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Genome-wide characterisation of replication and transcription changed induced by G4-stabilisation with PhenDC3

ABSTRACT: Genome-wide characterisation of replication and transcription changed induced by G4-stabilisation with PhenDC3

PROVIDER: PRJNA522010 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8568930.fastq.gz	Fastqsanger.gz
	SRR8568940.fastq.gz	Fastqsanger.gz
	SRR8568931.fastq.gz	Fastqsanger.gz
	SRR8568941.fastq.gz	Fastqsanger.gz
	SRR8568932.fastq.gz	Fastqsanger.gz

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Genome-wide characterisation of replication and transcription changed induced by G4-stabilisation with PhenDC3

Project description:Genome-wide characterisation of replication and transcription programs upon G4-stabilisation by PhenDC3

2019-06-01 | GSE126477 | GEO

Comparative genome-wide transcriptional profile after RTEL1 depletion and G4 stabilisation.

Project description:The goal of this study is to compare the transcription profile of mouse embryonic fibroblasts upon deletion of the helicase RTEL1 and stabilisation of G-quadruplexes (G4) with the G4 stabilisation drug TMPyP4.

2021-01-04 | GSE149850 | GEO

Comparative genome-wide transcriptional profile after RTEL1 depletion and G4 stabilisation.

Project description:Comparative genome-wide transcriptional profile after RTEL1 depletion and G4 stabilisation.

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DNA2 and MSH2 activities collectively mediate environmental chemical compound stabilized G4 for efficient telomere replication

Project description:G-quadruplexes (G4s) are widely existing stable DNA secondary structures in mammalian cells. A long-standing hypothesis is that timely resolution of G4s is needed for efficient and faithful DNA replication. In vitro, G4s may be unwound by helicases or alternatively resolved via DNA2 nuclease-mediated G4 cleavage. However, little is known about the biological significance and regulatory mechanism of the DNA2-mediated G4 removal pathway. Here, we report that DNA2 deficiency or its chemical inhibition leads to a significant accumulation of G4s and stalled replication forks at telomeres, which is demonstrated by a high-resolution technology: Single Molecular Analysis of Replicating DNA (SMARD). We further identify that the DNA repair complex MutSα (MSH2-MSH6) binds G4s and stimulates G4 resolution via DNA2-mediated G4 excision. MSH2 deficiency, similar to DNA2 deficiency or inhibition, causes G4 accumulation and defective telomere replication. Meanwhile, G4-stabilizing environmental compounds block G4 unwinding by helicases but not G4 cleavage by DNA2. Consequently, G4 stabilizers impair telomere replication and cause telomere fragility, especially in cells deficient in DNA2 or MSH2.

2025-08-07 | PXD059843 | Pride

Timeless collaborates with DDX11 to ensure processive replication of G4-forming DNA [RNA-seq]

Project description:Regions of DNA with the potential to form secondary structure pose a frequent and significant impediment to DNA replication that must be actively countered by cells in order to preserve genetic and epigenetic integrity. The fork protection complex (FPC), a conserved group of replisome-associated proteins, comprising Timeless, plays an important role in maintaining efficient replisome function. A previously unappreciated DNA binding domain in the C terminus of Timeless, which exhibits specificity towards G4 structures, acts in collaboration with the DDX11 helicase to ensure replication of G4 structures in vivo and maintenance of genetic and epigenetic stability. Using RNA-seq experiments, we show that (i) Timeless and DDX11 share common gene targets, (ii) the promoter of Timeless- and DDX11-dependent genes are enriched in G4 structures in the vicinity of their promoter and (iii) both Timeless and DDX11 share a common set of gene targets with the FANCJ helicase known to maintain epigenetic stability in the vicinity of G4 structures.

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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.

2023-06-28 | GSE235953 | GEO

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

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HLTF Prevents G4 Accumulation and Promotes G4-induced Fork Slowing to Maintain Genome Stability

Project description:G-quadruplexes (G4s) form throughout the genome and influence important cellular processes, but their deregulation can challenge DNA replication fork progression and threaten genome stability. Here, we demonstrate an unexpected, dual role for the dsDNA translocase HLTF in G4 metabolism. First, we find that HLTF is enriched at G4s in the human genome and suppresses G4 accumulation throughout the cell cycle using its ATPase activity. This function of HLTF affects telomere maintenance by restricting alternative lengthening of telomeres, a process stimulated by G4s. We also show that HLTF and MSH2, a mismatch repair factor that binds G4s, act in independent pathways to suppress G4s and to promote resistance to G4 stabilization. In a second, distinct role, HLTF restrains DNA synthesis upon G4 stabilization by suppressing PrimPol-dependent repriming. Together, the dual functions of HLTF in the G4 response prevent DNA damage and potentially mutagenic replication to safeguard genome stability.

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RTEL1 regulates G4/R-loops to avert replication-transcription collisions

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Geobacillus sp. G4 strain:G4

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