Open discussion platform of the COST action EuroMicropH. This discussion series is intended to stimulate an exchange on the different aspects of how microorganisms react to low pH conditions and why people are interested to investigate this subject.
Please register here for the upcoming meeting. To access the session, please follow the zoom link below.
23.09.2022 16:00 CEST
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https://tuwien.zoom.us/j/92961817473?pwd=NWc5aUlSRXRYb01tNkFQUnl1dnpVUT09
Meeting-ID: 929 6181 7473
Programm
16:00 Welcome
16:05 Bram Van den Bergh, VIB-KU Leuven
Mutations in respiratory complex I promote antibiotic persistence through alterations in intracellular acidity and protein synthesis
16:30 Daniela De Biase, Sapienza University of Rom and Fabio Giovannercole, University of Namur
Biochemical and Omic studies on Escherichia coli exposed to phosphinic compounds possessing antibacterial activity
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Abstracts
Mutations in respiratory complex I promote antibiotic persistence through alterations in intracellular acidity and protein synthesis
Bram Van den Bergh
Antibiotic persistence describes the presence of phenotypic variants within an isogenic bacterial population that are transiently tolerant to antibiotic treatment. Perturbations of metabolic homeostasis can promote antibiotic persistence, but the precise mechanisms are not well understood. Here, we use laboratory evolution, population-wide sequencing and biochemical characterizations to identify mutations in respiratory complex I and discover how they promote persistence in Escherichia coli. We show that persistence-inducing perturbations of metabolic homeostasis are associated with cytoplasmic acidification. Such cytoplasmic acidification is further strengthened by compromised proton pumping in the complex I mutants. While RpoS regulon activation induces persistence in the wild type, the aggravated cytoplasmic acidification in the complex I mutants leads to increased persistence via global shutdown of protein synthesis. Thus, we propose that cytoplasmic acidification, amplified by a compromised complex I, can act as a signaling hub for perturbed metabolic homeostasis in antibiotic persisters.
