ArticlePloS one2016
Epigenetic Repeat-Induced Gene Silencing in the Chromosomal and Extrachromosomal Contexts in Human Cells.
Article in PloS one, 2016. 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, 22 citations in OpenAlex.
- Extrachromosomal circular DNA: a potential clinical therapeutic target in malignant tumors.Cellular & molecular biology letters · 2026Review
- Translational insights from nonclinical studies of AAV gene therapies for hemophilia: mechanisms underpinning variability and durability of gene expression.Therapeutic advances in hematology · 2026Review
- Leveraging extrachromosomal DNA to fine-tune trials of targeted therapy for glioblastoma: opportunities and challenges.Nature reviews. Clinical oncology · 2022Review
- Review
- How Chaotic Is Genome Chaos?Cancers · 2021Review
- Length Polymorphism and Methylation Status of UPS29 Minisatellite of theInternational journal of molecular sciences · 2020Article
- AmpliconReconstructor integrates NGS and optical mapping to resolve the complex structures of focal amplifications.Nature communications · 2020Article
- The biogenesis and roles of extrachromosomal oncogene involved in carcinogenesis and evolution.American journal of cancer research · 2020Review
- Article
- Targeted amplification of a sequence of interest in artificial chromosome in mammalian cells.Nucleic acids research · 2019Article
- Circular DNA elements of chromosomal origin are common in healthy human somatic tissue.Nature communications · 2018Article
- Transcription-coupled changes in nuclear mobility of mammalian cis-regulatory elements.Science (New York, N.Y.) · 2018Article
- SIRT1 stabilizes extrachromosomal gene amplification and contributes to repeat-induced gene silencing.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A plasmid bearing both a replication initiation region and a matrix attachment region is spontaneously amplified in transfected mammalian cells and generates plasmid repeats in the extrachromosomal double minutes (DMs) or the chromosomal homogeneously staining region (HSR). Generally, the repeat sequences are subject to repeat-induced gene silencing, the mechanism of which remains to be elucidated. Previous research showed that gene expression from the same plasmid repeat was higher from repeats located at DMs than at the HSR, which may reflect the extrachromosomal environment of the DMs. In the current study, plasmid repeats in both DMs and HSR were associated with repressive histone modifications (H3K9me3, H3K9me2), and the levels of repressive chromatin markers were higher in HSR than in DMs. Inactive chromatin is known to spread to neighboring regions in chromosome arm. Here, we found that such spreading also occurs in extrachromosomal DMs. Higher levels of active histone modifications (H3K9Ac, H3K4me3, and H3K79me2) were detected at plasmid repeats in DMs than in HSR. The level of DNA CpG methylation was generally low in both DMs and HSR; however, there were some hypermethylated copies within the population of repeated sequences, and the frequency of such copies was higher in DMs than in HSR. Together, these data suggest a "DNA methylation-core and chromatin-spread" model for repeat-induced gene silencing. The unique histone modifications at the extrachromosomal context are discussed with regard to the model.
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