ABSTRACT
The major aetiological agent of human bacterial meningitis is Neisseria meningitidis. During the course of disease and host colonization, the bacterium has to withstand limited oxygen availability. Nitrogen oxide and nitrogen oxyanions are thought to be present, which may constitute an alternative sink for electrons from the N. meningitidis respiratory chain. A partial denitrification pathway is encoded by the aniA nitrite reductase gene and the norB nitric oxide reductase gene. Analysis of the completed genome sequences of two N. meningitidis strains is used to generate a model for the membrane-associated respiratory chain of this organism. Analysis of aniA expression indicates it to be controlled primarily by oxygen and secondarily by nitrite. The ability of N. meningitidis to denitrify relies on microaerobic growth conditions. Here we show that under microaerobic conditions nitrite supplements oxygen as an alternative respiratory substrate.
Subject(s)
Aerobiosis , Neisseria meningitidis/metabolism , Nitrites/metabolism , Antigens, Bacterial/physiology , Bacterial Outer Membrane Proteins/physiology , Genome, Bacterial , Neisseria meningitidis/genetics , Neisseria meningitidis/growth & developmentABSTRACT
A lacZ-based reporter gene system was used to identify the promoter of the Campylobacter jejuni iron-responsive gene regulator Fur. In other Gram-negative bacteria, the fur promoter is usually located directly upstream of the fur gene and is often autoregulated in response to iron. In this study we demonstrate that expression of the C. jejuni fur gene is controlled from two promoters located in front of the first and second open reading frames upstream of fur. Neither of these promoters was iron-regulated, and the presence of both promoters in front of fur gives higher expression of the lacZ reporter than with either promoter alone. Expression from two distal promoters might be a mechanism for regulating the level of the C. jejuni Fur protein in response to unknown stimuli.