In vivo genetic analysis of Pseudomonas aeruginosa carbon catabolic repression through the study of CrcZ pseudo-revertants shows that Crc-mediated metabolic robustness is needed for proficient bacterial virulence and antibiotic resistance
Hfq and Crc regulate P. aeruginosa carbon catabolic repression at the post-transcriptional level. In vitro work has shown that Hfq binds the target RNAs and Crc stabilizes the complex. A third element in the regulation is the small RNA CrcZ, which sequesters the Crc-Hfq complex under no catabolic re...
| Autores: | , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2023 |
| País: | España |
| Institución: | Consejo Superior de Investigaciones Científicas (CSIC) |
| Repositorio: | DIGITAL.CSIC. Repositorio Institucional del CSIC |
| OAI Identifier: | oai:digital.csic.es:10261/363516 |
| Acceso en línea: | http://hdl.handle.net/10261/363516 https://api.elsevier.com/content/abstract/scopus_id/85180006807 |
| Access Level: | acceso abierto |
| Palabra clave: | Catabolic repression Crc CrcZ Pseudomonas aeruginosa antibiotic resistance virulence |
| Sumario: | Hfq and Crc regulate P. aeruginosa carbon catabolic repression at the post-transcriptional level. In vitro work has shown that Hfq binds the target RNAs and Crc stabilizes the complex. A third element in the regulation is the small RNA CrcZ, which sequesters the Crc-Hfq complex under no catabolic repression conditions, allowing the translation of the target mRNAs. A ΔcrcZ mutant was generated and presented fitness defects and alterations in its virulence potential and antibiotic resistance. Eight pseudo-revertants that present different degrees of fitness compensation were selected. Notably, although Hfq is the RNA binding protein, most mutations occurred in Crc. This indicates that Crc is strictly needed for P. aeruginosa efficient carbon catabolic repression in vivo. The compensatory mutations restore in a different degree the alterations in antibiotic susceptibility and virulence of the ΔcrcZ mutant, supporting that Crc plays a fundamental role linking P. aeruginosa metabolic robustness, virulence, and antibiotic resistance. |
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