Rhizobacteria-mediated induced systemic resistence in Arabidopsis

Abstract

Upon primary pathogen attack, plants activate a diverse array of defense mechanisms at the site of primary infection. Besides this so-called basal resistance, plants have also the ability to enhance their defensive capacity against future pathogen attack. There are at least two types of biologically induced resistance. Classic systemic acquired resistance (SAR) results from infection by a necrotizing pathogen and is dependent on endogenous accumulation of salicylic acid (SA). Root colonization by non-pathogenic rhizobacteria can trigger an induced systemic resistance (ISR) response as well. The ISR signaling pathway differs from the SAR pathway, in that ISR functions independently of SA, but requires intact responsiveness to the plant hormones jasmonic acid (JA) and ethylene. Using the naturally occurring variation in ISR inducibility and basal resistance against the bacterial leaf pathogen P. syringae pv. tomato (Pst) in Arabidopsis, a dominant locus (ISR1) on chromosome III was identified that controls both ISR inducibility and basal resistance against Pst. Further physiological analysis revealed that genotypes carrying the recessive alleles of this alleles exhibit a reduced sensitivity to ethylene, indicating that the ISR1 gene encodes an ethylene signaling component that plays an important role in disease resistance. Additionally, we tested 11 Arabidopsis mutants with enhanced disease susceptibility to P. syringae pathogens for their ability to express ISR and SAR. In this screen we identified three Eds genes (Eds4, Eds8 and Eds10) that are involved in ISR, and two genes (Eds5 and Eds12) that are involved in SAR. The ISR-impaired mutants were found to be impaired in JA/ethylene-dependent signaling, whereas the SAR-impaired mutants were affected in SA-dependent signaling. To further examine the relationship between basal resistance and induced resistance, we assessed the effectiveness of SAR and ISR against different pathogens that are resisted through either SA-dependent basal defenses, or JA/ethylene-dependent basal defenses. SAR was highly effective against the oomycete Peronospora parasitica and turnip crinkle virus (TCV), which are both resisted through SA-dependent basal defenses, whereas ISR yielded only weak or no protection, respectively. Conversely, ISR was highly effective against Alternaria brassicicola, which is resisted through JA-dependent basal resistance, whereas SAR yielded no protection against this fungus. The bacterial pathogens P. syringae and Xanthomonas campestris that are both resisted through a combined action of SA- and JA/ethylene-dependent basal resistance, were sensitive to both ISR and ISR. Collectively, our results indicate that ISR is achieved by an enhancement of JA/ethylene-dependent basal resistance, whereas SAR is achieved by an enhancement of SA-dependent basal resistance. This conclusion points to a model in which induced resistance is expressed as a potentiation of either JA/ethylene dependent basal defenses (ISR), or SA-dependent basal defenses (SAR) upon challenge with a pathogen.