ArticleScientific reports2017
Critical role of quorum sensing-dependent glutamate metabolism in homeostatic osmolality and outer membrane vesiculation in Burkholderia glumae.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 16 citations in OpenAlex.
- Influence of nonpolar aliphatic amino acids on Pseudomonas aeruginosa for virulence factors production.Biotechnology and applied biochemistry · 2026Article
- AHL-differential quorum sensing regulation of amino acid metabolism inMicrobiology spectrum · 2024Article
- Conversations in the Gut: The Role of Quorum Sensing in Normobiosis.International journal of molecular sciences · 2023Review
- Identification of a Genetically Linked but Functionally Independent Two-Component System Important for Cell Division of the Rice PathogenFrontiers in microbiology · 2021Article
- Bacterial bug-out bags: outer membrane vesicles and their proteins and functions.Journal of microbiology (Seoul, Korea) · 2020Review
- Quorum Sensing Regulators AphA and OpaR Control Expression of the Operon Responsible for Biosynthesis of the Compatible Solute Ectoine.Applied and environmental microbiology · 2019Article
- Saline Environments as a Source of Potential Quorum Sensing Disruptors to Control Bacterial Infections: A Review.Marine drugs · 2019Review
- Article
- Glutamate uptake is important for osmoregulation and survival in the rice pathogen Burkholderia glumae.PloS one · 2018Article
- Article
- Group AFrontiers in immunology · 2018Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic homeostasis in cooperative bacteria is achieved by modulating primary metabolism in a quorum sensing (QS)-dependent manner. A perturbed metabolism in QS mutants causes physiological stress in the rice bacterial pathogen Burkholderia glumae. Here, we show that increased bacterial osmolality in B. glumae is caused by unusually high cellular concentrations of glutamate and betaine generated by QS deficiencies. QS negatively controls glutamate uptake and the expression of genes involved in the glutamine synthetase and glutamine oxoglutarate aminotransferase cycles. Thus, cellular glutamate levels were significantly higher in the QS mutants than in the wild type, and they caused hyperosmotic cellular conditions. Under the hypotonic conditions of the periplasm in the QS mutants, outer membrane bulging and vesiculation were observed, although these changes were rescued by knocking out the gltI gene, which encodes a glutamate transporter. Outer membrane modifications were not detected in the wild type. These results suggest that QS-dependent glutamate metabolism is critical for homeostatic osmolality. We suggest that outer membrane bulging and vesiculation might be the outcome of a physiological adaptation to relieve hypotonic osmotic stress in QS mutants. Our findings reveal how QS functions to maintain bacterial osmolality in a cooperative population.
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