Novel mechanisms of TolC-independent decreased bile-salt susceptibility in Escherichia coli
FEMS Microbiology Letters, ISSN: 1574-6968, Vol: 367, Issue: 10
2021
- 2Citations
- 11Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations2
- Citation Indexes2
- Captures11
- Readers11
- 11
Article Description
Bile salts, including sodium deoxycholate (DOC), are secreted into the intestine to aid fat digestion and contribute to antimicrobial protection. Gram-negative pathogens such as Escherichia coli, however, are highly resistant to DOC, using multiple mechanisms of which the multidrug efflux pump AcrAB-TolC is the dominant one. Given that TolC-mediated efflux masks the interaction of DOC with potential targets, we sought to identify those targets by identifying genes whose mutations cause an increase in the MIC to DOC relative to the ΔtolC parental strain, that lacks TolC-associated functional efflux pumps. Using a mutant screen, we isolated twenty independent spontaneous mutants that had a higher MIC than the E. coli parental ΔtolC strain. Whole genome sequencing of these mutants mapped most mutations to the ptsI or cyaA gene. Analysis of knock-out mutants and complementation showed that elimination of PtsI, a component of the carbohydrate phosphotransferase system, or one of the two key proteins involved in cAMP synthesis and signaling, adenylate cyclase (CyaA) or cAMP receptor protein (Crp) causes low-level increased resistance of a ΔtolC E. coli strain to DOC.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85101048008&origin=inward; http://dx.doi.org/10.1093/femsle/fnaa083; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85085538086&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/32407499; https://academic.oup.com/femsle/article/doi/10.1093/femsle/fnaa083/5837082; https://dx.doi.org/10.1093/femsle/fnaa083; https://academic.oup.com/femsle/article/367/10/fnaa083/5837082
Oxford University Press (OUP)
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