Affiliation:
1. Pathology Department, Division of Cell Biology and Immunology, University of Utah School of Medicine, Salt Lake City, Utah 84132-2501
Abstract
ABSTRACT
During the course of a urinary tract infection, substantial levels of nitric oxide and reactive nitrogen intermediates are generated. We have found that many uropathogenic strains of
Escherichia coli
display far greater resistance to nitrosative stress than the K-12 reference strain MG1655. By selecting and screening for uropathogenic
E. coli
transposon mutants that are unable to grow in the presence of acidified nitrite, the
cadC
gene product was identified as a key facilitator of nitrosative stress resistance. Mutation of
cadC
, or its transcriptional targets
cadA
and
cadB
, results in loss of significant production of the polyamine cadaverine and increased sensitivity to acidified nitrite. Exogenous addition of cadaverine or other polyamines rescues growth of
cad
mutants under nitrosative stress. In wild-type cells, the concentration of cadaverine produced per cell is substantially increased by exposure to acidified nitrite. The mechanism behind polyamine-mediated rescue from nitrosative stress is unclear, but it is not attributable solely to chemical quenching of reactive nitrogen species or reduction in mutation frequency.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Reference30 articles.
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