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

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 ac...

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Published inJournal of bacteriology Vol. 201; no. 2
Main Authors Orr, James S, Christensen, David G, Wolfe, Alan J, Rao, Christopher V
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 15.01.2019
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Abstract 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.
AbstractList 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.
Escherichia coli produces acetate during aerobic growth on various carbon sources. After consuming the carbon substrate, E. coli 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 E. coli 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 Escherichia coli during aerobic growth on sugars. In E. coli , 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. Escherichia coli produces acetate during aerobic growth on various carbon sources. After consuming the carbon substrate, E. coli 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 E. coli 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. IMPORTANCE Many microorganisms produce fermentation products during aerobic growth on sugars. One of the best-known examples is the production of acetate by Escherichia coli during aerobic growth on sugars. In E. coli , 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.
Many microorganisms produce fermentation products during aerobic growth on sugars. One of the best-known examples is the production of acetate by Escherichia coli during aerobic growth on sugars. In E. coli , 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. ABSTRACT Escherichia coli produces acetate during aerobic growth on various carbon sources. After consuming the carbon substrate, E. coli 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 E. coli 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. IMPORTANCE Many microorganisms produce fermentation products during aerobic growth on sugars. One of the best-known examples is the production of acetate by Escherichia coli during aerobic growth on sugars. In E. coli , 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.
Author Wolfe, Alan J
Christensen, David G
Orr, James S
Rao, Christopher V
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10.1128/AEM.03034-16
10.1128/jb.178.21.6238-6249.1996
10.1128/MMBR.69.1.12-50.2005
10.1038/msb4100050
10.1007/s10295-007-0244-2
10.1093/oxfordjournals.jbchem.a124616
10.1002/bit.260470103
10.1128/JB.185.21.6448-6455.2003
10.1002/0471142727.mb0117s79
10.1021/bp050073s
10.1111/j.1365-2958.2008.06186.x
10.1073/pnas.120163297
10.1016/j.molcel.2013.06.003
10.1042/BJ20130412
10.1016/0003-9861(75)90002-8
10.1371/journal.pone.0094816
10.1074/jbc.274.3.1745
10.1093/nar/gki108
10.1073/pnas.85.6.1888
10.1093/nar/29.9.e45
10.1038/nmeth.1318
10.1016/j.mib.2010.01.002
10.1016/j.ymben.2004.05.001
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Citation Orr JS, Christensen DG, Wolfe AJ, Rao CV. 2019. Extracellular acidic pH inhibits acetate consumption by decreasing gene transcription of the tricarboxylic acid cycle and the glyoxylate shunt. J Bacteriol 201:e00410-18. https://doi.org/10.1128/JB.00410-18.
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References Vazquez A (e_1_3_3_2_2) 2017
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References_xml – ident: e_1_3_3_8_2
  doi: 10.1016/j.tibtech.2006.09.001
– volume-title: Overflow metabolism: from yeast to marathon runners
  year: 2017
  ident: e_1_3_3_2_2
  contributor:
    fullname: Vazquez A
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  doi: 10.1128/AEM.03034-16
– ident: e_1_3_3_17_2
  doi: 10.1128/jb.178.21.6238-6249.1996
– ident: e_1_3_3_3_2
  doi: 10.1128/MMBR.69.1.12-50.2005
– ident: e_1_3_3_22_2
  doi: 10.1038/msb4100050
– ident: e_1_3_3_7_2
  doi: 10.1007/s10295-007-0244-2
– ident: e_1_3_3_15_2
  doi: 10.1093/oxfordjournals.jbchem.a124616
– ident: e_1_3_3_19_2
  doi: 10.1002/bit.260470103
– ident: e_1_3_3_12_2
  doi: 10.1128/JB.185.21.6448-6455.2003
– ident: e_1_3_3_21_2
  doi: 10.1002/0471142727.mb0117s79
– ident: e_1_3_3_10_2
  doi: 10.1021/bp050073s
– ident: e_1_3_3_20_2
  doi: 10.1111/j.1365-2958.2008.06186.x
– ident: e_1_3_3_23_2
  doi: 10.1073/pnas.120163297
– ident: e_1_3_3_5_2
  doi: 10.1016/j.molcel.2013.06.003
– ident: e_1_3_3_13_2
  doi: 10.1042/BJ20130412
– ident: e_1_3_3_11_2
  doi: 10.1016/0003-9861(75)90002-8
– ident: e_1_3_3_4_2
  doi: 10.1371/journal.pone.0094816
– ident: e_1_3_3_14_2
  doi: 10.1074/jbc.274.3.1745
– ident: e_1_3_3_26_2
  doi: 10.1093/nar/gki108
– ident: e_1_3_3_16_2
  doi: 10.1073/pnas.85.6.1888
– ident: e_1_3_3_25_2
  doi: 10.1093/nar/29.9.e45
– ident: e_1_3_3_24_2
  doi: 10.1038/nmeth.1318
– ident: e_1_3_3_6_2
  doi: 10.1016/j.mib.2010.01.002
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Snippet produces acetate during aerobic growth on various carbon sources. After consuming the carbon substrate, can further grow on the acetate. This phenomenon is...
Many microorganisms produce fermentation products during aerobic growth on sugars. One of the best-known examples is the production of acetate by Escherichia...
Escherichia coli produces acetate during aerobic growth on various carbon sources. After consuming the carbon substrate, E. coli can further grow on the...
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SubjectTerms 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
Title Extracellular Acidic pH Inhibits Acetate Consumption by Decreasing Gene Transcription of the Tricarboxylic Acid Cycle and the Glyoxylate Shunt
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