ArticleNucleic acids research2005
Mechanistic features of CAG*CTG repeat contractions in cultured cells revealed by a novel genetic assay.
Article in Nucleic acids research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 29 citations in OpenAlex.
- 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
- Modifiers of CAG/CTG Repeat Instability: Insights from Mammalian Models.Journal of Huntington's disease · 2021Review
- On the wrong DNA track: Molecular mechanisms of repeat-mediated genome instability.The Journal of biological chemistry · 2020Review
- MutSβ abundance and Msh3 ATP hydrolysis activity are important drivers of CTG•CAG repeat expansions.Nucleic acids research · 2017Article
- Contracting CAG/CTG repeats using the CRISPR-Cas9 nickase.Nature communications · 2016Article
- Non-LTR retrotransposons and microsatellites: Partners in genomic variation.Mobile genetic elements · 2013Review
- Coordinated processing of 3' slipped (CAG)n/(CTG)n hairpins by DNA polymerases β and δ preferentially induces repeat expansions.The Journal of biological chemistry · 2013Article
- Trinucleotide repeat expansions catalyzed by human cell-free extracts.Cell research · 2013Article
- Instability of CTG repeats is governed by the position of a DNA base lesion through base excision repair.PloS one · 2013Article
- Human mismatch repair protein hMutLα is required to repair short slipped-DNAs of trinucleotide repeats.The Journal of biological chemistry · 2012Article
- DNA mismatch repair complex MutSβ promotes GAA·TTC repeat expansion in human cells.The Journal of biological chemistry · 2012Article
- Nucleotide excision repair, mismatch repair, and R-loops modulate convergent transcription-induced cell death and repeat instability.PloS one · 2012Article
- Non-B DNA structure-induced genetic instability and evolution.Cellular and molecular life sciences : CMLS · 2010Review
- Zinc-finger directed double-strand breaks within CAG repeat tracts promote repeat instability in human cells.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Methods to determine DNA structural alterations and genetic instability.Methods (San Diego, Calif.) · 2009Review
- Article
- Replication in mammalian cells recapitulates the locus-specific differences in somatic instability of genomic GAA triplet-repeats.Nucleic acids research · 2006Article
- CAG*CTG repeat instability in cultured human astrocytes.Nucleic acids research · 2006Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Trinucleotide repeats (TNRs) undergo high frequency mutagenesis to cause at least 15 neurodegenerative diseases. To understand better the molecular mechanisms of TNR instability in cultured cells, a new genetic assay was created using a shuttle vector. The shuttle vector contains a promoter-TNR-reporter gene construct whose expression is dependent on TNR length. The vector harbors the SV40 ori and large T antigen gene, allowing portability between primate cell lines. The shuttle vector is propagated in cultured cells, then recovered and analyzed in yeast using selection for reporter gene expression. We show that (CAG*CTG)25-33 contracts at frequencies as high as 1% in 293T and 293 human cells and in COS-1 monkey cells, provided that the plasmid undergoes replication. Hairpin-forming capacity of the repeat sequence stimulated contractions. Evidence for a threshold was observed between 25 and 33 repeats in COS-1 cells, where contraction frequencies increased sharply (up 720%) over a narrow range of repeat lengths. Expression of the mismatch repair protein Mlh1 does not correlate with repeat instability, suggesting contractions are independent of mismatch repair in our system. Together, these findings recapitulate certain features of human genetics and therefore establish a novel cell culture system to help provide new mechanistic insights into CAG*CTG repeat instability.
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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.