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

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

PROVIDER: PRJNA678867 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11685469_1.fastq.gz	Fastqsanger.gz
	SRR11685469_2.fastq.gz	Fastqsanger.gz
	SRR11685470_1.fastq.gz	Fastqsanger.gz
	SRR11685470_2.fastq.gz	Fastqsanger.gz
	SRR11685471_1.fastq.gz	Fastqsanger.gz

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RTEL1 Regulates G4/R-Loops to Avert Replication-Transcription Collisions.

Project description:Regulator of telomere length 1 (RTEL1) is an essential helicase that maintains telomere integrity and facilitates DNA replication. The source of replication stress in Rtel1-deficient cells remains unclear. Here, we report that loss of RTEL1 confers extensive transcriptional changes independent of its roles at telomeres. The majority of affected genes in Rtel1-/- cells possess G-quadruplex (G4)-DNA-forming sequences in their promoters and are similarly altered at a transcriptional level in wild-type cells treated with the G4-DNA stabilizer TMPyP4 (5,10,15,20-Tetrakis-(N-methyl-4-pyridyl)porphine). Failure to resolve G4-DNAs formed in the displaced strand of RNA-DNA hybrids in Rtel1-/- cells is suggested by increased R-loops and elevated transcription-replication collisions (TRCs). Moreover, removal of R-loops by RNaseH1 overexpression suppresses TRCs and alleviates the global replication defects observed in Rtel1-/- and Rtel1PIP_box knockin cells and in wild-type cells treated with TMPyP4. We propose that RTEL1 unwinds G4-DNA/R-loops to avert TRCs, which is important to prevent global deregulation in both transcription and DNA replication.

| S-EPMC7773548 | biostudies-literature

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

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

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

2021-01-04 | GSE161597 | GEO

Yra1-bound R loops cause orientation-independent transcription-replication collisions and telomere instability

Project description:R loops are an important source of genome instability largely due to its negative impact on replication progression. Yra1/ALY is an abundant RNA-binding factor conserved from yeast to humans and required for mRNA export, but its excess cause lethality and genome instability. Here, we show that Yra1 binds RNA-DNA hybrids in vitro and when artificially overexpressed is recruited to chromatin in an RNA-DNA hybrid-dependent manner stabilizing R loops and converting them into replication obstacles in vivo. Importantly, excess of Yra1 increases R loop-mediated genome instability caused by transcription-replication collisions regardless of whether they are co-directional or head-on. It also induces telomere shortening and senescence, consistent with a defect in telomere replication. Our results indicate that R loops form transiently in cells regardless of replication and, after stabilization by excess Yra1, they compromise genome integrity, in agreement with a two-step model of R loop-mediated genome instability. This work opens new perspectives to understand transcription-associated genome instability in repair-deficient cells, including tumoral cells.

2018-06-27 | GSE113580 | GEO

G4-dependent DNA loops regulate gene expression [RNA-seq]

Project description:RNAPII is mainly responsible for mRNA transcription and plays a vital role in gene expression. In light of the above results showing that cellular G4s are highly correlated with RNAPII-mediated DNA loops, we performed the RNA-seq to evaluate how G4-dependent long-range DNA interactions modulate gene expression. We revealed that PDS treatment modulates the expression of not only genes with G4 in their promoters, but also those with promoters being connected with distal G4 through RNAPII-linked long-range DNA interactions.

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RAD52 resolves replication-transcription collisions to mitigate R-loop induced genome instability

Project description:Collisions of transcription and replication machinery on the same DNA strand can pose a significant threat to genomic stability. These collision occur in part due to of RNA-DNA hybrids termed R-loops, in which a newly synthesized RNA molecule hybridizes with the DNA template strand. This study investigated the novel role of RAD52, a known DNA repair factor, in preventing collisions by managing R-loop formation and resolution. We show that RAD52 deficiency increases R-loop accumulation, exacerbating collisions and resulting in elevated DNA damage. Further, RAD52's ability to interact with the transcription machinery, coupled with its capacity to facilitate R-loop dissolution, highlights its role in preventing collisions. Lastly, we provide the first evidence of an increased mutational burden at conserved R-loop sites in human tumor samples. In summary, this study underscores the importance of RAD52 in orchestrating the delicate balance between replication and transcription processes to prevent collisions and maintain genome stability.

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2016-09-01 | E-MTAB-2943 | biostudies-arrayexpress