Rhizobacteria-mediated induced systemic resistance in Arabidopsis

Selected strains of rhizosphere bacteria have been shown to reduce disease by activating a resistance mechanism in the plant called rhizobacteria-mediated induced systemic resistance (ISR). ISR resembles pathogen-induced systemic acquired resistance (SAR), in that both types of induced resistance render uninfected plant parts more resistant towards a broad spectrum of pathogens. The spectrum of effectiveness of ISR and SAR largely overlaps but is also partly divergent. In contrast to SAR, ISR induced by Pseudomonas fluorescens WCS417r is independent of salicylic acid (SA) and PR gene activation. Instead, ISR follows a signaling pathway in which components from the jasmonic acid (JA) and ethylene (ET) response are successively engaged to trigger a defense reaction that, like SAR, is controlled by the regulatory factor NPRI. To investigate the role of JA and ET in ISR, their production was monitored in ISR-expressing plants. Neither JA nor ET production changed upon induction of ISR. From this we postulate that ISR is mediated via an increase in the plants sensitivity to JA and ET. This is supported by the potentiated expression of the JA-inducible gene AtVSP observed in challenged, ISR-expressing plants. Moreover, preliminary results indicate that the ACC oxidase activity is enhanced in ISR-expressing plants, providing a greater potential to produce ET upon challenge. In our search for ISR-related genes we identified two genes that show altered expression upon induction of ISR: the JA-inducible gene AtVSP, which shows an enhanced level of expression in challenged, ISR-expressing plants, and a root-specific, ET-inducible thaumatin-like gene, which is activated upon colonization of the roots with ISR-inducing rhizobacteria. Moreover, we identified a locus (ISRI) on chromosome 3 that controls the expression of ISR. Arabidopsis genotypes that are affected in this locus are also less sensitive to ET. Together, these data confirm the important role of JA and ET in ISR signaling. Cross-talk between SA- and JA-dependent pathways can result in inhibition of JA-mediated defense responses. For instance, chemical agents that activate the SAR pathway, e. g. SA and benzothiadiazole (BTH), can affect the JA-dependent wound response, which plays a role in defense against insects. We investigated possible antagonistic interactions between the SAR pathway and the ISR pathway. Simultaneous activation of SAR and ISR in Arabidopsis resulted in an additive effect on the level of induced protection against Pseudomonas syringae pv. tomato. In Arabidopsis genotypes that are blocked in either SAR or ISR, this additive effect was not evident. Moreover, induction of ISR did not affect the expression of the SAR marker gene PR-I in plants expressing SAR. Together, these observations demonstrate that the SAR and the ISR pathway are compatible and that there is no significant cross-talk between these pathways. Therefore, combining SAR and ISR provides an attractive tool for the improvement of disease control