Evidence map›Paper›PMID 25940904›Full record

ArticleGenes & development2015

Regulation of recombination at yeast nuclear pores controls repair and triplet repeat stability.

Xiaofeng A Su, Vincent Dion, Susan M Gasser, Catherine H Freudenreich

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

83 citing papers in PubMed, 131 citations in OpenAlex.

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  11. Nucleoporins cooperate with Polycomb silencers to promote transcriptional repression and repair at DNA double-strand breaks.Proceedings of the National Academy of Sciences of the United States of America · 2025
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23 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Xiaofeng A SuDepartment of Biology, Tufts University, Medford, Massachusetts 02155, USA;
Vincent DionFriedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland;
Susan M GasserFriedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland; Faculty of Natural Sciences, University of Basel, CH-4056 Basel, Switzerland.
Catherine H FreudenreichDepartment of Biology, Tufts University, Medford, Massachusetts 02155, USA; Program in Genetics, Tufts University, Medford, Massachusetts 02155, USA; catherine.freudenreich@tufts.edu.
Friedrich Miescher Institute · CHTufts University · US

Funding

Mutations Arising During DNA RepairP01GM105473 · NIGMS · BRANDEIS UNIVERSITY · PI LOVETT, SUSAN THOMAS · 2014 to 2018
$8.6M
NIGMS NIH HHS P01 GM105473NIGMS NIH HHS P01GM105473
6 · The paper itself

Abstract

Secondary structure-forming DNA sequences such as CAG repeats interfere with replication and repair, provoking fork stalling, chromosome fragility, and recombination. In budding yeast, we found that expanded CAG repeats are more likely than unexpanded repeats to localize to the nuclear periphery. This positioning is transient, occurs in late S phase, requires replication, and is associated with decreased subnuclear mobility of the locus. In contrast to persistent double-stranded breaks, expanded CAG repeats at the nuclear envelope associate with pores but not with the inner nuclear membrane protein Mps3. Relocation requires Nup84 and the Slx5/8 SUMO-dependent ubiquitin ligase but not Rad51, Mec1, or Tel1. Importantly, the presence of the Nup84 pore subcomplex and Slx5/8 suppresses CAG repeat fragility and instability. Repeat instability in nup84, slx5, or slx8 mutant cells arises through aberrant homologous recombination and is distinct from instability arising from the loss of ligase 4-dependent end-joining. Genetic and physical analysis of Rad52 sumoylation and binding at the CAG tract suggests that Slx5/8 targets sumoylated Rad52 for degradation at the pore to facilitate recovery from acute replication stress by promoting replication fork restart. We thereby confirmed that the relocation of damage to nuclear pores plays an important role in a naturally occurring repair process.

Indexed as

Recombination, GeneticDNA RepairNuclear PoreProtein TransportSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsS PhaseSumoylationTrinucleotide RepeatsSaccharomyces cerevisiae ProteinsCAG repeatschromosome fragilitynuclear organizationnuclear porerepeat expansionSlx5/Slx8

Identifiers

PMID25940904
PMCPMC4441049
OpenAlexW2128926534

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.