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Promoter G-quadruplex folding precedes transcription and is controlled by chromatin

ABSTRACT: Promoter G-quadruplex folding precedes transcription and is controlled by chromatin

PROVIDER: PRJNA681342 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13161600.fastq.gz	Fastqsanger.gz
	SRR13161700.fastq.gz	Fastqsanger.gz
	SRR13161800.fastq.gz	Fastqsanger.gz
	SRR13161601.fastq.gz	Fastqsanger.gz
	SRR13161701.fastq.gz	Fastqsanger.gz

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Promoter G-quadruplex folding precedes transcription and is controlled by chromatin

Project description:Four stranded DNA G-quadruplex (G4) structures are common features of the human genome that are primarily found in active promoters associated with elevated transcription. Here, we explore the relationship between the folding of G4s in promoters, transcription and chromatin state. Transcriptional inhibition by DRB or by triptolide reveals that promoter G4 formation, as assessed G4 ChIP-seq, is not reliant on transcriptional activity. Establishing a link between G4 formation and chromatin accessibility, we demonstrate that chromatin compaction leads to loss of promoter G4s accompanied by a corresponding loss of RNA polymerase II (Pol II). Furthermore, pre-treatment of cells with a G4-stabilising ligand can mitigate Pol II loss at promoters induced by chromatin compaction. Overall, our findings show that G4 formation is fostered in accessible chromatin and does not require active transcription. Furthermore, our findings suggest that G4s have a role to recruit Pol II to promote transcription.

2021-03-31 | GSE162299 | GEO

Promoter G-quadruplex folding precedes transcription and is controlled by chromatin.

Project description:BackgroundFour-stranded G-quadruplexes (G4s) are DNA secondary structures in the human genome that are primarily found in active promoters associated with elevated transcription. Here, we explore the relationship between the folding of promoter G4s, transcription and chromatin state.ResultsTranscriptional inhibition by DRB or by triptolide reveals that promoter G4 formation, as assessed by G4 ChIP-seq, does not depend on transcriptional activity. We then show that chromatin compaction can lead to loss of promoter G4s and is accompanied by a corresponding loss of RNA polymerase II (Pol II), thus establishing a link between G4 formation and chromatin accessibility. Furthermore, pre-treatment of cells with a G4-stabilising ligand mitigates the loss of Pol II at promoters induced by chromatin compaction.ConclusionsOverall, our findings show that G4 folding is coupled to the establishment of accessible chromatin and does not require active transcription.

| S-EPMC8103603 | biostudies-literature

Stress promotes RNA G-quadruplex folding in human cells

Project description:Guanine (G)-rich nucleic acids can fold into G-quadruplex (G4) structures under permissive conditions. Although many RNAs contain sequences that fold into RNA G4s (rG4s) in vitro, their folding and functions in vivo are not well understood. Here, we showed that the folding of putative rG4s in human cells into rG4 structures was dynamically induced by stress. By using high-throughput dimethylsulfate probing, we identified hundreds of endogenous stress-induced rG4s. Our results demonstrated that stress-induced rG4s were enriched in mRNA 3′-untranslated regions and enhanced mRNA stability. Furthermore, stress-induced rG4 folding was readily reversible upon stress removal. In summary, our study revealed the dynamic regulation of rG4 folding in living human cells and suggests suggested that widespread rG4 motifs may have a global regulatory impact on mRNA stability and cellular stress response.

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Stress promotes RNA G-quadruplex folding in human cells

Project description:Stress promotes RNA G-quadruplex folding in human cells

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Epigenetic regulation by dynamic RNA G-quadruplex folding and unfolding (CHART-Seq)

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Epigenetic regulation by dynamic RNA G-quadruplex folding and unfolding (ChIP-Seq)

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G-Quadruplex structures are stable and detectable in human genomic DNA.

Project description:The G-quadruplex is an alternative DNA structural motif that is considered to be functionally important in the mammalian genome. Herein, we address the hypothesis that G-quadruplex structures can exist within double-stranded genomic DNA using a G-quadruplex-specific probe. An engineered antibody is employed to enrich for DNA containing G-quadruplex structures, followed by deep sequencing to detect and map G-quadruplexes at high resolution in genomic DNA from human breast adenocarcinoma cells. Our high sensitivity structure-based pull-down strategy enables the isolation of genomic DNA fragments bearing a single as well as multiple G-quadruplex structures. Stable G-quadruplex structures are found in sub-telomeres, gene bodies and gene regulatory regions. For a sample of identified target genes, we show that G-quadruplex stabilizing ligands can modulate transcription. These results confirm the existence of G-quadruplex structures and their persistence in human genomic DNA. Four independent libraries have been enriched in DNA G-quadruplex structures using a G-quadruplex-specific probe. One genomic input library was sequenced as control. Deep-sequencing of these libraries allowed the mapping of G-quadruplexes on the genome.

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DNA 5-methylcytosine regulates genome-wide formation of G-quadruplex structures [WGBS]

Project description:G-quadruplex structures (G4s) have been identified in genomes of multiple organisms and proven to play important epigenetic regulatory roles in various cellular functions. However, the G4 formation mechanism remains largely unknown. Here, we found a negative correlation between DNA 5mC methylation and G4 abundance. The abundance of genomic G4s significantly increased when the whole-genome methylation level was reduced in DNMT1-knockout cells. This increase was then suppressed by DNMT1 over-expression. And more G4s were detected in the hypomethylated cancer cell line HepG2 and rectal cancer tissues. Besides, 5mC modification significantly inhibited G4 formation of the potential G-quadruplex sequences (PQSs). The transcription of genes with 5mC modification sites in their promoter PQSs was affected after treatment with G4 stabilizer pyridostatin or methylation inhibitor 5-aza-dC. The global reduction of genomic methylation elevates gene transcription levels through increased G4s. Taken together, DNA 5mC methylation prevents PQSs from folding into G4s in genomes.

2024-06-20 | GSE270034 | GEO

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