Abstract
The hemorrhagic septicemic disease vibriosis caused by Vibrio anguillarum shows noticeable similarities to invasive septicemia in humans, and in this case, the V. anguillarum–host system has the potential to serve as a model for understanding native eukaryotic host–pathogen interactions. Iron acquisition, as a fierce battle occurring between pathogenic V. anguillarum and the fish host, is a pivotal step for virulence. In this article, advances in defining the roles of iron uptake pathways in growth and virulence of V. anguillarum have been summarized, divided into five aspects, including siderophore biosynthesis and secretion, iron uptake, iron release, and regulation of iron uptake. Understanding the molecular mechanisms of iron acquisition will have important implications for the pathogenicity of this organism.
Highlights
The Gram-negative bacterium Vibrio anguillarum is a pathogen that causes vibriosis with lethal hemorrhagic septicemia in aquatic animals worldwide (Toranzo et al, 2005)
V. anguillarum, like most other organisms, has an absolute requirement for iron to synthesize a large number of crucial enzymes, which are involved in many fundamental cellular processes, such as cytochromes for cell respiration, ribonucleotide reductase for the biosynthesis of DNA precursors, and enzymes for the tricarboxylic acid (TCA) cycle (Crosa et al, 2004)
We describe the developments in understanding the molecular mechanisms of iron acquisition systems in V. anguillarum, divided into the following aspects: siderophore biosynthesis and secretion, iron uptake, iron release, and regulation of iron uptake
Summary
The Gram-negative bacterium Vibrio anguillarum is a pathogen that causes vibriosis with lethal hemorrhagic septicemia in aquatic animals worldwide (Toranzo et al, 2005). One is mediated by a 65 kb pJM1 plasmid, which contains most of the genes encoding for biosynthesis and transport proteins of the siderophore anguibactin (Naka et al, 2013b).
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