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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE161597 | GEO | 2021/01/04

REPOSITORIES: GEO

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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

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

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

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RNAPII-dependent ATM signaling at collisions with replication forks

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Unscheduled DNA replication in G1 causes genome instability and damage signatures indicative of replication collisions

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

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Chromatin conformation regulates the coordination between DNA replication and transcription

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

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Rif1 regulates initiation timing of late replication origins throughout the S. cerevisiae genome

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-01 | E-GEOD-55156 | biostudies-arrayexpress

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.

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Dicer in action at replication-transcription collisions.

Project description:Maintaining genome stability at sites of transcription and replication collision is a major challenge to cells. Recently, we have shown that in Schizosaccharomyces pombe Dicer promotes transcription termination at these sites, facilitating DNA replication and preventing replication fork restart that would otherwise occur via homologous recombination at the expense of genome stability. This novel role of Dicer could further explain its previously described role as a tumor suppressor.

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The cohesin acetyltransferase Eco1 coordinates rDNA replication and transcription

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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The nature of mutations induced by replication–transcription collisions.

Project description:The DNA replication and transcription machineries share a common DNA template and thus can collide with each other co-directionally or head-on. Replication–transcription collisions can cause replication fork arrest, premature transcription termination, DNA breaks, and recombination intermediates threatening genome integrity. Collisions may also trigger mutations, which are major contributors to genetic disease and evolution. However, the nature and mechanisms of collision-induced mutagenesis remain poorly understood. Here we reveal the genetic consequences of replication–transcription collisions in actively dividing bacteria to be two classes of mutations: duplications/deletions and base substitutions in promoters. Both signatures are highly deleterious but are distinct from the previously well-characterized base substitutions in the coding sequence. Duplications/deletions are probably caused by replication stalling events that are triggered by collisions; their distribution patterns are consistent with where the fork first encounters a transcription complex upon entering a transcription unit. Promoter substitutions result mostly from head-on collisions and frequently occur at a nucleotide that is conserved in promoters recognized by the major ? factor in bacteria. This substitution is generated via adenine deamination on the template strand in the promoter open complex, as a consequence of head-on replication perturbing transcription initiation. We conclude that replication–transcription collisions induce distinct mutation signatures by antagonizing replication and transcription, not only in coding sequences but also in gene regulatory elements.

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