Resistance in Escherichia coli

Escheridia coli cells with a disrupted copA gene exhibit decreased resistance to copper. This apparent copper sensitivity could be complemented by introduction of a plasmid expressing ecCopA or CopB of En. hirae. Coj A-disrupted strains were still relatively resistant to copper salts, which can be attributed to other genes involved in copper tolerance in Es. coli (Silver and Phung, 1996). However, these other functions that participate in copper resistance are still largely unclear. 

ATP-dependent uptake of copper into everted membrane vesicles from cells expressing ecCopA could be demonstrated. Transport was inhibited by the classical P-type ATPase inhibitor vanadate. Dithiothreitol, a strong reductant, was required for ecCopA-catalyzed Cu uptake, suggesting that the substrate of ecCopA is Cu(l). Thus the function of ecCopA resembles that of the En. hirae CopB ATPase by functioning as a copper efflux pump in vivo when excess copper is present in the cytoplasm (Rensing et al., 2000). 

The copper-inducible regulator CueR, which activates the transcription of the ecCopA copper efflux system, has recently been identihed in 

The promoters of ecCopA and YacK are apparently regulated by CueR. Both copper and silver are inducers, but not zinc or mercury. The loss of copper activation at both promoters in the cueR deletion strain can be rescued by complementing it with a plasmid carrying the gene. Interaction between CueR and the ecCopA promoter has been shown with a DNase I protection assay. It showed that CueR binds in vitro to a sequence with dyad symmetry within a 19-spacer sequence in the promoter (Stoyanov et al., 2001). CueR is thus the primary copper-responsive activator of the ecCopA copper efflux system of Es. coli. 

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Multiresistant Escherichia coli have been selected by the use of broad-spectrum antimicrobials in both livestock and humans (36). The development of antimicrobial resistance in Escherichia coli creates problems due to the high propensity of these bacteria to disseminate antimicrobial resistance genes. Resistance genes have been traced from Escherichia coli in animals to Escherichia coli in humans. Escherichia coli 0157 H7 has been recently recognized as an important human pathogen (37). lire mode of its transmission is primarily through the food, but person-to-person transmission has been also identified in some day-care center and nursing home outbreaks (38). 

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S ATP + hygromycin B <1> (<1> responsible for resistance against hygromycin B, an aminocyclitol antibiotic [1] resistance to hygromycin B also occurs in Escherichia coli, where a plasmid encodes a hygromycin B phos-... 

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Her research interests originally focused on biological cell membranes, first working on phosphate transport in Escherichia coli and then the plasma membrane proton ATPase in Saccharomyces cerevisiae. While isolating vanadate-resistant mutants in yeast, she became fascinated with work showing that oral administration of vanadium salts alleviated symptoms of diabetes and switched her research focus to that area. She has pursued the insulin-enhancing mechanism of vanadium salts and complexes in cell culture, the STZ-induced diabetic rat, and human type 2 diabetic patients. The National Institutes of Health, the American Heart Association, and the American Diabetes Association have funded the work in her laboratory. Willsky has lectured all around the world and published both research articles and book chapters in this area. 

Multicopy plasmids offer a limited, but still instructive comparison. Plasmids are replicating clusters of genes in bacteria. Under certain conditions they confer beneficial traits (such as resistance against antibiotics) on the bacterial host. They can also be passed on by conjugation between cells. A well elucidated mechanism of copy number control of abundant plasmids relies on a frans-acting inhibitor and czs-acting activator. For example, the ColE 1 plasmid in Escherichia coli blocks the action of the RNA primer (activator) by... 

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