ArticleGenetics2015
MSH3 Promotes Dynamic Behavior of Trinucleotide Repeat Tracts In Vivo.
Article in Genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed.
- Mismatch repair MLH complexes make distinct contributions to post-replicative mismatch repair versus trinucleotide repeat expansions.bioRxiv : the preprint server for biology · 2026Article
- Msh2-Msh3 DNA-binding is not sufficient to promote trinucleotide repeat expansions in Saccharomyces cerevisiae.Genetics · 2025Article
- Review
- Massive contractions of myotonic dystrophy type 2-associated CCTG tetranucleotide repeats occur via double-strand break repair with distinct requirements for DNA helicases.G3 (Bethesda, Md.) · 2024Article
- Elevated MSH2 MSH3 expression interferes with DNA metabolism in vivo.Nucleic acids research · 2023Article
- Review
- Genomic Instability and Cancer Risk Associated with Erroneous DNA Repair.International journal of molecular sciences · 2021Review
- Review
- Variable number tandem repeats mediate the expression of proximal genes.Nature communications · 2021Article
- Alternative DNA StructuresMicrobiology and molecular biology reviews : MMBR · 2021Review
- HDAC3 deacetylates the DNA mismatch repair factor MutSβ to stimulate triplet repeat expansions.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- On the wrong DNA track: Molecular mechanisms of repeat-mediated genome instability.The Journal of biological chemistry · 2020Review
- Trinucleotide repeat instability during double-strand break repair: from mechanisms to gene therapy.Current genetics · 2019Review
- The central role of DNA damage and repair in CAG repeat diseases.Disease models & mechanisms · 2018Review
- Loss of MSH2 and MSH6 due to heterozygous germline defects in MSH3 and MSH6.Familial cancer · 2017Article
- DNA mismatch repair in trinucleotide repeat instability.Science China. Life sciences · 2017Review
- MutSβ abundance and Msh3 ATP hydrolysis activity are important drivers of CTG•CAG repeat expansions.Nucleic acids research · 2017Article
- Break-induced replication links microsatellite expansion to complex genome rearrangements.BioEssays : news and reviews in molecular, cellular and developmental biology · 2017Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Trinucleotide repeat (TNR) expansions are the underlying cause of more than 40 neurodegenerative and neuromuscular diseases, including myotonic dystrophy and Huntington's disease, yet the pathway to expansion remains poorly understood. An important step in expansion is the shift from a stable TNR sequence to an unstable, expanding tract, which is thought to occur once a TNR attains a threshold length. Modeling of human data has indicated that TNR tracts are increasingly likely to expand as they increase in size and to do so in increments that are smaller than the repeat itself, but this has not been tested experimentally. Genetic work has implicated the mismatch repair factor MSH3 in promoting expansions. Using Saccharomyces cerevisiae as a model for CAG and CTG tract dynamics, we examined individual threshold-length TNR tracts in vivo over time in MSH3 and msh3Δ backgrounds. We demonstrate, for the first time, that these TNR tracts are highly dynamic. Furthermore, we establish that once such a tract has expanded by even a few repeat units, it is significantly more likely to expand again. Finally, we show that threshold- length TNR sequences readily accumulate net incremental expansions over time through a series of small expansion and contraction events. Importantly, the tracts were substantially stabilized in the msh3Δ background, with a bias toward contractions, indicating that Msh2-Msh3 plays an important role in shifting the expansion-contraction equilibrium toward expansion in the early stages of TNR tract expansion.
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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.