Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41598-017-05219-x
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dc.titleDirect and convenient measurement of plasmid stability in lab and clinical isolates of E. coli
dc.contributor.authorChen, S
dc.contributor.authorLarsson, M
dc.contributor.authorRobinson, R.C
dc.contributor.authorChen, S.L
dc.date.accessioned2020-10-20T09:11:15Z
dc.date.available2020-10-20T09:11:15Z
dc.date.issued2017
dc.identifier.citationChen, S, Larsson, M, Robinson, R.C, Chen, S.L (2017). Direct and convenient measurement of plasmid stability in lab and clinical isolates of E. coli. Scientific Reports 7 (1) : 4788. ScholarBank@NUS Repository. https://doi.org/10.1038/s41598-017-05219-x
dc.identifier.issn20452322
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/178316
dc.description.abstractPlasmids are important mobile elements in bacteria, contributing to evolution, virulence, and antibiotic resistance. Natural plasmids are generally large and maintained at low copy number and thus prone to be lost. Therefore, dedicated plasmid maintenance systems have evolved, leading to plasmid loss rates as low as 1 per 107 divisions. These low rates complicate studies of plasmid loss, as traditional techniques for measuring plasmid loss are laborious and not quantitative. To overcome these limitations, we leveraged a stringent negative selection system to develop a method for performing direct, quantitative measurements of plasmid loss in E. coli. We applied our method to gain mechanistic insights into a heterologously reconstituted segregation system in lab strains and clinical isolates of E. coli. We also performed direct stability studies of a currently circulating resistance plasmid in a clinical isolate, strain EC958, which is a member of the rapidly expanding global ST131 E. coli clone. Our results establish the foundational assays required to screen for small molecules targeting plasmid stability, which could complement current strategies for reducing the spread of antibiotic resistance, complementing other strategies for treating antibiotic resistant bacteria. © 2017 The Author(s).
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectbacterial DNA
dc.subjectchloramphenicol
dc.subjectantibiotic resistance
dc.subjectbacterial genome
dc.subjectDNA replication
dc.subjectdrug effect
dc.subjectEscherichia coli
dc.subjectgenetics
dc.subjectgrowth, development and aging
dc.subjectplasmid
dc.subjectChloramphenicol
dc.subjectDNA Replication
dc.subjectDNA, Bacterial
dc.subjectDrug Resistance, Bacterial
dc.subjectEscherichia coli
dc.subjectGenome, Bacterial
dc.subjectPlasmids
dc.typeArticle
dc.contributor.departmentDEPT OF MEDICINE
dc.contributor.departmentDEPT OF CHEMICAL & BIOMOLECULAR ENGG
dc.description.doi10.1038/s41598-017-05219-x
dc.description.sourcetitleScientific Reports
dc.description.volume7
dc.description.issue1
dc.description.page4788
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