Plant defenses against pathogens and insects are regulated differentially by cross-communicating signal transduction pathways in which salicylic acid (SA) and jasmonic acid (JA) play key roles. In this study, we investigated the molecular mechanism of the antagonistic effect of SA on JA signaling. Arabidopsis plants unable to accumulate SA produced 25-fold higher levels of JA and showed enhanced expression of the JA-responsive genes LOX2 , PDF1.2 , and VSP in response to infection by Pseudomonas syringae pv tomato DC3000, indicating that in wild-type plants, pathogen-induced SA accumulation is associated with the suppression of JA signaling. Analysis of the Arabidopsis mutant npr1 , which is impaired in SA signal transduction, revealed that the antagonistic effect of SA on JA signaling requires the regulatory protein NPR1. Nuclear localization of NPR1, which is essential for SA-mediated defense gene expression, is not required for the suppression of JA signaling, indicating that cross-talk between SA and JA is modulated through a novel function of NPR1 in the cytosol.

Plant defenses against pathogens and insects are regulated differentially by cross-communicating signaling pathways in which salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) play key roles. To understand how plants integrate pathogen-and insect-induced signals into specific defense responses, we monitored the dynamics of SA, JA, and ET signaling in Arabidopsis after attack by a set of microbial pathogens and herbivorous insects with different modes of attack. Arabidopsis plants were exposed to a pathogenic leaf bacterium (Pseudomonas syringae pv. tomato), a pathogenic leaf fungus (Alternaria brassicicola), tissuechewing caterpillars (Pieris rapae), cell-content-feeding thrips (Frankliniella occidentalis), or phloem-feeding aphids (Myzus persicae). Monitoring the signal signature in each plant-attacker combination showed that the kinetics of SA, JA, and ET production varies greatly in both quantity and timing. Analysis of global gene expression profiles demonstrated that the signal signature characteristic of each Arabidopsis-attacker combination is orchestrated into a surprisingly complex set of transcriptional alterations in which, in all cases, stress-related genes are overrepresented. Comparison of the transcript profiles revealed that consistent changes induced by pathogens and insects with very different modes of attack can show considerable overlap. Of all consistent changes induced by A. brassicicola, Pieris rapae, and F. occidentalis, more than 50% also were induced consistently by P. syringae. Notably, although these four attackers all stimulated JA biosynthesis, the majority of the changes in JA-responsive gene expression were attacker specific. All together, our study shows that SA, JA, and ET play a primary role in the orchestration of the plant's defense response, but other regulatory mechanisms, such as pathway cross-talk or additional attacker-induced signals, eventually shape the highly complex attacker-specific defense response.

This paper examines induced resistance (SAR) in plants against various insect and pathogenic invaders. SAR confers quantitative protection against a broad spectrum of microorganisms in a manner comparable to immunization in mammals, although the underlying mechanisms differ. Discussed here are the molecular events underlying SAR: the mechanisms involved in SAR, including lignification and other structural barriers, pathogenesis-related proteins and their expression, and the signals for SAR including salicylic acid. Recent findings on the biological role of systemin, ethylene, jasmonates, and electrical signals are reviewed. Chemical activators of SAR comprise inorganic compounds, natural compounds, and synthetic compounds. Plants known to exhibit SAR and induced systemic resistance are listed.

In a variety of plant species, the development of necrotic lesions in response to pathogen infection leads to induction of generalized disease resistance in uninfected tissues. A well-studied example of this "immunity" reaction is systemic acquired resistance (SAR) in tobacco. SAR is characterized by the development of a disease-resistant state in plants that have reacted hypersensitively to previous infection by tobacco mosaic virus. Here, we show that the onset of SAR correlates with the coordinate induction of nine classes of mRNAs. Salicylic acid, a candidate for the endogenous signal that activates the resistant state, induces expression of the same "SAR genes." A novel synthetic immunization compound, methyl-2,6-dichloroisonicotinic acid, also induces both resistance and SAR gene expression. These observations are consistent with the hypothesis that induced resistance results at least partially from coordinate expression of these SAR genes. A model is presented that ties pathogen-induced necrosis to the biosynthesis of salicylic acid and the induction of SAR.

In Arabidopsis, systemic acquired resistance against pathogens has been associated with the accumulation of salicylic acid (SA) and the expression of the pathogenesis-related proteins PR-1, PR-2, and PR-5. We report here the isolation of two nonallelic mutants impaired in the pathway leading to SA biosynthesis. These SA induction-deficient ( sid ) mutants do not accumulate SA after pathogen inoculation and are more susceptible to both virulent and avirulent forms of Pseudomonas syringae and Peronospora parasitica. However, sid mutants are not as susceptible to these pathogens as are transgenic plants expressing the nahG gene encoding an SA hydroxylase that degrades SA to catechol. In contrast to NahG plants, only the expression of PR-1 is strongly reduced in sid mutants, whereas PR-2 and PR-5 are still expressed after pathogen attack. Furthermore, the accumulation of the phytoalexin camalexin is normal. These results indicate that SA-independent compensation pathways that do not operate in NahG plants are active in sid mutants. One of the mutants is allelic to eds5 (for enhanced disease susceptibility), whereas the other mutant has not been described previously. INTRODUCTIONInfection with necrotizing pathogens often leads to the subsequent systemic induction of resistance. This is referred to as systemic acquired resistance (SAR), which is characterized by a long-lasting defense response against a broad spectrum of pathogens (Kuc, 1982;Ryals et al., 1994;Sticher et al., 1997). After the initial observation that treatment of plants with salicylic acid (SA) leads to resistance (White, 1979), several lines of evidence have shown that SA is associated with SAR. The expression of a number of pathogenesis-related (PR) proteins is highly correlated with acquired resistance Uknes et al., 1992). The synthesis of PR proteins can be induced by treatment with SA and also by the application of functional analogs of SA, such as 2,6-dichloroisonicotinic acid (INA;Métraux et al., 1991) or benzo(1,2,3)thiadiazole-7-carbothioic acid S -methyl ester (BTH; Görlach et al., 1996).The accumulation of SA in plant tissues correlates with the presence of PR proteins and resistance (Malamy et al., 1990;Métraux et al., 1990;Yalpani et al., 1991). In addition, transgenic tobacco (Gaffney et al., 1993) and Arabidopsis plants that express the Pseudomonas putida nahG gene, encoding an SA hydroxylase, which degrades SA to catechol, are hypersusceptible to infection with virulent pathogens and cannot develop SAR. Experiments with NahG plants also showed that SA is involved in gene-for-gene defense responses . These findings provide strong evidence for the involvement of SA in SAR.SA also has been proposed to be the systemic signal for SAR (Malamy et al., 1990;Métraux et al., 1990). However, although SA synthesized in infected leaves can be shown to be transported to uninfected leaves in tobacco and cucumber (Shulaev et al., 1995;Mölders et al., 1996), grafting experiments with tobacco plants expressing NahG, cholera toxin, or reduced levels of ...