SALICYLIC ACID-MEDIATED SIGNAL TRANSDUCTION IN DISEASE RESISTANCE
D KLESSIG, J DURNER, S ZHANG, D WENDEHENNE, H DU, Z CHEN and M ANDERSON
Waksman Institute, Rutgers University, Piscataway, NJ 08854, USA
Background and objectives
During the past several years, we have used a variety of biochemical, molecular and genetic approaches to identify components of the host signal-transduction pathway(s) activated during plant defence responses to pathogen attack. A critical component in the signalling cascade leading to PR gene activation is salicylic acid (SA). To help elucidate the mechanisms of SA action, several tobacco proteins which interact with SA have been identified. In addition, several other potential components in the SA-mediated signalling pathway have been uncovered.
Results and conclusions
Proteins with which SA interact include catalase and ascorbate peroxidase [1, 2]. SA inhibits these two major H2O2- scavenging enzymes by serving as an one-electron donating substrate. In so doing, it is converted to a phenolic radical, which may be responsible for SA-induced tepid peroxidation. Lipid peroxides induce PR-1 genes; thus the signals that activate defence gene expression may be generated, in part, by SA's interaction with these enzymes. SABP2 is another SA-binding protein. The affinity for SA of this low-MW, soluble protein (Kd = 9O nM) is 150-fold higher than that of catalase. SABP2 has even higher affinity for the commercial plant defence activator benzothiadiazole which is more effective at inducing PR gene expression than SA. SA treatment rapidly and transiently activates a MAP kinase, termed SIPK for SA-induced protein kinase. SIPK is also activated by TMV infection, a variety of pathogen-derived elicitors (e.g. elicitins) and other stresses (e.g. wounding). A second MAP kinase, called WIPK because it was first discovered to be wound-induced at the MRNA level, is also activated by TMV  but, surprisingly, not by wounding. Both transcription and post-translational phosphorylation are required for its activation by TMV, which is N-gene-initiated but SA-independent. Another plant defence signalling compound may be nitric oxide (NO). Administration of NO donors or recombinant NO synthase to tobacco induces PR-1 (and PAL) gene expression. These genes are similarly activated by treatment with the second messengers of the mammalian NO signalling cascade, cGMP and cADP ribose. These results, together with those obtained with inhibitors of guanylate cyclase and Ca2+ channels, suggest that critical players in animal NO signalling are also operative in plant defence responses.
1. Chen Z, Silva H, Klessig DF, 1993. Science 262, 1883-1886.
2. Turner J, Klessig DF, 1995. Proceedings of the National Academy of Sciences, USA 92, 11312-11316.