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MOB rules: Antibiotic Exposure Reprograms Metabolism to Mobilize Bacillus subtilis in Competitive Interactions
Yongjin Liu1, Sandra LaBonte1,2, Courtney Brake3
1Biochemistry and Biophysics Department, Texas A&M University, AgriLife Research, College Station, Texas, USA.
Biorxiv : the Preprint Server for Biology
|April 2, 2024
Summary
Bacillus subtilis mobilizes in response to subinhibitory antibiotic concentrations. This study identifies key regulators and metabolic shifts enabling this coordinated population movement.
Area of Science:
- Microbiology
- Bacterial Physiology
- Systems Biology
Background:
- Antibiotics exhibit dose-dependent effects, with subinhibitory concentrations triggering varied bacterial responses.
- Bacillus subtilis mobilizes via a population-spreading mechanism when exposed to bacteriostatic translation inhibitors.
- The regulatory mechanisms governing antibiotic-induced bacterial mobilization remain largely unknown.
Approach:
- Investigated the regulatory functions essential for Bacillus subtilis mobilization under subinhibitory chloramphenicol exposure.
- Analyzed changes in gene expression and metabolism, mapping them to a regulatory protein network.
- Utilized reporter genes for pdhA and pucA to visualize metabolic compartmentalization within the mobilized population.
Key Points:
- Several transcriptional regulators coordinate metabolic reprogramming, including glycolysis, nucleotide, and amino acid metabolism, to support bacterial mobilization.
- Identified pdhA and pucA gene expression and metabolite abundance as key indicators of mobilized population metabolic states.
- Demonstrated that Bacillus subtilis mounts a coordinated mobile response through a regulated metabolic adaptation to chloramphenicol.
Conclusions:
- Uncovered a network of transcriptional regulators controlling metabolic shifts crucial for Bacillus subtilis population mobilization.
- Highlighted the distinct metabolic profiles within different regions of the mobilized bacterial population.
- Revealed a regulated, population-level response enabling coordinated movement and adaptation to subinhibitory antibiotic stress.
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