Induction of acid tolerance at neutral pH in log‐phase
            <i>Escherichia coli</i>
            by medium filtrates from organisms grown at acidic pH

Rowbury,; Goodson, Michael S.

doi:10.1046/j.1472-765x.1998.00370.x

Cited by 18 publications

(24 citation statements)

References 12 publications

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“…Also, high-density acid resistance of E. coli does not appear to involve a secreted factor. For similar reasons, the phenomenon we describe is different from that reported earlier for E. coli acid habituation, which also involved an uncharacterized secreted product (41)(42)(43).…”

Section: Discussioncontrasting

confidence: 99%

Products of theEscherichia coliAcid Fitness Island Attenuate Metabolite Stress at Extremely Low pH and Mediate a Cell Density-Dependent Acid Resistance

2007

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Escherichia coli has an ability, rare among the Enterobacteriaceae, to survive extreme acid stress under various host (e.g., human stomach) and nonhost (e.g., apple cider) conditions. Previous microarray studies have exposed a cluster of 12 genes at 79 centisomes collectively called an acid fitness island (AFI). Four AFI genes, gadA, gadX, gadW, and gadE, were already known to be involved in an acid resistance system that consumes an intracellular proton through the decarboxylation of glutamic acid. However, roles for the other eight AFI gene products were either unknown or subject to conflicting findings. Two new aspects of acid resistance are described that require participation of five of the remaining eight AFI genes. YhiF (a putative regulatory protein), lipoprotein Slp, and the periplasmic chaperone HdeA protected E. coli from organic acid metabolites produced during fermentation once the external pH was reduced to pH 2.5. HdeA appears to handle protein damage caused when protonated organic acids diffuse into the cell and dissociate, thereby decreasing internal pH. In contrast, YhiF-and Slp-dependent systems appear to counter the effects of the organic acids themselves, specifically succinate, lactate, and formate, but not acetate. A second phenomenon was defined by two other AFI genes, yhiD and hdeD, encoding putative membrane proteins. These proteins participate in an acid resistance mechanism exhibited only at high cell densities (>10 8 CFU per ml). Densitydependent acid resistance does not require any demonstrable secreted factor and may involve cell contactdependent activation. These findings further define the complex physiology of E. coli acid resistance.

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Section: Discussioncontrasting

confidence: 99%

Products of theEscherichia coliAcid Fitness Island Attenuate Metabolite Stress at Extremely Low pH and Mediate a Cell Density-Dependent Acid Resistance

2007

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“…When cells are stressed with a relatively milder acidic pH, the physiology of the cells undergoes an adaptive process, known as the acid tolerance response (ATR), which is a process that facilitates enhanced production of various proteins (e.g., acid pumps, chaperones, DNA repair and membrane proteins) required to efficiently counteract acid damage and maintain viability during exposure to low pH (9,15,17,41,51). The molecular basis of the ATR has been studied extensively in Escherichia coli (44), Salmonella enterica serovar Typhimurium (16,18), and oral streptococcal species (51).…”

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confidence: 99%

Inactivation of VicK Affects Acid Production and Acid Survival of Streptococcus mutans

et al. 2009

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The regulation of acid production in and the tolerance to low pH of the cariogenic bacterium Streptococcus mutans have garnered considerable attention since both of these properties contribute substantially to the virulence of this organism. Frequent or prolonged exposure to acid end products, mainly lactic acid, that are present following the consumption of dietary sugars erodes the dental enamel, thereby initiating dental caries. Here we report the involvement of the S. mutans VicK sensor kinase in both the acidogenicity and the aciduricity of this bacterium. When cultures were supplemented with glucose, the glycolytic rate of a VicK null mutant was significantly decreased compared to the glycolytic rate of the wild type (P < 0.05), suggesting that there was impaired acid production. Not surprisingly, the VicK deletion mutant produced less lactic acid, while an acid tolerance response assay revealed that loss of VicK significantly enhanced the survival of S. mutans (P < 0.05). Compared to the survival rates of the wild type, the survival rates of the VicK-deficient mutant were drastically increased when cultures were grown at pH 3.5 with or without preexposure to a signal pH (pH 5.5). Global transcriptional analysis using DNA microarrays and S. mutans wild-type UA159 and VicK deletion mutant strains grown at neutral and low pH values revealed that loss of VicK significantly affected expression of 89 transcripts more than twofold at pH 5.5 (P < 0.001). The affected transcripts included genes with putative functions in transport and maintenance of cell membrane integrity. While our results provide insight into the acid-inducible regulon of S. mutans, here we imply a novel role for VicK in regulating intracellular pH homeostasis in S. mutans.

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“…Two findings indicate that the process inducing alkali sensitization at acidic pH described here is quite distinct from that leading to acid tolerance (Rowbury and Goodson 1998). First, alkali sensitization induction needs a low molecular weight dialysable component (Table 1) whereas acid tolerance induction by extracellular induction components does not.…”

Section: -----------------------------------------------------mentioning

confidence: 81%

“…and Goodson 1998) suggest that ideas on how inducible processes occur in bacteria may have to be re-thought. It has generally been considered that inducible processes switched on by chemical agents in bacteria involve the entry of the chemical stimulus into the cell or a cell compartment (e.g.…”

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confidence: 99%

The role of regulatory gene products in alkali sensitization by extracellular medium components in Escherichia coli

Rowbury

Hussain

1998

Letters in Applied Microbiology

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become alkali sensitized on transfer from pH 7·0 to pH 5·5 but they also secrete extracellular agents which induce alkali sensitivity when added (in neutralized filtrates) to organisms growing at pH 7·0. In contrast, filtrates from cultures grown at pH 7·0 have no effect. Filtrates were inactivated by protease but not by heat treatment in a boiling water-bath, suggesting that a very heat-stable protein is involved in alkali sensitivity induction. A heatstable low molecular weight component (or components) may also be needed for induction, or the induction protein itself may be of low molecular weight. Strains with lesions in hns, fur or himA produced almost inactive filtrates and it therefore appears that H-NS, Fur and IHF are involved in synthesis of the induction components. As the presence of protease during incubation at pH 5·5 totally abolished alkali sensitization of strain 1829 while inhibition of sensitization induction occurred if the induction components were removed by filtration or dialysis during pH 5·5 incubation, it is proposed that the extracellular induction components (EICs) are essential for the original sensitization response. These results suggest that sensitization induction occurs by a different mechanism to that which is believed to occur for most bacterial inducible response systems; these are claimed to involve exclusively intracellular reactions and components whereas the present response involves functioning of extracellular components.

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Induction of acid tolerance at neutral pH in log‐phase Escherichia coli by medium filtrates from organisms grown at acidic pH

Cited by 18 publications

References 12 publications

Products of theEscherichia coliAcid Fitness Island Attenuate Metabolite Stress at Extremely Low pH and Mediate a Cell Density-Dependent Acid Resistance

Products of theEscherichia coliAcid Fitness Island Attenuate Metabolite Stress at Extremely Low pH and Mediate a Cell Density-Dependent Acid Resistance

Inactivation of VicK Affects Acid Production and Acid Survival of Streptococcus mutans

The role of regulatory gene products in alkali sensitization by extracellular medium components in Escherichia coli

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