3F3A cell line. We analyzed the effect of Dexamethasone treatment on the transcriptome in these four cell lines.

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HIRA-mediated loading of histone variant H3.3 controls androgen-induced transcription by regulation of AR/BRD4 complex assembly at enhancers

Project description:HIRA-mediated loading of histone variant H3.3 controls androgen-induced transcription by regulation of AR/BRD4 complex assembly at enhancers

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RPA interacts with HIRA and regulates H3.3 deposition at gene regulatory elements in mammalian cells

Project description:The incorporation of histone variant H3.3 has been implicated in the formation and maintenance of specialized chromatin structure in metazoan cells. H3.3 is enriched in promoters, regulatory elements and genebody, and HIRA is required for H3.3 enrichment in these regions. But the mechanism of regulating H3.3 deposition by HIRA remains elusive. By screening a custom library of small hairpin RNAs (shRNAs) targeting known chromatin regulators, we identify single-stranded DNA binding protein RPA as being critically required for deposition of newly synthesized H3.3. RPA interacts with HIRA and H3.3 and co-localizes with HIRA at gene promoters and some regulatory elements across genome wide. Deletion of RPA dramatically reduces the enrichment of HIRA and newly synthesized H3.3 at these regions and reduced nascent anti-sense transcription. Taken together, our data demonstrate that RPA functions as new regulator of H3.3 deposition in promoter and some regulatory elements by recruiting HIRA and reveal a novel mechanism for RPA in chromatin and gene regulation.

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The role of histone variant H3.3 regulation by HIRA in hematopoiesis (ChIP-Seq)

Project description:Histone variants contribute to the complexity of the chromatin landscape and play an integral role in defining DNA domains and regulating gene expression. The histone H3 variant H3.3 is incorporated into genic elements independent of DNA replication by its chaperone HIRA. Here we demonstrate that Hira is required for the self-renewal of adult hematopoietic stem cells (HSCs) and to restrain erythroid differentiation. Deletion of Hira led to rapid depletion of HSCs while differentiated hematopoietic cells remained largely unaffected. Depletion of HSCs after Hira deletion was accompanied by increased expression of bivalent and erythroid genes, which were exacerbated upon cell division and paralleled increased erythroid differentiation. Assessing H3.3 occupancy identified a subset of polycomb-repressed chromatin in HSCs that depend on HIRA to maintain the inaccessible, H3.3-occupied state for gene repression. HIRA-dependent H3.3 incorporation thus defines distinct repressive chromatin that represses erythroid differentiation of HSCs.

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HIRA-mediated loading of histone variant H3.3 controls androgen-induced transcription by regulation of AR/BRD4 complex assembly at enhancers [ChIP-Seq]

Project description:HIRA-mediated loading of histone variant H3.3 controls androgen-induced transcription by regulation of AR/BRD4 complex assembly at enhancers [ChIP-Seq]

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