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Rtf2 is Important for Replication Fork Barrier Activity of RTS1 via Splicing of Rtf1

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

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE192344 | GEO | 2021/12/24

REPOSITORIES: GEO

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Schizosaccharomyces pombe Rtf2 is important for replication fork barrier activity of RTS1 via splicing of Rtf1.

Project description:Arrested replication forks, when restarted by homologous recombination, result in error-prone DNA syntheses and non-allelic homologous recombination. Fission yeast RTS1 is a model fork barrier used to probe mechanisms of recombination-dependent restart. RTS1 barrier activity is entirely dependent on the DNA binding protein Rtf1 and partially dependent on a second protein, Rtf2. Human RTF2 was recently implicated in fork restart, leading us to examine fission yeast Rtf2's role in more detail. In agreement with previous studies, we observe reduced barrier activity upon rtf2 deletion. However, we identified Rtf2 to be physically associated with mRNA processing and splicing factors and rtf2 deletion to cause increased intron retention. One of the most affected introns resided in the rtf1 transcript. Using an intronless rtf1, we observed no reduction in RFB activity in the absence of Rtf2. Thus, Rtf2 is essential for correct rtf1 splicing to allow optimal RTS1 barrier activity.

| S-EPMC10473836 | biostudies-literature

Rtf2 is Important for Replication Fork Barrier Activity of RTS1 via Splicing of Rtf1 [cDNA-Seq]

Project description:This study investigated the role Rtf2 plays on the replication fork barrier (RFB) activity of RTS1 in S. pombe. We confirm Rtf2 is important for the full barrier activity of the RTS1-Rtf1 RFB. We show that Rtf2 does not enact its enhancing effect on RTS1 RFB activity via binding to Region A of RTS1, but instead we find it to be closely associated with several splicing factors. Analysis of cells deleted for rtf2 by cDNA-Seq reveal splicing defects specifically effecting intron retention, including for the Rtf1 transcript. We show that intron retention within rtf1 is responsible for the reduced barrier activity of RTS1 when rtf2 is deleted. This study reveals Rtf2 to be an important factor for maintaining efficient splicing within the cell.

2021-12-24 | GSE192343 | GEO

Rtf2 is Important for Replication Fork Barrier Activity of RTS1 via Splicing of Rtf1 [Pu-Seq]

2021-12-24 | GSE192342 | GEO

Rtf2 is Important for Replication Fork Barrier Activity of RTS1 via Splicing of Rtf1

Project description:Rtf2 is Important for Replication Fork Barrier Activity of RTS1 via Splicing of Rtf1

| PRJNA791210 | ENA

Rtf2 is Important for Replication Fork Barrier Activity of RTS1 via Splicing of Rtf1 [cDNA-Seq]

Project description:Rtf2 is Important for Replication Fork Barrier Activity of RTS1 via Splicing of Rtf1 [cDNA-Seq]

| PRJNA791218 | ENA

Rtf2 is Important for Replication Fork Barrier Activity of RTS1 via Splicing of Rtf1 [Pu-Seq]

Project description:Rtf2 is Important for Replication Fork Barrier Activity of RTS1 via Splicing of Rtf1 [Pu-Seq]

| PRJNA791219 | ENA

Rtf1-mediated eukaryotic site-specific replication termination.

Project description:The molecular mechanisms mediating eukaryotic replication termination and pausing remain largely unknown. Here we present the molecular characterization of Rtf1 that mediates site-specific replication termination at the polar Schizosaccharomyces pombe barrier RTS1. We show that Rtf1 possesses two chimeric myb/SANT domains: one is able to interact with the repeated motifs encoded by the RTS1 element as well as the elements enhancer region, while the other shows only a weak DNA binding activity. In addition we show that the C-terminal tail of Rtf1 mediates self-interaction, and deletion of this tail has a dominant phenotype. Finally, we identify a point mutation in Rtf1 domain I that converts the RTS1 element into a replication barrier of the opposite polarity. Together our data establish that multiple protein DNA and protein-protein interactions between Rtf1 molecules and both the repeated motifs and the enhancer region of RTS1 are required for site-specific termination at the RTS1 element.

| S-EPMC2535681 | biostudies-literature

Mechanism for inverted-repeat recombination induced by a replication fork barrier.

Project description:Replication stress and abundant repetitive sequences have emerged as primary conditions underlying genomic instability in eukaryotes. To gain insight into the mechanism of recombination between repeated sequences in the context of replication stress, we used a prokaryotic Tus/Ter barrier designed to induce transient replication fork stalling near inverted repeats in the budding yeast genome. Our study reveals that the replication fork block stimulates a unique recombination pathway dependent on Rad51 strand invasion and Rad52-Rad59 strand annealing activities, Mph1/Rad5 fork remodelers, Mre11/Exo1/Dna2 resection machineries, Rad1-Rad10 nuclease and DNA polymerase δ. Furthermore, we show recombination at stalled replication forks is limited by the Srs2 helicase and Mus81-Mms4/Yen1 nucleases. Physical analysis of the replication-associated recombinants revealed that half are associated with an inversion of sequence between the repeats. Based on our extensive genetic characterization, we propose a model for recombination of closely linked repeats that can robustly generate chromosome rearrangements.

| S-EPMC8748988 | biostudies-literature

Gene duplication and deletion caused by over-replication at a fork barrier.

Project description:Replication fork stalling can provoke fork reversal to form a four-way DNA junction. This remodelling of the replication fork can facilitate repair, aid bypass of DNA lesions, and enable replication restart, but may also pose a risk of over-replication during fork convergence. We show that replication fork stalling at a site-specific barrier in fission yeast can induce gene duplication-deletion rearrangements that are independent of replication restart-associated template switching and Rad51-dependent multi-invasion. Instead, they resemble targeted gene replacements (TGRs), requiring the DNA annealing activity of Rad52, the 3'-flap nuclease Rad16-Swi10, and mismatch repair protein Msh2. We propose that excess DNA, generated during the merging of a canonical fork with a reversed fork, can be liberated by a nuclease and integrated at an ectopic site via a TGR-like mechanism. This highlights how over-replication at replication termination sites can threaten genome stability in eukaryotes.

| S-EPMC10676400 | biostudies-literature

Direct observation of stalled fork restart via fork regression in the T4 replication system.

Project description:The restart of a stalled replication fork is a major challenge for DNA replication. Depending on the nature of the damage, different repair processes might be triggered; one is template switching, which is a bypass of a leading-strand lesion via fork regression. Using magnetic tweezers to study the T4 bacteriophage enzymes, we have reproduced in vitro the complete process of template switching. We show that the UvsW DNA helicase in cooperation with the T4 holoenzyme can overcome leading-strand lesion damage by a pseudostochastic process, periodically forming and migrating a four-way Holliday junction. The initiation of the repair process requires partial replisome disassembly via the departure of the replicative helicase. The results support the role of fork regression pathways in DNA repair.

| S-EPMC3858903 | biostudies-literature

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