ArticleFrontiers in microbiology2015
The inactivation of RNase G reduces the Stenotrophomonas maltophilia susceptibility to quinolones by triggering the heat shock response.
Article in Frontiers in microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- The world of ribonucleases from pseudomonads: a short trip through the main features and singularities.Microbial biotechnology · 2021Review
- Advances in the Microbiology of Stenotrophomonas maltophilia.Clinical microbiology reviews · 2021Article
- Antibiotic resistance: Time of synthesis in a post-genomic age.Computational and structural biotechnology journal · 2021Review
- Analysis of multidrug resistance inVirulence · 2019Article
- Global Analysis of Genes Essential for Francisella tularensis Schu S4 GrowthJournal of bacteriology · 2019Article
- Substantial Contribution of SmeDEF, SmeVWX, SmQnr, and Heat Shock Response to Fluoroquinolone Resistance in Clinical Isolates ofFrontiers in microbiology · 2019Article
- Overexpression of the Efflux Pumps SmeVWX and SmeDEF Is a Major Cause of Resistance to Co-trimoxazole in Stenotrophomonas maltophilia.Antimicrobial agents and chemotherapy · 2018Article
- Genome-wide analysis shows that RNase G plays a global role in the stability of mRNAs in Stenotrophomonas maltophilia.Scientific reports · 2017Article
- Effect of antibiotics on bacterial populations: a multi-hierachical selection process.F1000Research · 2017Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Quinolone resistance is usually due to mutations in the genes encoding bacterial topoisomerases. However, different reports have shown that neither clinical quinolone resistant isolates nor in vitro obtained Stenotrophomonas maltophilia mutants present mutations in such genes. The mechanisms so far described consist on efflux pumps' overexpression. Our objective is to get information on novel mechanisms of S. maltophilia quinolone resistance. For this purpose, a transposon-insertion mutant library was obtained in S. maltophilia D457. One mutant presenting reduced susceptibility to nalidixic acid was selected. Inverse PCR showed that the inactivated gene encodes RNase G. Complementation of the mutant with wild-type RNase G allele restored the susceptibility to quinolones. Transcriptomic and real-time RT-PCR analyses showed that several genes encoding heat-shock response proteins were expressed at higher levels in the RNase defective mutant than in the wild-type strain. In agreement with this situation, heat-shock reduces the S. maltophilia susceptibility to quinolone. We can then conclude that the inactivation of the RNase G reduces the susceptibility of S. maltophilia to quinolones, most likely by regulating the expression of heat-shock response genes. Heat-shock induces a transient phenotype of quinolone resistance in S. maltophilia.
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