SIGNALING POTENTIAL OF IRON IN PLANT-MICROBE INTERACTIONS - THE PATHOGENIC SWITCH OF IRON TRANSPORT IN ERWINIA-CHRYSANTHEMI

Although competition for iron has long been recognized in bacterial virulence and animal host defence, its role in plant pathogenesis has only been clarified recently, with the soft rot pathogen Erwinia chrysanthemi. A functional genetic system encoding the production and utilization of the siderophore chrysobactin is required for symptom expansion on African violets and chrysobactin has been detected in 24-h old diseased tissues. It was also established that the transcriptional activity of the fct cbs operon representative of this system, encoding transport and biosynthetic functions, is negatively regulated by iron. In this study, Escherichia coli lacZ was used as a reporter gene to analyse the expression of this operon at the onset of infection. A series of fct::lac chromosomal fusions regulated by iron were constructed and the behaviour of one engineered strain was analysed in planta; induction of LacZ activity appeared to occur after 10 h following leaf inoculation and to be subject to variations over time typical of the regulatory response to iron. In contrast to parental cells, engineered cells thus disrupted in the production and utilization of chrysobactin gave rise to a necrotic front associated with a downshift in viable counts. These data, for the first time, provide direct evidence of in vivo regulation of an iron-controlled function associated with pathogenicity and demonstrate (i) that expression of the chrysobactin-mediated iron uptake system contributes greatly to invasive growth of the pathogen, and (ii) that plant extracellular fluids can be detected by pathogens as iron-limited environments.