Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (666 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Any DNA sequence capable of independent replication or a molecule that possesses a replication origin and which is therefore potentially capable of being replicated in a suitable cell. (Singleton and Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Replicons; Replication Unit; Replication Units; Unit, Replication; Units, Replication.
Where it fits in the MeSH classification
- Broader topics
- Genome Components
- Narrower topics
- Replication Origin
Related concepts
- Replication Origin
Research landscape
PubMed indexes 7,314 records tagged with the MeSH heading “Replicon” (counts retrieved 2026-10-29). 689 of them (9.4%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 2,566 records.
Reviews account for 706 records (9.7%) and meta-analyses for 1. Randomized controlled trials number 8 (0.1%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 2,175 |
| 2000-2009 | 2,566 |
| 2010-2019 | 1,884 |
| 2020 onward | 689 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 706 | 9.7% |
| Meta-analyses | 1 | 0.0% |
| Randomized controlled trials | 8 | 0.1% |
Method: PubMed query "Replicon"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in genetics and genomics
Genetic findings vary widely in strength. A variant linked to a condition in one study may not replicate in other ancestries, and most common variants have small effects that are meaningful only in aggregate. Studies of rare, high-impact variants can support strong causal claims about a gene, while association studies describe statistical links that need functional and independent replication. Check the sample size, the ancestry of participants, whether results were replicated, and whether a laboratory or clinical outcome was actually measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| MOB-suite: software tools for clustering, reconstruction and typing of plasmids from draft assemblies | 2018 | Research article Design not recorded in structured metadata | 907 | cc by PMID 30052170 · DOI · PMC6159552 |
| Replication landscape of the human genome | 2016 | Research article Design not recorded in structured metadata | 295 | cc by PMID 26751768 · DOI · PMC4729899 |
| Involvement of G-quadruplex regions in mammalian replication origin activity | 2019 | Research article Design not recorded in structured metadata | 179 | cc by PMID 31332171 · DOI · PMC6646384 |
| License to Replicate: Mechanisms of Licensing Eukaryotic Origins for DNA Replication | 2026 | Review article Design not recorded in structured metadata | 3 | cc by PMID 41423967 · DOI · PMC12719912 |
MOB-suite: software tools for clustering, reconstruction and typing of plasmids from draft assemblies [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Large-scale bacterial population genetics studies are now routine due to cost-effective Illumina short-read sequencing.
- Closing excerpt
- com/phac-nml/mob-suite.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (238 words)
Large-scale bacterial population genetics studies are now routine due to cost-effective Illumina short-read sequencing. However, analysing plasmid content remains difficult due to incomplete assembly of plasmids. Bacterial isolates can contain any number of plasmids and assembly remains complicated due to the presence of repetitive elements. Numerous tools have been developed to analyse plasmids but the performance and functionality of the tools are variable. The MOB-suite was developed as a set of modular tools for reconstruction and typing of plasmids from draft assembly data to facilitate characterization of plasmids. Using a set of closed genomes with publicly available Illumina data, the MOB-suite identified contigs of plasmid origin with both high sensitivity and specificity (95 and 88 %, respectively). In comparison, plasmidfinder demonstrated high specificity (99 %) but limited sensitivity (50 %). Using the same dataset of 377 known plasmids, MOB-recon accurately reconstructed 207 plasmids so that they were assigned to a single grouping without other plasmid or chromosomal sequences, whereas plasmidSPAdes was only able to accurately reconstruct 102 plasmids. In general, plasmidSPAdes has a tendency to merge different plasmids together, with 208 plasmids undergoing merge events. The MOB-suite reduces the number of errors but produces more hybrid plasmids, with 84 plasmids undergoing both splits and merges. The MOB-suite also provides replicon typing similar to plasmidfinder but with the inclusion of relaxase typing and prediction of conjugation potential. The MOB-suite is written in Python 3 and is available from https://github.com/phac-nml/mob-suite.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30052170 · DOI · PMC6159552
Replication landscape of the human genome [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Despite intense investigation, human replication origins and termini remain elusive.
- Closing excerpt
- This novel panorama of replication reveals how chromatin and transcription modulate the initiation process to create cell-type-specific replication programs.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (151 words)
Despite intense investigation, human replication origins and termini remain elusive. Existing data have shown strong discrepancies. Here we sequenced highly purified Okazaki fragments from two cell types and, for the first time, quantitated replication fork directionality and delineated initiation and termination zones genome-wide. Replication initiates stochastically, primarily within non-transcribed, broad (up to 150 kb) zones that often abut transcribed genes, and terminates dispersively between them. Replication fork progression is significantly co-oriented with the transcription. Initiation and termination zones are frequently contiguous, sometimes separated by regions of unidirectional replication. Initiation zones are enriched in open chromatin and enhancer marks, even when not flanked by genes, and often border 'topologically associating domains' (TADs). Initiation zones are enriched in origin recognition complex (ORC)-binding sites and better align to origins previously mapped using bubble-trap than λ-exonuclease. This novel panorama of replication reveals how chromatin and transcription modulate the initiation process to create cell-type-specific replication programs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26751768 · DOI · PMC4729899
Involvement of G-quadruplex regions in mammalian replication origin activity [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Genome-wide studies of DNA replication origins revealed that origins preferentially associate with an Origin G-rich Repeated Element (OGRE), potentially forming G-quadruplexes (G4).
