ArticleBMC molecular biology2007
Somatic CTG*CAG repeat instability in a mouse model for myotonic dystrophy type 1 is associated with changes in cell nuclearity and DNA ploidy.
Article in BMC molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Somatic and intergenerational G4C2 hexanucleotide repeat instability in a human C9orf72 knock-in mouse model.Nucleic acids research · 2024Article
- Challenges and Considerations of Preclinical Development for iPSC-Based Myogenic Cell Therapy.Cells · 2024Review
- Modifiers of CAG/CTG Repeat Instability: Insights from Mammalian Models.Journal of Huntington's disease · 2021Review
- Double-strand break repair plays a role in repeat instability in a fragile X mouse model.DNA repair · 2019Article
- The Repeat Expansion Diseases: The dark side of DNA repair.DNA repair · 2015Review
- Environmental stress induces trinucleotide repeat mutagenesis in human cells.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Elevated Muscle-Specific miRNAs in Serum of Myotonic Dystrophy Patients Relate to Muscle Disease Progress.PloS one · 2015Article
- The role of CUGBP1 in age-dependent changes of liver functions.Ageing research reviews · 2012Review
- Article
- Continuous and periodic expansion of CAG repeats in Huntington's disease R6/1 mice.PLoS genetics · 2010Article
- Microsatellite repeat instability and neurological disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2009Review
- ATR protects the genome against CGG.CCG-repeat expansion in Fragile X premutation mice.Nucleic acids research · 2008Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTrinucleotide instability is a hallmark of degenerative neurological diseases like Huntington's disease, some forms of spinocerebellar ataxia and myotonic dystrophy type 1 (DM1). To investigate the effect of cell type and cell state on the behavior of the DM1 CTG*CAG repeat, we studied a knock-in mouse model for DM1 at different time points during ageing and followed how repeat fate in cells from liver and pancreas is associated with polyploidization and changes in nuclearity after the onset of terminal differentiation.
resultsAfter separation of liver hepatocytes and pancreatic acinar cells in pools with 2n, 4n or 8n DNA, we analyzed CTG*CAG repeat length variation by resolving PCR products on an automated PAGE system. We observed that somatic CTG*CAG repeat expansion in our DM1 mouse model occurred almost uniquely in the fraction of cells with high cell nuclearity and DNA ploidy and aggravated with aging.
conclusionOur findings suggest that post-replicative and terminal-differentiation events, coupled to changes in cellular DNA content, form a preconditional state that influences the control of DNA repair or recombination events involved in trinucleotide expansion in liver hepatocytes and pancreatic acinar cells.
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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.