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Integrated HPV18 acts as enhancer-like RNA and form phase-separated condensates to promote oncogenic genes expression.

ABSTRACT: Integrated HPV18 acts as enhancer-like RNA and form phase-separated condensates to promote oncogenic genes expression.

PROVIDER: PRJNA1051147 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27180601_1.fastq.gz	Fastqsanger.gz
	SRR27180601_2.fastq.gz	Fastqsanger.gz
	SRR27180602_1.fastq.gz	Fastqsanger.gz
	SRR27180602_2.fastq.gz	Fastqsanger.gz
	SRR27180603_1.fastq.gz	Fastqsanger.gz

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Integrated HPV18 acts as enhancer-like RNA and form phase-separated condensates to promote oncogenic genes expression.

Project description:Most of the cervical cancers are caused by human papillomavirus (HPV) infection. It has been known that, in HeLa cells, HPV18 viral genome is integrated at chromosome 8q24.21 and activates transcription of proto-oncogene c-Myc. However, the mechanism of how the integrated HPV fragment exhibits transcription activation function has not been fully elucidated. In this study, we found that HPV18 transcripts themselves have an enhancer RNA-like function to activate their proximal genes including CCAT1-5L and c-Myc. We showed that the human genome-integrated HPV18 genes are activated by transcription coregulators BRD4, Mediator. The transcribed HPV18 RNAs form a liquid-like condensate at chromosome 8q24.21 locus, which in turn accumulates RNA polymerase II. Moreover, we identified uncharacterized transcript from Upstream Region of CCAT1-5L, named URC. The URC RNA is transcribed as a chimera RNA with HPV18 and is composed of 3'-untranslated region of HPV18 transcript. We found that the URC contributes to stabilization of HPV18 RNAs by supplying a poly-adenylation site for HPV18 transcript. Our findings suggest that HPV18 integration at 8q24.21 locus causes HPV18-URC chimera RNA and promotes tumorigenesis through RNA-based liquid droplet formation.

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lncRNA DIGIT and BRD3 protein form phase-separated condensates to regulate endoderm differentiation [RIP-seq]

Project description:lncRNA DIGIT and BRD3 protein form phase-separated condensates to regulate endoderm differentiation

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lncRNA DIGIT and BRD3 protein form phase-separated condensates to regulate endoderm differentiation

Project description:lncRNA DIGIT and BRD3 protein form phase-separated condensates to regulate endoderm differentiation

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lncRNA DIGIT and BRD3 protein form phase-separated condensates to regulate endoderm differentiation

Project description:Gene programs that control differentiation are regulated through the interplay between DNA, RNA, and protein. Cooperation among these fundamental cellular components can occur through highly structured interactions connecting domains formed by specific sequences of nucleotides, ribonucleotides, and/or amino acids and also through the assembly of biomolecular condensates. Here, we show that endoderm differentiation is regulated through the interaction of the long noncoding (lnc) RNA DIGITand the bromodomain and extra-terminal (BET) domain family protein BRD3. BRD3 forms phase-separated condensates that contain DIGIT, occupies enhancers of endoderm transcription factors, and is required for endoderm differentiation. Purified BRD3 binds to acetylated histone H3 lysine 18 (H3K18ac) in vitro and occupies regions of the genome enriched in H3K18ac during endoderm differentiation, including the key transcription factors that regulate endoderm differentiation. DIGIT is also enriched in regions of H3K18ac, and depletion of DIGIT results in decreased recruitment of BRD3 to these regions. Our findings support a model where cooperation between DIGIT and BRD3 at regions of H3K18ac regulates the transcription factors that drive endoderm differentiation and suggest a broader role for protein-lncRNA phase-separated condensates as regulators of transcription in development.

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lncRNA DIGIT and BRD3 protein form phase-separated condensates to regulate endoderm differentiation [RIP-seq]

Project description:lncRNA DIGIT and BRD3 protein form phase-separated condensates to regulate endoderm differentiation [RIP-seq]

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Phase-separated NDF−FACT condensates facilitate transcription elongation on chromatin [PRO-Seq]

Project description:How the facilitates chromatin transcription (FACT) complex enables RNA polymerase II to overcome chromatin barriers in cells remains poorly understood—especially given the limited direct interactions of FACT with polymerases, DNA or nucleosomes. Here we demonstrate that phase separation, mediated by nucleosome destabilizing factor (NDF), is a key mechanism enabling the function of FACT during transcription elongation. Through biochemical and single-molecule assays, we found that NDF−FACT condensates create specialized biochemical environments that enhance transcription efficiency approximately 20-fold compared with FACT alone. These dynamic condensates form on transcribing RNA polymerase II and travel along chromatin, where they promote efficient nucleosome disassembly at barriers while retaining histones on DNA to preserve chromatin integrity. In human stem cells, disruption of these condensates leads to genome-wide transcriptional defects and chromatin instability, mirroring the effects of FACT depletion. By showing that phase separation enhances FACT function during transcription elongation, our study reveals a key mechanism that preserves chromatin integrity and transcriptional homeostasis in human stem cells.

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Phase-separated NDF−FACT condensates facilitate transcription elongation on chromatin [TT-Seq]

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