Signaling by two-component system noncognate partners promotes intrinsic tolerance to polymyxin B in uropathogenic Escherichia coli
| Autor: | Erin J. Breland, Ellisa W. Zhang, Holly M. Scott Algood, Charles W. Stratton, Maria Hadjifrangiskou, Navleen K. Gill, Jonathan E. Schmitz, Sarah C. Hanks, Kirsten R. Guckes |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.drug_class Polymyxin 030106 microbiology Biology medicine.disease_cause Ferric Compounds Biochemistry Article Microbiology 03 medical and health sciences Bacterial Proteins Transcriptional regulation medicine Uropathogenic Escherichia coli Molecular Biology Escherichia coli Polymyxin B Ions Regulation of gene expression Reverse Transcriptase Polymerase Chain Reaction Escherichia coli Proteins Histidine kinase Drug Tolerance Gene Expression Regulation Bacterial Cell Biology Two-component regulatory system Anti-Bacterial Agents Response regulator 030104 developmental biology Protein Binding Signal Transduction Transcription Factors medicine.drug |
| Zdroj: | Science signaling |
| ISSN: | 1937-9145 1945-0877 |
| DOI: | 10.1126/scisignal.aag1775 |
| Popis: | Bacteria use two-component systems (TCSs) to react appropriately to environmental stimuli. Typical TCSs comprise a sensor histidine kinase that acts as a receptor coupled to a partner response regulator that coordinates changes in bacterial behavior, often through its activity as a transcriptional regulator. TCS interactions are typically confined to cognate pairs of histidine kinases and response regulators. We describe two distinct TCSs in uropathogenic Escherichia coli (UPEC) that interact to mediate a response to ferric iron. The PmrAB and QseBC TCSs were both required for proper transcriptional response to ferric iron. Ferric iron induced the histidine kinase PmrB to phosphotransfer to both its cognate response regulator PmrA and the noncognate response regulator QseB, leading to transcriptional responses coordinated by both regulators. Pretreatment of the UPEC strain UTI89 with ferric iron led to increased resistance to polymyxin B that required both PmrA and QseB. Similarly, pretreatment of several UPEC isolates with ferric iron increased tolerance to polymyxin B. This study defines physiologically relevant cross talk between TCSs in a bacterial pathogen and provides a potential mechanism for antibiotic resistance of some strains of UPEC. |
| Databáze: | OpenAIRE |
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