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J Bacteriol. 2016 Sep 9;198(19):2662-72. doi: 10.1128/JB.00030-16. Print 2016 Oct 1.

The UbiI (VisC) Aerobic Ubiquinone Synthase Is Required for Expression of Type 1 Pili, Biofilm Formation, and Pathogenesis in Uropathogenic Escherichia coli.

Author information

1
Department of Pathology, Microbiology & Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
2
Department of Chemical and Biomolecular Engineering, Vanderbilt University, Tennessee, USA.
3
Department of Molecular, Cellular & Developmental Biology, University of Michigan-Ann Arbor, Ann Arbor, Michigan, USA.
4
Department of Molecular Microbiology & Microbial Pathogenesis, Washington University School of Medicine in Saint Louis, St. Louis, Missouri, USA.
5
Department of Pathology, Microbiology & Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA maria.hadjifrangiskou@vanderbilt.edu.

Abstract

Uropathogenic Escherichia coli (UPEC), which causes the majority of urinary tract infections (UTI), uses pilus-mediated adherence to initiate biofilm formation in the urinary tract. Oxygen gradients within E. coli biofilms regulate expression and localization of adhesive type 1 pili. A transposon mutant screen for strains defective in biofilm formation identified the ubiI (formerly visC) aerobic ubiquinone synthase gene as critical for UPEC biofilm formation. In this study, we characterized a nonpolar ubiI deletion mutant and compared its behavior to that of wild-type bacteria grown under aerobic and anoxic conditions. Consistent with its function as an aerobic ubiquinone-8 synthase, deletion of ubiI in UPEC resulted in reduced membrane potential, diminished motility, and reduced expression of chaperone-usher pathway pili. Loss of aerobic respiration was previously shown to negatively impact expression of type 1 pili. To determine whether this reduction in type 1 pili was due to an energy deficit, wild-type UPEC and the ubiI mutant were compared for energy-dependent phenotypes under anoxic conditions, in which quinone synthesis is undertaken by anaerobic quinone synthases. Under anoxic conditions, the two strains exhibited wild-type levels of motility but produced diminished numbers of type 1 pili, suggesting that the reduction of type 1 pilus expression in the absence of oxygen is not due to a cellular energy deficit. Acute- and chronic-infection studies in a mouse model of UTI revealed a significant virulence deficit in the ubiI mutant, indicating that UPEC encounters enough oxygen in the bladder to induce aerobic ubiquinone synthesis during infection.

IMPORTANCE:

The majority of urinary tract infections are caused by uropathogenic E. coli, a bacterium that can respire in the presence and absence of oxygen. The bladder environment is hypoxic, with oxygen concentrations ranging from 4% to 7%, compared to 21% atmospheric oxygen. This work provides evidence that aerobic ubiquinone synthesis must be engaged during bladder infection, indicating that UPEC bacteria sense and use oxygen as a terminal electron acceptor in the bladder and that this ability drives infection potential despite the fact that UPEC is a facultative anaerobe.

PMID:
27161114
PMCID:
PMC5019064
DOI:
10.1128/JB.00030-16
[Indexed for MEDLINE]
Free PMC Article

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