Brem D, Pelludat C, Rakin A, Jacobi C A, Heesemann J
Max von Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie, Pettenkoferstr. 9a, 80336 München, Germany1.
Microbiology (Reading). 2001 May;147(Pt 5):1115-1127. doi: 10.1099/00221287-147-5-1115.
Yersinia enterocolitica O:8, biogroup (BG) IB, strain WA-C carries a high-pathogenicity island (HPI) including iron-repressible genes (irp1-9, fyuA) for biosynthesis and uptake of the siderophore yersiniabactin (Ybt). The authors report the functional analysis of irp6,7,8, which show 98-99% similarity to the corresponding genes ybtP,Q,X on the HPI of Yersinia pestis. It was demonstrated that irp6,7 are involved in ferric (Fe)-Ybt utilization and mouse virulence of Y. enterocolitica, thus confirming corresponding results for Y. pestis. Additionally it was shown that inactivation of the ampG-like gene irp8 did not affect either Fe-Ybt utilization or mouse virulence. To determine whether irp6, irp7 and fyuA (encoding the outer-membrane Fe-Ybt/pesticin receptor FyuA) are sufficient to mediate Fe-Ybt transport/utilization, these genes were transferred into Escherichia coli entD,F and into non-pathogenic Y. enterocolitica, BG IA, strain NF-O. Surprisingly, E. coli entD,F but not Y. enterocolitica NF-O gained the capability to utilize exogenous Fe-Ybt as a result of this gene transfer, although both strains expressed functional FyuA (pesticin sensitivity). These results suggest that besides irp6, irp7 and fyuA, additional genes are required for sufficient Fe-Ybt transport/utilization. Finally, it was shown that irp6, irp7 and fyuA but not irp8 are involved in controlling Ybt biosynthesis and fyuA gene expression: irp6 and/or irp7 mutation leads to upregulation whereas fyuA mutation leads to downregulation. However, fyuA-dependent control of Ybt biosynthesis could be bypassed in a fyuA mutant by ingredients of chrome azurol S (CAS) siderophore indicator agar.
小肠结肠炎耶尔森菌O:8，生物群（BG）IB，WA - C菌株携带一个高致病性岛（HPI），其中包括用于耶尔森菌素（Ybt）生物合成和摄取的铁抑制基因（irp1 - 9，fyuA）。作者报告了irp6、7、8的功能分析，这些基因与鼠疫耶尔森菌HPI上的相应基因ybtP、Q、X具有98 - 99%的相似性。结果表明，irp6、7参与小肠结肠炎耶尔森菌的铁（Fe）- Ybt利用和小鼠毒力，从而证实了鼠疫耶尔森菌的相应结果。此外，研究表明，类ampG基因irp8的失活既不影响Fe - Ybt利用，也不影响小鼠毒力。为了确定irp6、irp7和fyuA（编码外膜Fe - Ybt/鼠疫菌素受体FyuA）是否足以介导Fe - Ybt转运/利用，将这些基因转入大肠杆菌entD、F和非致病性小肠结肠炎耶尔森菌BG IA菌株NF - O。令人惊讶的是，尽管两种菌株都表达功能性FyuA（鼠疫菌素敏感性），但基因转移后，大肠杆菌entD、F获得了利用外源性Fe - Ybt的能力，而非致病性小肠结肠炎耶尔森菌NF - O却没有。这些结果表明，除了irp6、irp7和fyuA外，还需要其他基因才能实现充分的Fe - Ybt转运/利用。最后，研究表明，irp6、irp7和fyuA而非irp8参与控制Ybt生物合成和fyuA基因表达：irp6和/或irp7突变导致上调，而fyuA突变导致下调。然而，在fyuA突变体中，铬天青S（CAS）铁载体指示琼脂的成分可以绕过fyuA对Ybt生物合成的依赖性控制。
