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Interplay of cellular cAMP levels, ^S activity and oxidative stress resistance in Escherichia coli

¹ Department Chemie, Biotechnologie, Technische Universitaet Muenchen;
² Department of Molecular, Cellular and Developmental Biology, University of Michigan;
³ Deutsches Krebsforschungszentrum, Department Cell Cycle Control and Carcinogenesis;
⁴ Technische Universitaet Muenchen

ABSTRACT

Hypochlorous acid (HOCl), the active ingredient of household bleach, functions as powerful antimicrobial that is used not only in numerous industrial applications but also in the mammalian host defense. Here we show that multicopy expression of cpdA, encoding the cAMP phosphodiesterase, leads to a dramatically increased resistance of E. coli to HOCl stress as well as to the unrelated hydrogen peroxide (H2O2) stress. This general oxidative stress resistance is apparently caused by the CpdA-mediated decrease in cellular cAMP levels, which leads to the partial inactivation of the global transcriptional regulator CRP. Down regulation of CRP in turn causes the de-repression of rpoS, encoding the alternative sigma factor S, which activates the general stress response in E. coli. We found that these highly oxidative stress resistant cells have a substantially increased capacity to combat HOCl-mediated insults and to degrade reactive oxygen species. Mutational analysis revealed that the DNA protecting protein, Dps, the catalase, KatE, and the exonuclease III, XthA, play the predominant roles in conferring the high resistance of rpoS overexpressing strains towards HOCl and H2O2 stress. Our results demonstrate the close regulatory interplay between cellular cAMP levels, S activity and oxidative stress resistance in E. coli.

⁵ E-mail: jeannette.winter{at}ch.tum.de