SummaryFerritins are multimeric iron storage proteins encoded by a four-member gene family in Arabidopsis (AtFer1-4). To investigate whether iron sequestration in ferritins is a part of an iron-withholding defense system induced in response to bacterial invasion, we used Arabidopsis thaliana as a susceptible host for the pathogenic bacterium Erwinia chrysanthemi. In this study, we used a T-DNA insertion mutant line to show that the lack of a functional AtFer1 gene resulted in an enhanced susceptibility of Arabidopsis plants to E. chrysanthemi. We found that the AtFer1 gene is upregulated during infection, with a biphasic accumulation of the transcript at critical time points 0.5 and 24 h post-infection (p.i.). The activation of AtFer1 expression observed at 24 h p.i. was independent of the iron-dependent regulatory sequence (IDRS) known to mediate the transcriptional response of the AtFer1 gene to iron excess and to nitric oxide. Upregulation of AtFer1 gene expression was compromised after inoculation with an E. chrysanthemi siderophore null mutant. Infiltration of the purified siderophores chrysobactin and desferrioxamine strongly increased AtFer1 transcript abundance and it did not occur with the iron-loaded forms of these siderophores. We found that neither oxidative stress nor nitric oxide was involved in the plant response to chrysobactin. Our data show that ferritin accumulation during infection of Arabidopsis by E. chrysanthemi is a basal defense mechanism which is mainly activated by bacterial siderophores. The potential role of siderophores in this process is discussed.

Iron is an essential element for most living organisms, and pathogens are likely to compete with their hosts for the acquisition of this element. The bacterial plant pathogen Dickeya dadantii has been shown to require its siderophore-mediated iron uptake system for systemic disease progression on several host plants, including Arabidopsis thaliana. In this study, we investigated the effect of the iron status of Arabidopsis on the severity of disease caused by D. dadantii. We showed that symptom severity, bacterial fitness and the expression of bacterial pectate lyase-encoding genes were reduced in iron-deficient plants. Reduced symptoms correlated with enhanced expression of the salicylic acid defence plant marker gene PR1. However, levels of the ferritin coding transcript AtFER1, callose deposition and production of reactive oxygen species were reduced in iron-deficient infected plants, ruling out the involvement of these defences in the limitation of disease caused by D. dadantii. Disease reduction in iron-starved plants was also observed with the necrotrophic fungus Botrytis cinerea. Our data demonstrate that the plant nutritional iron status can control the outcome of an infection by acting on both the pathogen's virulence and the host's defence. In addition, iron nutrition strongly affects the disease caused by two soft rot-causing plant pathogens with a large host range. Thus, it may be of interest to take into account the plant iron status when there is a need to control disease without compromising crop quality and yield in economically important plant species.