- Closing excerpt
- Altogether, these results converge to the functional importance of OGRE/G4 elements in DNA replication initiation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (152 words)
Genome-wide studies of DNA replication origins revealed that origins preferentially associate with an Origin G-rich Repeated Element (OGRE), potentially forming G-quadruplexes (G4). Here, we functionally address their requirements for DNA replication initiation in a series of independent approaches. Deletion of the OGRE/G4 sequence strongly decreased the corresponding origin activity. Conversely, the insertion of an OGRE/G4 element created a new replication origin. This element also promoted replication of episomal EBV vectors lacking the viral origin, but not if the OGRE/G4 sequence was deleted. A potent G4 ligand, PhenDC3, stabilized G4s but did not alter the global origin activity. However, a set of new, G4-associated origins was created, whereas suppressed origins were largely G4-free. In vitro Xenopus laevis replication systems showed that OGRE/G4 sequences are involved in the activation of DNA replication, but not in the pre-replication complex formation. Altogether, these results converge to the functional importance of OGRE/G4 elements in DNA replication initiation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31332171 · DOI · PMC6646384
License to Replicate: Mechanisms of Licensing Eukaryotic Origins for DNA Replication [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Accurate and timely genome replication is a universal feature of living organisms and a prerequisite for cell proliferation.
- Closing excerpt
- In this review, we highlight similarities and differences in licensing mechanisms between yeast and metazoa.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (125 words)
Accurate and timely genome replication is a universal feature of living organisms and a prerequisite for cell proliferation. In eukaryotes, genomic DNA replication initiates in two steps, origin licensing and origin firing, reflecting the loading and activation of the MCM replicative helicase motor on origin DNA. Biochemical reconstitution of these steps in the budding yeast model system signified a major advance towards understanding the molecular and structural details of eukaryotic replication initiation events. With recent successes in reconstituting origin licensing with purified human proteins, a mechanistic picture is beginning to emerge on how DNA replication initiates in higher eukaryotes and how it deviates from the paradigms established in budding yeast. In this review, we highlight similarities and differences in licensing mechanisms between yeast and metazoa.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41423967 · DOI · PMC12719912
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The multifarious, multireplicon Burkholderia cepacia complex [5]
- Research article Maintaining genome stability at the replication fork [6]
- Research article DNA replication origin activation in space and time [7]
- Research article Replication fork stalling at natural impediments [8]
- Research article The plasticity of DNA replication forks in response to clinically relevant genotoxic stress [9]
- Research article Eukaryotic DNA replication origins: many choices for appropriate answers [10]
References
- Robertson J, Nash JHE. MOB-suite: software tools for clustering, reconstruction and typing of plasmids from draft assemblies. . 2018. PMID 30052170 · DOI · PMC6159552
- Petryk N, Kahli M, d'Aubenton-Carafa Y, Jaszczyszyn Y, Shen Y, Silvain M, et al.. Replication landscape of the human genome. . 2016. PMID 26751768 · DOI · PMC4729899
- Prorok P, Artufel M, Aze A, Coulombe P, Peiffer I, Lacroix L, et al.. Involvement of G-quadruplex regions in mammalian replication origin activity. . 2019. PMID 31332171 · DOI · PMC6646384
- Frisbie V, Bleichert F. License to Replicate: Mechanisms of Licensing Eukaryotic Origins for DNA Replication. . 2026. PMID 41423967 · DOI · PMC12719912
- Mahenthiralingam E, Urban TA, Goldberg JB. The multifarious, multireplicon Burkholderia cepacia complex. Nat Rev Microbiol. 2005. PMID 15643431 · DOI
- Branzei D, Foiani M. Maintaining genome stability at the replication fork. Nat Rev Mol Cell Biol. 2010. PMID 20177396 · DOI
- Fragkos M, Ganier O, Coulombe P, Méchali M. DNA replication origin activation in space and time. Nat Rev Mol Cell Biol. 2015. PMID 25999062 · DOI
- Mirkin EV, Mirkin SM. Replication fork stalling at natural impediments. Microbiol Mol Biol Rev. 2007. PMID 17347517 · DOI · PMC1847372
- Berti M, Cortez D, Lopes M. The plasticity of DNA replication forks in response to clinically relevant genotoxic stress. Nat Rev Mol Cell Biol. 2020. PMID 32612242 · DOI
- Méchali M. Eukaryotic DNA replication origins: many choices for appropriate answers. Nat Rev Mol Cell Biol. 2010. PMID 20861881 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.