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Linkage between Catecholate Siderophores and the Multicopper Oxidase CueO in Escherichia coli. Gregor Grass, 2004.The multicopper oxidase CueO had previously been demonstrated to exhibit phenoloxidase activity and was implicated in intrinsic copper resistance in Escherichia coli . Catecholates can potentially reduce Cu(II) to the prooxidant Cu(I) . In this report we provide evidence that CueO protects E . coli cells by oxidizing enterobactin, the catechol iron siderophore of E . coli, in the presence of copper . In vitro, a mixture of enterobactin and copper was toxic for E . coli cells, but the addition of purified CueO led to their survival . Deletion of fur resulted in copper hypersensitivity that was alleviated by additional deletion of entC, preventing synthesis of enterobactin . In addition, copper added together with 2,3-dihydroxybenzoic acid or enterobactin was able to induce a  (cueO-lacZ)
operon fusion more efficiently than copper alone . The reaction
product of the 2,3-dihydroxybenzoic acid oxidation by CueO that can
complex Cu(II) ions was determined by gas chromatography-mass
spectroscopy and identified as 2-carboxymuconate .
Altered Susceptibility of Candida glabrata Bloodstream Isolates to Triazoles at Clinically Relevant pH Values: Comparison of the NCCLS M27-A2, Sensititre YeastOne, and Etest Methods. Manjunath P. Pai, 2004.We studied the MICs of triazoles against 15 Candida glabrata clinical isolates by the NCCLS M27-A2, Sensititre YeastOne, and Etest methods by using media at pHs 6.0, 7.0, and 7.4 . Thirteen isolates were less susceptible to triazoles at pH 6.0 and more susceptible to triazoles at pH 7.4 compared to pH 7.0 . rpoS Mutations and Loss of General Stress Resistance in Escherichia coli Populations as a Consequence of Conflict between Competing Stress Responses. Lucinda Notley-McRobb, 2002.The general stress resistance of Escherichia coli is controlled by the RpoS sigma factor (  S), but mutations in rpoS are surprisingly common in natural and laboratory populations . Evidence for the selective advantage of losing rpoS was obtained from experiments with nutrient-limited bacteria at different growth rates . Wild-type bacteria were rapidly displaced by rpoS mutants in both glucose- and nitrogen-limited chemostat populations . Nutrient limitation led to selection and sweeps of rpoS null mutations and loss of general stress resistance . The rate of takeover by rpoS mutants was most rapid (within 10 generations of culture) in slower-growing populations that initially express higher
S levels . Competition for core RNA polymerase is the likeliest explanation for reduced expression from distinct promoters dependent on
70 and involved in the hunger response to nutrient limitation . Indeed, the mutation of rpoS led to significantly higher expression of genes contributing to the high-affinity glucose scavenging system required for the hunger response . Hence, rpoS polymorphism in E . coli populations may be viewed as the result of competition between the hunger response, which requires sigma factors other than
S for expression, and the maintenance of the ability to withstand external stresses . The extent of external stress significantly influences the spread of rpoS mutations . When acid stress was simultaneously applied to glucose-limited cultures, both the phenotype and frequency of rpoS mutations were attenuated in line with the level of stress . The conflict between the hunger response and maintenance of stress resistance is a potential weakness in bacterial regulation .
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