ArticleMolecular and cellular biology2007
Postreplication repair inhibits CAG.CTG repeat expansions in Saccharomyces cerevisiae.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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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.
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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.
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Who cites it
40 citing papers in PubMed, 54 citations in OpenAlex.
- Overcoming natural replication barriers formed by DNA structures and the role of repositioning to the nuclear periphery.DNA repair · 2025Review
- Recurrent DNA nicks drive massive expansions of (GAA)Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Creation and resolution of non-B-DNA structural impediments during replication.Critical reviews in biochemistry and molecular biology · 2022Article
- Homologous recombination within repetitive DNA.Current opinion in genetics & development · 2021Review
- Restarted replication forks are error-prone and cause CAG repeat expansions and contractions.PLoS genetics · 2021Article
- On the wrong DNA track: Molecular mechanisms of repeat-mediated genome instability.The Journal of biological chemistry · 2020Review
- Large-scale contractions of Friedreich's ataxia GAA repeats in yeast occur during DNA replication due to their triplex-forming ability.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Defects in the GINS complex increase the instability of repetitive sequences via a recombination-dependent mechanism.PLoS genetics · 2019Article
- Cis- and Trans-Modifiers of Repeat Expansions: Blending Model Systems with Human Genetics.Trends in genetics : TIG · 2018Review
- Precarious maintenance of simple DNA repeats in eukaryotes.BioEssays : news and reviews in molecular, cellular and developmental biology · 2017Review
- Review
- Replication stalling and DNA microsatellite instability.Biophysical chemistry · 2017Review
- Differential requirement of Srs2 helicase and Rad51 displacement activities in replication of hairpin-forming CAG/CTG repeats.Nucleic acids research · 2017Article
- Small molecule inhibitors uncover synthetic genetic interactions of human flap endonuclease 1 (FEN1) with DNA damage response genes.PloS one · 2017Article
- Contracting CAG/CTG repeats using the CRISPR-Cas9 nickase.Nature communications · 2016Article
- Expansion of Interstitial Telomeric Sequences in Yeast.Cell reports · 2015Article
- Genetic Interactions Implicating Postreplicative Repair in Okazaki Fragment Processing.PLoS genetics · 2015Article
- Regulation of recombination at yeast nuclear pores controls repair and triplet repeat stability.Genes & development · 2015Article
- Increased meiotic crossovers and reduced genome stability in absence of Schizosaccharomyces pombe Rad16 (XPF).Genetics · 2014Article
- NuA4 initiates dynamic histone H4 acetylation to promote high-fidelity sister chromatid recombination at postreplication gaps.Molecular cell · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Trinucleotide repeats (TNRs) are unique DNA microsatellites that can expand to cause human disease. Recently, Srs2 was identified as a protein that inhibits TNR expansions in Saccharomyces cerevisiae. Here, we demonstrate that Srs2 inhibits CAG . CTG expansions in conjunction with the error-free branch of postreplication repair (PRR). Like srs2 mutants, expansions are elevated in rad18 and rad5 mutants, as well as the PRR-specific PCNA alleles pol30-K164R and pol30-K127/164R. Epistasis analysis indicates that Srs2 acts upstream of these PRR proteins. Also, like srs2 mutants, the pol30-K127/164R phenotype is specific for expansions, as this allele does not alter mutation rates at dinucleotide repeats, at nonrepeating sequences, or for CAG . CTG repeat contractions. Our results suggest that Srs2 action and PRR processing inhibit TNR expansions. We also investigated the relationship between PRR and Rad27 (Fen1), a well-established inhibitor of TNR expansions that acts at 5' flaps. Our results indicate that PRR protects against expansions arising from the 3' terminus, presumably replication slippage events. This work provides the first evidence that CAG . CTG expansions can occur by 3' slippage, and our results help define PRR as a key cellular mechanism that protects against expansions.
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Registered trials
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.