Iron is an essential element for most organisms because it catalyzes redox reactions and is required for many cellular processes. On the other hand, iron excess can damage cells due to iron’s highly reactive properties. Therefore iron uptake, transport, storage and use are tightly regulated in plants. Under iron deficient conditions the model plant Arabidopsis thaliana expresses the ferric reductase oxidase gene FRO2 and the iron-regulated transporter gene IRT1 to increase iron uptake from the soil. In addition, it activates biosynthesis and excretion of phenolic compounds to increase iron solubility via the expression of the transcription factor MYB72 and the glucosidase gene BGLU42, amongst others. Surprisingly, upon colonization of A. thaliana roots by the beneficial bacterium P. simiae this highly regulated process is affected and the expression of FRO2, IRT1, MYB72 and BGLU42 is induced. Interestingly, MYB72 and BGLU42 are required for the onset of induced systemic resistance. Thus, activation of at least part of the iron deficiency response is essential for the induction of systemic resistance by P. simiae WCS417. So far, it is unknown how this response is activated. We decided to investigate how and why the iron deficiency response is activated in A. thaliana roots in response to P. simiae WCS417. We are studying whether activation of the iron deficiency response sustains the growth promotion seen upon colonization by beneficial rhizobacteria. Moreover, we wonder whether ISR is similar to previously reported iron deficiency-induced resistance. Several studies report that iron-deficient plants are less sensitive to Botrytis cinerea and Dickeya dadantii. Thus, ISR and iron deficiency-induced resistance might both be mediated by activation of the iron deficiency response and be similar downstream of this activation. These hypotheses are investigated using an in vitro and a hydroponic set-up that allows us to control iron availability in the medium.