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Laboratoire des Interactions Plantes Pathogènes UMR 217 INRA/UMPC/AgroParisTech, 16 rue Claude Bernard 75005 Paris, France; Isotopenlabor der TNF, Universität zu Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany; Institut für Physik, Universität zu Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany; Unité de Microbiologie et Genetique, UMR CNRS/INSA/UCB 5122, 69622 Villeurbanne, France; Laboratoire d'Ingénierie des Protéines et Contrôle Métabolique Institut Jacques Monod/CNRS/Universités Paris 6 & 7, 2 place Jussieu 75251 Paris cedex 05, France
* To whom correspondence should be addressed. Email: franza{at}inapg.fr.
| Abstract |
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During infection the phytopathogenic enterobacterium E. chrysanthemi has to cope with iron limiting conditions and production of reactive oxygen species by plant cells. Previous studies have shown that a tight control of the bacterial intracellular iron content is necessary for full virulence. E. chrysanthemi genome possesses two loci that could be devoted to iron storage: the bfr gene encoding a haem-containing bacterioferritin and the ftnA gene coding for a paradigmatic ferritin. To assess the role of these proteins in the physiology of this pathogen, we constructed ferritin deficient mutants by reverse genetics. Unlike the bfr mutant, the ftnA mutant had increased sensitivity to iron deficiency and to redox stress conditions. Interestingly, the bfr ftnA mutant displayed an intermediate phenotype for the sensitivity to these stresses. Whole cell analysis by Mössbauer spectrocopy showed that the main iron storage protein is FtnA and that there is an increase in the ferrous/ferric iron ratio in the ftnA and bfr ftnA mutants. We found that the ftnA gene expression is positively controlled by iron and the transcriptional repressor Fur via the small antisens RNA RyhB. bfr gene expression is induced at the stationary phase of growth. The sigmaS transcriptional factor is necessary for this control. Pathogenicity tests showed that the FtnA ferritin and the Bfr bacterioferritin contribute differentialy to the virulence of E. chrysanthemi depending on the host indicating the importance of a perfect control of iron homeostasis in this bacterial species during infection.
| Appl. Environ. Microbiol. | Infect. Immun. | Eukaryot. Cell |
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| Mol. Cell. Biol. | J. Virol. | Microbiol. Mol. Biol. Rev. |
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