Induced resistance: an enhancement of basal resistance?

Upon primary pathogen attack, plants activate resistance mechanisms at the site of 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 aquired resistance (SAR) results from infection by a necrotizing pathogen and is dependant on endogenous accumulation of salicylic acid (SA). Root colonization by non-pathogenic rhizobacteria can trigger an induced systemic resistance (ISR) response as well, which functions independantly of SA and requires intact responsiveness to the plant hormones jasmonic acid (JA) and ethylene (ET). A screen for genotypes impaired in either ISR or SAR revealed that ecotypes RLD1 and Ws-0, as well as the enhanced disease suspectibility mutants eds4-1, eds8-1 and eds10-1, are impaired in WCS417r-mediated ISR, whereas mutants eds5-1 and eds12-1 are impaired in pathogen-induced SAR. Analysis of JA-, ET- and SA-responsiveness revealed that the ISR-impaired genotypes are affected in signaling compounds contributing to JA/ET-dependent basal against P. syringae, while the SAR-impaired genotypes are affected in compounds contributing to SA-dependent basal resistance against P. syringae. To further examine the relationship between basal resistance and induced resistance, the effectiveness of SAR and ISR was assessed against different Arabidopsis pathogens that are resisted through JA/ET-dependent basal resistance, SA-dependent basal resistance, or a combination of JA/ET- and SA-dependent basal resistance. This analysis revealed that ISR is effective predominantly against pathogens that are resisted through JA/ET-dependent basal resistance, whereas SAR is effective against pathogens that are resisted through SA-dependent basal resistance. Collectively, our results suggest that ISR constitutes an enhancement of JA/ET-dependent basal resistance, whereas SAR is achieved through an enhanced expression of SA-dependent basal resistance.