Nitrogen (N) is essential for life and is a major limiting factor of plant growth. Because soils frequently lack sufficient N, large quantities of inorganic N fertilizers are added to soils for crop production. However, nitrate, urea, and ammonium are a major source of global pollution, because much of the N that is not taken up by plants enters streams, groundwater, and lakes, where it affects algal production and causes an imbalance in aquatic food webs. Many agronomical data indicate that the higher use of N fertilizers during the green revolution had an impact on the incidence of crop diseases. In contrast, examples in which a decrease in N fertilization increases disease severity are also reported, indicating that there is a complex relationship linking N uptake and metabolism and the disease infection processes. Thus, although it is clear that N availability affects disease, the underlying mechanisms remain unclear. The aim of this review is to describe current knowledge of the mechanisms that link plant N status to the plant's response to pathogen infection and to the virulence and nutritional status of phytopathogens.
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.
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