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G4-DNA Formation and Chromatin Remodelling are Interdependent in Human Cells

ABSTRACT: G4-DNA Formation and Chromatin Remodelling are Interdependent in Human Cells

PROVIDER: PRJNA988071 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25040753_1.fastq.gz	Fastqsanger.gz
	SRR25040753_2.fastq.gz	Fastqsanger.gz
	SRR25040754_1.fastq.gz	Fastqsanger.gz
	SRR25040754_2.fastq.gz	Fastqsanger.gz
	SRR25040755_1.fastq.gz	Fastqsanger.gz

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G4-DNA Formation and Chromatin Remodelling are Interdependent in Human Cells [RNA-seq]

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G4-DNA Formation and Chromatin Remodelling are Interdependent in Human Cells [RNA-seq]

Project description:DNA G-quadruplexes (G4s) have been identified as important biological targets for transcriptional, translational, and epigenetic regulation. The stabilisation of G4s with small molecule ligands has emerged as a technique to regulate gene expression and as a potential therapeutic approach for human diseases. Here, we demonstrate that ligand stabilisation of G4s causes altered chromatin accessibility dependant on the targeting specificity of the molecule. In particular, stabilisation of a target G4 using the highly specific GTC365 ligand resulted in differential accessibility of 61 genomic regions, while the broad targeted GQC-05 ligand stabilised many G4s and induced a global shift towards increased accessibility of gene promoter regions. Interestingly, while we observed distinct effects of each ligand on RNA expression levels and the induction of DNA double-stranded breaks, both ligands modified DNA damage response pathways. Our work represents the dual possibility of G4-stabilising ligands for specific or global chromatin modulation via unique targeting characteristics.

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G4-DNA Formation and Chromatin Remodelling are Interdependent in Human Cells [ATAC-seq]

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G4-DNA formation and chromatin remodelling are interdependent in human cells.

Project description:DNA G-quadruplexes (G4s) have been identified as important biological targets for transcriptional, translational, and epigenetic regulation. The stabilisation of G4s with small molecule ligands has emerged as a technique to regulate gene expression and as a potential therapeutic approach for human diseases. Here, we demonstrate that ligand stabilisation of G4s causes altered chromatin accessibility dependent on the targeting specificity of the molecule. In particular, stabilisation of a target G4 using the highly specific GTC365 ligand resulted in differential accessibility of 61 genomic regions, while the broad-targeting G4 ligand, GQC-05, stabilised many G4s and induced a global shift towards increased accessibility of gene promoter regions. Interestingly, while we observed distinct effects of each ligand on RNA expression levels and the induction of DNA double-stranded breaks, both ligands modified DNA damage response pathways. Our work represents the dual possibility of G4-stabilising ligands for specific or global chromatin modulation via unique targeting characteristics.

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G4-DNA Formation and Chromatin Remodelling are Interdependent in Human Cells

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

2023-06-28 | GSE235954 | GEO

TERRA regulates DNA G-quadruplex formation and ATRX loading on chromatin

Project description:The genome consists of non-B-DNA structures such as G-quadruplexes (G4) that are involved in the regulation of genome stability and transcription. Telomeric-repeat containing RNA (TERRA) is capable of folding into G-quadruplex and interacting with chromatin remodeler ATRX. Here we show that TERRA modulates ATRX occupancy on repetitive sequences and over genes, and maintains DNA G-quadruplex structures at TERRA target and non-target sites in mouse embryonic stem cells. TERRA prevents ATRX from binding to subtelomeric regions and represses H3K9me3 formation. G4 ChIP-seq reveals that G4 abundance decreases at accessible chromatin regions, particularly at transcription start sites (TSS) after TERRA depletion; such G4 reduction at TSS is associated with elevated ATRX occupancy and differentially expressed genes. Loss of ATRX alleviates the effect of gene repression caused by TERRA depletion. Immunostaining analyses demonstrate that knockdown of TERRA diminishes DNA G4 signals, whereas silencing ATRX elevates G4 formation. Our results uncover an epigenetic regulation by TERRA that sequesters ATRX and preserves DNA G4 structures.

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Zuo1 supports G4 structure formation and directs repair towards nucleotide excision repair

Project description:Nucleic acids can fold into G-quadruplex (G4) structures that can fine tune biological processes. Proteins are required to recognize G4 structures and coordinate their function. We identify Zuo1 as a novel G4-binding protein in a yeast one-hybrid screen. Biochemical and molecular experiments in yeast confirm that Zuo1 specifically binds to G4 structures in vitro and in vivo. In vivo in the absence of Zuo1 less G4 structures form, cell growth slows and cells become UV sensitive. Subsequent experiments reveal that these cellular changes are due to reduced levels of G4 structures. Interestingly, Zuo1 function and binding to G4 structures results in the recruitment of nucleotide excision repair (NER) factors, which has a positive effect on genome stability. Cells lacking functional NER as well as Zuo1 accumulate G4s structures, which become accessible for translesion synthesis. Our results suggest a model in which Zuo1 supports NER function and regulates the choice of the DNA repair pathway near G4 structures.

2020-06-23 | GSE149502 | GEO

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