ArticleAmerican journal of human genetics2005
Role of replication and CpG methylation in fragile X syndrome CGG deletions in primate cells.
Article in American journal of human genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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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Who cites it
26 citing papers in PubMed, 51 citations in OpenAlex.
- Creation and resolution of non-B-DNA structural impediments during replication.Critical reviews in biochemistry and molecular biology · 2022Article
- Mechanisms of theInternational journal of molecular sciences · 2022Review
- On the wrong DNA track: Molecular mechanisms of repeat-mediated genome instability.The Journal of biological chemistry · 2020Review
- The G-rich Repeats inGenetics · 2018Article
- Inheritable epigenetic response towards foreign DNA entry by mammalian host cells: a guardian of genomic stability.Epigenetics · 2018Review
- Of Men and Mice: Modeling the Fragile X Syndrome.Frontiers in molecular neuroscience · 2018Article
- Review
- DNA Replication Dynamics of the GGGGCC Repeat of the C9orf72 Gene.The Journal of biological chemistry · 2015Article
- Quadruplex formation by both G-rich and C-rich DNA strands of the C9orf72 (GGGGCC)8•(GGCCCC)8 repeat: effect of CpG methylation.Nucleic acids research · 2015Article
- Modeling diseases of noncoding unstable repeat expansions using mutant pluripotent stem cells.World journal of stem cells · 2015Review
- Inferring short tandem repeat variation from paired-end short reads.Nucleic acids research · 2014Article
- The DNA replication program is altered at the FMR1 locus in fragile X embryonic stem cells.Molecular cell · 2014Article
- Review
- Epigenetic mechanisms and genome stability.Clinical epigenetics · 2011Article
- Role of transcript and interplay between transcription and replication in triplet-repeat instability in mammalian cells.Nucleic acids research · 2011Article
- Tissue- and age-specific DNA replication patterns at the CTG/CAG-expanded human myotonic dystrophy type 1 locus.Nature structural & molecular biology · 2010Article
- DNA instability at chromosomal fragile sites in cancer.Current genomics · 2010Article
- Secondary structure formation and DNA instability at fragile site FRA16B.Nucleic acids research · 2010Article
- A distinct DNA-methylation boundary in the 5'- upstream sequence of the FMR1 promoter binds nuclear proteins and is lost in fragile X syndrome.American journal of human genetics · 2009Article
- Replisome stalling and stabilization at CGG repeats, which are responsible for chromosomal fragility.Nature structural & molecular biology · 2009Article
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
Instability of the fragile X CGG repeat involves both maternally derived expansions and deletions in the gametes of full-mutation males. It has also been suggested that the absence of aberrant CpG methylation may enhance repeat deletions through an unknown process. The effect of CGG tract length, DNA replication direction, location of replication initiation, and CpG methylation upon CGG stability were investigated using an SV40 primate replication system. Replication-dependant deletions with 53 CGG repeats were observed when replication was initiated proximal to the repeat, with CGG as the lagging-strand template. When we initiated replication further from the repeat, while maintaining CGG as the lagging-strand template or using CCG as the lagging-strand template, significant instability was not observed. CpG methylation of the unstable template stabilized the repeat, decreasing both the frequency and the magnitude of deletion events. Furthermore, CpG methylation slowed the efficiency of replication for all templates. Interestingly, replication forks displayed no evidence of a block at the CGG repeat tract, regardless of replication direction or CpG methylation status. Templates with 20 CGG repeats were stable under all circumstances. These results reveal that CGG deletions occur during replication and are sensitive to replication-fork dynamics, tract length, and CpG methylation.
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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.