ArticlePLoS genetics2017
Genetic plasticity of the Shigella virulence plasmid is mediated by intra- and inter-molecular events between insertion sequences.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
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- The emergence of metabolisms through Earth history and implications for biospheric evolution.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Article
- Fecal microbiome profiling of children withMicrobiology spectrum · 2025Article
- Can Nature Overcome Invasive Gastrointestinal Infections?International journal of molecular sciences · 2025Review
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- Evolution, persistence, and host adaption of a gonococcal AMR plasmid that emerged in the pre-antibiotic era.PLoS genetics · 2023Article
- The parABSm system is involved in megaplasmid partitioning and genome integrity maintenance in Thermus thermophilus.G3 (Bethesda, Md.) · 2023Article
- A ParDE toxin-antitoxin system is responsible for the maintenance of theFrontiers in cellular and infection microbiology · 2023Article
- Evolutionary and genomic insights into the long-term colonization ofEmerging microbes & infections · 2022Article
- How Do Transposable Elements Activate Expression of Transcriptionally Silent Antibiotic Resistance Genes?International journal of molecular sciences · 2022Review
- The VirF21:VirF30 protein ratio is affected by temperature and impacts Shigella flexneri host cell invasion.FEMS microbiology letters · 2022Article
- Virulence plasmid pINV as a genetic signature forMicrobial genomics · 2022Article
- A Highly Unstable and Elusive Plasmid That Encodes the Type III Secretion System Is Necessary for Full Virulence in the Marine Fish PathogenInternational journal of molecular sciences · 2022Article
- Maintenance of the Shigella sonnei Virulence Plasmid Is Dependent on Its Repertoire and Amino Acid Sequence of Toxin-Antitoxin Systems.Journal of bacteriology · 2022Article
- What makes a megaplasmid?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Article
- Article
- Evaluation of a Live AttenuatedPathogens (Basel, Switzerland) · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Acquisition of a single copy, large virulence plasmid, pINV, led to the emergence of Shigella spp. from Escherichia coli. The plasmid encodes a Type III secretion system (T3SS) on a 30 kb pathogenicity island (PAI), and is maintained in a bacterial population through a series of toxin:antitoxin (TA) systems which mediate post-segregational killing (PSK). The T3SS imposes a significant cost on the bacterium, and strains which have lost the plasmid and/or genes encoding the T3SS grow faster than wild-type strains in the laboratory, and fail to bind the indicator dye Congo Red (CR). Our aim was to define the molecular events in Shigella flexneri that cause loss of Type III secretion (T3S), and to examine whether TA systems exert positional effects on pINV. During growth at 37°C, we found that deletions of regions of the plasmid including the PAI lead to the emergence of CR-negative colonies; deletions occur through intra-molecular recombination events between insertion sequences (ISs) flanking the PAI. Furthermore, by repositioning MvpAT (which belongs to the VapBC family of TA systems) near the PAI, we demonstrate that the location of this TA system alters the rearrangements that lead to loss of T3S, indicating that MvpAT acts both globally (by reducing loss of pINV through PSK) as well as locally (by preventing loss of adjacent sequences). During growth at environmental temperatures, we show for the first time that pINV spontaneously integrates into different sites in the chromosome, and this is mediated by inter-molecular events involving IS1294. Integration leads to reduced PAI gene expression and impaired secretion through the T3SS, while excision of pINV from the chromosome restores T3SS function. Therefore, pINV integration provides a reversible mechanism for Shigella to circumvent the metabolic burden imposed by pINV. Intra- and inter-molecular events between ISs, which are abundant in Shigella spp., mediate plasticity of S. flexneri pINV.
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