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Título

The cellular abundance of chemoreceptors, chemosensory signaling proteins, sensor histidine kinases, and solute binding proteins of Pseudomonas aeruginosa provides insight into sensory preferences and signaling mechanisms

AutorMatilla, Miguel A. CSIC ORCID; Génova, Roberta CSIC ORCID; Martín-Mora, David CSIC ORCID; Maaß, S.; Becher, Dörte; Krell, Tino CSIC ORCID
Palabras claveChemotaxis
Chemoreceptor
Sensor histidine kinases
Solute binding protein
Chemosensory pathway
Protein abundance
Pseudomonas aeruginosa
Fecha de publicación2023
EditorMultidisciplinary Digital Publishing Institute
CitaciónInternational Journal of Molecular Sciences 24: 1363 (2023)
ResumenChemosensory pathways and two-component systems are important bacterial signal transduction systems. In the human pathogen Pseudomonas aeruginosa, these systems control many virulence traits. Previous studies showed that inorganic phosphate (Pi) deficiency induces virulence. We report here the abundance of chemosensory and two-component signaling proteins of P. aeruginosa grown in Pi deficient and sufficient media. The cellular abundance of chemoreceptors differed greatly, since a 2400-fold difference between the most and least abundant receptors was observed. For many chemoreceptors, their amount varied with the growth condition. The amount of chemoreceptors did not correlate with the magnitude of chemotaxis to their cognate chemoeffectors. Of the four chemosensory pathways, proteins of the Che chemotaxis pathway were most abundant and showed little variation in different growth conditions. The abundance of chemoreceptors and solute binding proteins indicates a sensing preference for amino acids and polyamines. There was an excess of response regulators over sensor histidine kinases in two-component systems. In contrast, ratios of the response regulators CheY and CheB to the histidine kinase CheA of the Che pathway were all below 1, indicative of different signaling mechanisms. This study will serve as a reference for exploring sensing preferences and signaling mechanisms of other bacteria.
Versión del editorhttp://dx.doi.org/10.3390/ijms24021363
URIhttp://hdl.handle.net/10261/310090
DOI10.3390/ijms24021363
Identificadoresdoi: 10.3390/ijms24021363
issn: 1422-0067
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