ArticleNucleic acids research1998
Cloned human FMR1 trinucleotide repeats exhibit a length- and orientation-dependent instability suggestive of in vivo lagging strand secondary structure.
Article in Nucleic acids research, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 58 citations in OpenAlex.
- Article
- G-Quadruplexes in Repeat Expansion Disorders.International journal of molecular sciences · 2023Review
- The mechanism of replication stalling and recovery within repetitive DNA.Nature communications · 2022Article
- The polyG diseases: a new disease entity.Acta neuropathologica communications · 2022Review
- On the wrong DNA track: Molecular mechanisms of repeat-mediated genome instability.The Journal of biological chemistry · 2020Review
- Repeat Instability in the Fragile X-Related Disorders: Lessons from a Mouse Model.Brain sciences · 2019Article
- Of Men and Mice: Modeling the Fragile X Syndrome.Frontiers in molecular neuroscience · 2018Article
- DNA Replication Dynamics of the GGGGCC Repeat of the C9orf72 Gene.The Journal of biological chemistry · 2015Article
- Exploring possible DNA structures in real-time polymerase kinetics using Pacific Biosciences sequencer data.BMC bioinformatics · 2015Article
- DNA triplet repeat expansion and mismatch repair.Annual review of biochemistry · 2015Review
- Epigenetics, autism spectrum, and neurodevelopmental disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2013Review
- Potassium bromate, a potent DNA oxidizing agent, exacerbates germline repeat expansion in a fragile X premutation mouse model.Human mutation · 2010Article
- Translation of the FMR1 mRNA is not influenced by AGG interruptions.Nucleic acids research · 2009Article
- Mutation spectra in fragile X syndrome induced by deletions of CGG*CCG repeats.The Journal of biological chemistry · 2009Review
- Hijacking of the mismatch repair system to cause CAG expansion and cell death in neurodegenerative disease.DNA repair · 2008Review
- ATR protects the genome against CGG.CCG-repeat expansion in Fragile X premutation mice.Nucleic acids research · 2008Article
- Repair of DNA double-strand breaks within the (GAA*TTC)n sequence results in frequent deletion of the triplet-repeat sequence.Nucleic acids research · 2008Article
- Deficiency of RecA-dependent RecFOR and RecBCD pathways causes increased instability of the (GAA*TTC)n sequence when GAA is the lagging strand template.Nucleic acids research · 2007Article
- An origin of DNA replication in the promoter region of the human fragile X mental retardation (FMR1) gene.Molecular and cellular biology · 2007Article
- Double-strand breaks in the myotonic dystrophy type 1 and the fragile X syndrome triplet repeat sequences induce different types of mutations in DNA flanking sequences in Escherichia coli.Nucleic acids research · 2006Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
The normal human FMR1 gene contains a genetically stable (CGG) n trinucleotide repeat which usually carries interspersed AGG triplets. An increase in repeat number and the loss of interspersions results in array instability, predominantly expansion, leading to FMR1 gene silencing. Instability is directly related to the length of the uninterrupted (CGG) n repeat and is widely assumed to be related to an increased propensity to form G-rich secondary structures which lead to expansion through replication slippage. In order to investigate this we have cloned human FMR1 arrays with internal structures representing the normal, intermediate and unstable states. In one replicative orientation, arrays show a length-dependent instability, deletions occurring in a polar manner. With longer arrays these extend into the FMR1 5'-flanking DNA, terminating at either of two short CGG triplet arrays. The orientation-dependent instability suggests that secondary structure forms in the G-rich lagging strand template, resolution of which results in intra-array deletion. These data provide direct in vivo evidence for a G-rich lagging strand secondary structure which is believed to be involved in the process of triplet expansion in humans.
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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.