INTERACTION BETWEEN SAR AND OTHER DEFENSE PATHWAYS
It is impossible to understand SAR fully without studying its interaction with other biological processes. It is hypothesized that plant defense pathways interact synergistically or antagonistically to fine-tune responses according to the challenging organism(s). Different responses may confer resistance to the same pathogen. On the other hand, activation of one pathway may lead to cross-talk inhibition of another that is less effective against the pathogen. Cross-talk between different defense pathways is reviewed elsewhere. Here, I focus on interactions involving components of SAR.
As mentioned earlier, NPR1 is required for other induced resistance pathways, including ISR induced by the nonpathogenic bacterium P. fluorescens. Like SAR, ISR protects plants against a range of pathogens, but it is independent of SA and PRgene induction. ISR is blocked in the jar1 (jasmonic acid resistant 1) and etr1(ethylene resistant 1) mutants, indicating a requirement for JA and C2H4 signaling components. The Arabidopsis ecotypes RLD and Ws, which fail to develop ISR, carry a recessive mutation that causes C2H4-insensitivity. Two previously identified mutants, eds4 and eds8, which are insensitive to C2H4 and JA, respectively, are also impaired in ISR. However, a third eds mutant, eds10, responds normally to both hormones and develops normal SAR but is blocked for ISR, suggesting that EDS10 is a novel component of ISR. ISR requires NPR1 at a point downstream of JAR1 and ETR1. NPR1 is therefore an important regulator of induced defense responses downstream of either SA or JA/C2H4 and may differentially regulate these responses according to upstream signals. Furthermore, simultaneous induction of SAR and ISR has an additive effect on the level of induced resistance against P. syringae. Therefore, NPR1 is able to function in both of these pathways simultaneously.
There are also examples of cross-resistance where insect feeding can induce aspects of SAR. This has been observed in response to aphids and whiteflies, which are sucking insects and therefore do minimal damage to the tissue. The idea that plants perceive some insects as pathogens rather than herbivores is supported by the identification of an R gene that confers resistance to aphids and nematodes. It makes sense for the plant to activate SAR when attacked by such insects if they act as vectors for pathogens. Evidence for coregulation by SA and JA signaling also comes from a gene expression profiling study in which 55 genes were induced by treatment with either SA or JA.