1.2.5S
RECEPTOR-MEDIATED PATHOGEN RECOGNITION AND SIGNAL TRANSDUCTION IN PLANT DEFENCE

D SCHEEL1, H HIRT2, T KROJ1, W LIGTERING2, D NENNSTIEL1, T NÜRNBERGER1, M TSCHÖPE1, H ZINECKER1 and U ZUR NIEDEN1

1Institut für Pflanzenbiochemie, Weinberg 3, D-06120 Halle (Saale), Germany; 2Institut für Mikrobiologie und Genetik, Dr-Bohr-Gasse 9, A-1030 Wien, Austria

Background and objectives
Plants apparently recognize potentially pathogenic organisms through receptors on their surface that specifically bind signal molecules, so-called elicitors, derived from pathogen or plant-surface structures and thereby initiate signalling cascades activating a multicomponent defence response. The coupling of this general type of non-self recognition with inducible defence reactions is believed to be an early event in plant evolution.

Results and conclusions
Cultured parsley cells and a glycoprotein elicitor from hyphal cell walls of the plant pathogenic oomycete Phytophthora sojae are the experimental system used to investigate the molecular mechanisms underlying recognition and signalling events. The oligopeptide fragment Pep-13 of this glycoprotein stimulates a multicomponent defence response in cultured parsley cells that is identical with the reaction to the glycoprotein and very similar to the response of intact plants to infection with the fungus. This elicitor is therefore believed to act as a recognition signal in this non-host plant/pathogen interaction, which is perceived by the plant cell through a plasma membrane receptor [1, 2].

Early elements of the plant response are ion fluxes across the plasma membrane, activation of a MAP kinase and the production of reactive oxygen species, the oxidative burst, followed by defence gene activation and phytoalexin accumulation. Activation of the elicitor-responsive ion channels, the most rapid reaction, has been found to be necessary and sufficient for all other reactions of the plant cells [3, 4]. Inhibition of elicitor-stimulated production of reactive oxygen species with diphenylene iodonium, an inhibitor of the mammalian NADPH oxidase, blocks defence gene activation and phytoalexin accumulation without affecting ion fluxes, MAP kinase activation, cell viability and constitutive gene expression [4, 5]. Mimicking the oxidative burst in the absence of elicitor by addition of appropriate amounts of potassium superoxide to the medium of cultured parsley cells stimulates phytoalexin accumulation but not ion fluxes. In contrast, hydrogen peroxide either added directly to, or generated in the culture medium by glucose and glucose oxidase does not stimulate any defence response [4]. Upon receptor-mediated activation, the MAP kinase is translocated to the nucleus where it might interact with transcription factors that induce expression of defence genes [5].

In summary, our results demonstrate a causal relationship between early and late elicitor reactions, establish a sequence of signalling events from receptor-mediated activation of ion channels through MAP kinase activation, the oxidative burst, and defence gene activation to phytoalexin production, and suggest that within this signal transduction chain the superoxide anion radical, rather than hydrogen peroxide, triggers defence gene activation and phytoalexin accumulation.

References
1. Nürnberger T, Nennstiel D, Jabs T et al., 1994. Cell 78, 449-460.
2. Nürnberger T, Nennstiel D, Hahlbrock K, Scheel D, 1995. Proceedings of the National Academy of Sciences, USA 92, 2338-2342.
3. Zimmermann S, Nürnberger T, Frachisse J-M et al., 1997 Proceedings of the National Academy of Sciences, USA 94, 2751-2755.
4. Jabs T, Tschöpe M, Colling C, Hahlbrock K, Scheel D, 1997. Proceedings of the National Academy of Sciences, USA 94, 4800-4805.
5. Ligterink W, Kroj T, zur Nieden U, Hirt H, Scheel D, 1997. Science 276, 2054-2057.