IutB participates in the ferric-vulnibactin utilization system in Vibrio vulnificus M2799

作者：Kawano Hiroaki; Miyamoto Katsushiro; Negoro Miho; Zushi Eriko; Tsuchiya Takahiro; Tanabe Tomotaka; Funahashi Tatsuya; Tsujibo Hiroshi^*

来源：Biometals, 2017, 30(2): 203-216.

DOI：10.1007/s10534-017-9994-0

• Clinical isolate
• Siderophore
• Siderophore-interacting protein
• Ferric-siderophore reductase
• Aerobactin
• Desferrioxamine B

Vibrio vulnificus, an opportunistic pathogen that causes a serious, often fatal, infection in humans, requires iron for its growth. This bacterium utilizes iron from the environment via the vulnibactin-mediated iron uptake system. The mechanisms of vulnibactin biosynthesis, vulnibactin export, and ferric-vulnibactin uptake systems have been reported, whereas the ferric-vulnibactin reduction mechanism in the cell remains unclear. The results of our previous study showed that VuuB, a member of the flavin adenine dinucleotide-containing siderophore-interacting protein family, is a ferric-vulnibactin reductase, but there are other reductases that can complement for the defective vuuB. The aim of this study was to identify these proteins that can complement the loss of function of VuuB. We constructed mutants of genes encoding putative reductases in V. vulnificus M2799, and analyzed their growth under low-iron conditions. Complementation analyses confirmed that IutB, which functions as a ferric-aerobactin reductase, participates in ferric-vulnibactin reduction in the absence of VuuB. This is the first genetic evidence that ferric-vulnibactin is reduced by a member of the ferric-siderophore reductase protein family. In the aerobactin-utilization system, IutB plays a major role in ferric-aerobactin reduction in V. vulnificus M2799, and VuuB and DesB can compensate for the defect of IutB. Furthermore, the expression of iutB and desB was found to be regulated by iron and a ferric uptake regulator.

• 出版日期2017-4