ArticlePloS one2011
Unusual structures are present in DNA fragments containing super-long Huntingtin CAG repeats.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Role of Bβ1 overexpression in the pathogenesis of SCA12.Movement disorders : official journal of the Movement Disorder Society · 2024Article
- Subcellular Localization And Formation Of Huntingtin Aggregates Correlates With Symptom Onset And Progression In A Huntington'S Disease Model.Brain communications · 2020Article
- Antagonistic pleiotropy in mice carrying a CAG repeat expansion in the range causing Huntington's disease.Scientific reports · 2019Article
- Sex-dependent behavioral impairments in the HdhQ350/+ mouse line.Behavioural brain research · 2018Article
- XJB-5-131-mediated improvement in physiology and behaviour of the R6/2 mouse model of Huntington's disease is age- and sex- dependent.PloS one · 2018Article
- CTG repeat-targeting oligonucleotides for down-regulating Huntingtin expression.Nucleic acids research · 2017Article
- Potential molecular consequences of transgene integration: The R6/2 mouse example.Scientific reports · 2017Article
- Impaired Nitric Oxide Mediated Vasodilation In The Peripheral Circulation In The R6/2 Mouse Model Of Huntington's Disease.Scientific reports · 2016Article
- Expression levels of DNA replication and repair genes predict regional somatic repeat instability in the brain but are not altered by polyglutamine disease protein expression or age.Human molecular genetics · 2014Article
- Article
- Right ventricular dysfunction in the R6/2 transgenic mouse model of Huntington's disease is unmasked by dobutamine.Journal of Huntington's disease · 2014Article
- Restriction endonuclease TseI cleaves A:A and T:T mismatches in CAG and CTG repeats.Nucleic acids research · 2013Article
- Direct evidence of progressive cardiac dysfunction in a transgenic mouse model of Huntington's disease.Journal of Huntington's disease · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundIn the R6/2 mouse model of Huntington's disease (HD), expansion of the CAG trinucleotide repeat length beyond about 300 repeats induces a novel phenotype associated with a reduction in transcription of the transgene. METHODOLOGY/PRINCIPAL
findingsWe analysed the structure of polymerase chain reaction (PCR)-generated DNA containing up to 585 CAG repeats using atomic force microscopy (AFM). As the number of CAG repeats increased, an increasing proportion of the DNA molecules exhibited unusual structural features, including convolutions and multiple protrusions. At least some of these features are hairpin loops, as judged by cross-sectional analysis and sensitivity to cleavage by mung bean nuclease. Single-molecule force measurements showed that the convoluted DNA was very resistant to untangling. In vitro replication by PCR was markedly reduced, and TseI restriction enzyme digestion was also hindered by the abnormal DNA structures. However, significantly, the DNA gained sensitivity to cleavage by the Type III restriction-modification enzyme, EcoP15I. CONCLUSIONS/SIGNIFICANCE: "Super-long" CAG repeats are found in a number of neurological diseases and may also appear through CAG repeat instability. We suggest that unusual DNA structures associated with super-long CAG repeats decrease transcriptional efficiency in vitro. We also raise the possibility that if these structures occur in vivo, they may play a role in the aetiology of CAG repeat diseases such as HD.
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