Extracellular Acidic pH Inhibits Acetate Consumption by Decreasing Gene Transcription of the Tricarboxylic Acid Cycle and the Glyoxylate Shunt

• Published in: Journal of bacteriology Vol. 201; no. 2
• Main Authors: Orr, James S, Christensen, David G, Wolfe, Alan J, Rao, Christopher V
• Format: Journal Article
• Language: English
• Published: United States American Society for Microbiology 15.01.2019
• Subjects: Acetates - metabolism; Acetic acid; Adaptation, Physiological; Aerobiosis; Amino acids; Bacteriology; BASIC BIOLOGICAL SCIENCES; Carbon; Carbon sources; Catabolism; Citric Acid Cycle - drug effects; Consumption; Culture Media - chemistry; E coli; Environmental Exposure; Escherichia coli - drug effects; Escherichia coli - growth & development; Escherichia coli - metabolism; Gene expression; Gene Expression Regulation, Bacterial - drug effects; Genes; Glucose; Glucose - metabolism; Glyoxylates - metabolism; Hydrogen-Ion Concentration; Magnesium; Microbiology; Microorganisms; Mutants; pH effects; Substrates; Sugar; Transcription; Transcription, Genetic - drug effects; Tricarboxylic acid cycle; acetate; carbon metabolism; Escherichia coli
• ISSN: 0021-9193; 1098-5530
• DOI: 10.1128/JB.00410-18

produces acetate during aerobic growth on various carbon sources. After consuming the carbon substrate, can further grow on the acetate. This phenomenon is known as the acetate switch, where cells transition from producing acetate to consuming it. In this study, we investigated how pH governs the acetate switch. When was grown on a glucose-supplemented medium initially buffered to pH 7, the cells produced and then consumed the acetate. However, when the initial pH was dropped to 6, the cells still produced acetate but were only able to consume it when little (<10 mM) acetate was produced. When significant acetate was produced in acidic medium, which occurs when the growth medium contains magnesium, amino acids, and sugar, the cells were unable to consume the acetate. To determine the mechanism, we characterized a set of metabolic mutants and found that those defective in the tricarboxylic acid (TCA) cycle or glyoxylate shunt exhibited reduced rates of acetate consumption. We further found that the expression of the genes in these pathways was reduced during growth in acidic medium. The expression of the genes involved in the AckA-Pta pathway, which provides the principal route for both acetate production and consumption, was also inhibited in acidic medium but only after glucose was depleted, which correlates with the acetate consumption phase. On the basis of these results, we conclude that growth in acidic environments inhibits the expression of the acetate catabolism genes, which in turn prevents acetate consumption. Many microorganisms produce fermentation products during aerobic growth on sugars. One of the best-known examples is the production of acetate by during aerobic growth on sugars. In , acetate production is reversible: once the cells consume the available sugar, they can consume the acetate previously produced during aerobic fermentation. We found that pH affects the reversibility of acetate production. When the cells produce significant acetate during growth in acidic environments, they are unable to consume it. Unconsumed acetate may accumulate in the cell and inhibit the expression of pathways required for acetate catabolism. These findings demonstrate how acetate alters cell metabolism; they also may be useful for the design of aerobic fermentation processes.