Properties of an L‐glutamate‐induced acid tolerance response which involves the functioning of extracellular induction components

Rowbury, R. J.; Humphrey, T. J.; Goodson, Margaret

doi:10.1046/j.1365-2672.1999.00676.x

Cited by 19 publications

(13 citation statements)

References 19 publications

(33 reference statements)

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“…AstE hydrolyzes N 2 -succinylglutamate into succinate and L-glutamate. L-glutamate has been identified to be involved in acid stress response in E. coli [53], [54]. Recent studies have demonstrated that n-butanol response in Lactobacillus brevis [55] downregulated the acid stress response significantly (Winkler and Kao, manuscript submitted).…”

Section: Resultsmentioning

confidence: 99%

Genomic Library Screens for Genes Involved in n-Butanol Tolerance in Escherichia coli

2011

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Backgroundn-Butanol is a promising emerging biofuel, and recent metabolic engineering efforts have demonstrated the use of several microbial hosts for its production. However, most organisms have very low tolerance to n-butanol (up to 2% (v/v)), limiting the economic viability of this biofuel. The rational engineering of more robust n-butanol production hosts relies upon understanding the mechanisms involved in tolerance. However, the existing knowledge of genes involved in n-butanol tolerance is limited. The goal of this study is therefore to identify E. coli genes that are involved in n-butanol tolerance.Methodology/Principal FindingsUsing a genomic library enrichment strategy, we identified approximately 270 genes that were enriched or depleted in n-butanol challenge. The effects of these candidate genes on n-butanol tolerance were experimentally determined using overexpression or deletion libraries. Among the 55 enriched genes tested, 11 were experimentally shown to confer enhanced tolerance to n-butanol when overexpressed compared to the wild-type. Among the 84 depleted genes tested, three conferred increased n-butanol resistance when deleted. The overexpressed genes that conferred the largest increase in n-butanol tolerance were related to iron transport and metabolism, entC and feoA, which increased the n-butanol tolerance by 32.8±4.0% and 49.1±3.3%, respectively. The deleted gene that resulted in the largest increase in resistance to n-butanol was astE, which enhanced n-butanol tolerance by 48.7±6.3%.Conclusions/SignificanceWe identified and experimentally verified 14 genes that decreased the inhibitory effect of n-butanol tolerance on E. coli. From the data, we were able to expand the current knowledge on the genes involved in n-butanol tolerance; the results suggest that an increased iron transport and metabolism and decreased acid resistance may enhance n-butanol tolerance. The genes and mechanisms identified in this study will be helpful in the rational engineering of more robust biofuel producers.

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Section: Resultsmentioning

confidence: 99%

Genomic Library Screens for Genes Involved in n-Butanol Tolerance in Escherichia coli

2011

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“…Previous studies have shown that phosphate and cAMP help in acid adaptation (Rowbury et al . ). It is possible that the reduced concentrations of the hydroxylamine in the pH 3·6 cells could be the result of its conversion to ammonium by hydroxylamine reductase (Bernheim and Hochstein ).…”

Section: Discussionmentioning

confidence: 97%

Acid stress induces differential accumulation of metabolites inEscherichia coliO26:H11

2018

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Shiga toxin producing non-O157 E. coli strains such as E. coli O26 are responsible for a growing number of food-related illnesses in the United States and around the world. From food production to consumption, micro-organisms in foods experience dramatic pH fluctuations by organic acids introduced either during food processing or by inorganic acids in the stomach. Acid exposure induces specific metabolite accumulation in bacterial cells. Understanding the survival mechanisms of pathogenic micro-organisms by studying the metabolome would be helpful in introducing effective hurdles and thus ensuring food safety.

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“…These results indicate that rpoS deficiency in HEC-RM did not affect acid resistance when they were adapted under moderate acid condition. Although rpoS is a regulatory gene involved in acid resistance, E. coli has two other non-rpoSdependent acid resistance mechanisms enhanced by either glutamate or arginine, which are associated with the consumption of protons by decarboxylase systems when these amino acids are present in the growth medium (13,24,33). TSB contains both amino acids; therefore, the activities of these two nonrpoS-dependent systems probably account for the observation that the rpoS-deficient mutant still possessed acid resistance in simulated gastric fluid by prior exposure to moderate acid condition.…”

Section: Resultsmentioning

confidence: 99%

Adaptation of Escherichia coli O157:H7 to pH Alters Membrane Lipid Composition, Verotoxin Secretion, and Resistance to Simulated Gastric Fluid Acid

Yuk

Marshall

2004

Appl Environ Microbiol

140

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The influence of adaptation to pH (from pH 5.0 to 9.0) on membrane lipid composition, verotoxin concentration, and resistance to acidic conditions in simulated gastric fluid (SGF) (pH 1.5, 37°C) was determined for Escherichia coli O157:H7 (HEC, ATCC 43895), an rpoS-deficient mutant of ATCC 43895 (HEC-RM, FRIK 816-3), and nonpathogenic E. coli (NPEC, ATCC 25922). Regardless of the strain, D values (in SGF) of acid-adapted cells were higher than those of non-acid-adapted cells, with HEC adapted at pH 5.0 having the greatest D value, i.e., 25.6 min. Acid adaptation increased the amounts of palmitic acid (C16:0) and decreased cis-vaccenic acid (C18:17c) in the membrane lipids of all strains. The ratio of cis-vaccenic acid to palmitic acid increased at acidic pH, causing a decrease in membrane fluidity. HEC adapted to pH 8.3 and HEC-RM adapted to pH 7.3 exhibited the greatest verotoxin concentrations (2,470 and 1,460 ng/ml, respectively) at approximately 10 8 CFU/ml. In addition, the ratio of extracellular to intracellular verotoxin concentration decreased at acidic pH, possibly due to the decrease of membrane fluidity. These results suggest that while the rpoS gene does not influence acid resistance in acid-adapted cells it does confer decreased membrane fluidity, which may increase acid resistance and decrease verotoxin secretion.

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Properties of an L‐glutamate‐induced acid tolerance response which involves the functioning of extracellular induction components

Cited by 19 publications

References 19 publications

Genomic Library Screens for Genes Involved in n-Butanol Tolerance in Escherichia coli

Genomic Library Screens for Genes Involved in n-Butanol Tolerance in Escherichia coli

Acid stress induces differential accumulation of metabolites inEscherichia coliO26:H11

Adaptation of Escherichia coli O157:H7 to pH Alters Membrane Lipid Composition, Verotoxin Secretion, and Resistance to Simulated Gastric Fluid Acid

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