Cell wall-degrading enzymes from Erwinia carotovora cooperate in the salicylic acid-independent induction of a plant defense response

The virulence of the plant pathogen Erwinia carotovora subsp. carotovora is dependent on the production and secretion of a large variety of plant cell wall-degrading enzymes, including several pectinases and cellulases. Treatment of tobacco plants with culture filtrates (CFs) from the pathogen (cont...

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Veröffentlicht in:Molecular plant-microbe interactions 1998-01, Vol.11 (1), p.23-32
Hauptverfasser: Vidal, S, Eriksson, A.R.B, Montesano, M, Denecke, J, Palva, E.T
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Sprache:eng
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Zusammenfassung:The virulence of the plant pathogen Erwinia carotovora subsp. carotovora is dependent on the production and secretion of a large variety of plant cell wall-degrading enzymes, including several pectinases and cellulases. Treatment of tobacco plants with culture filtrates (CFs) from the pathogen (containing the secreted cell wall-degrading enzymes) induces both local and systemic expression of genes involved in plant defense response. We have characterized the contribution of individually produced cell wall-degrading enzymes from E. carotovora subsp. carotovora in their ability to trigger local and systemic induction of a defense-related gene (coding for a basic beta-1,3-glucanase) as well as resistance to this pathogen in tobacco. Our results show that mainly pectic enzymes and to some extent one cellulase induce expression of the beta-1,3-glucanase gene. Cellulases appear to act cooperatively in the defense gene induction when added in combination with pectic enzymes. Similarly, pectinases and cellulases cooperate in triggering systemic resistance to the pathogen. Salicylic acid (SA) does not appear to be involved in this process, as systemic resistance was induced similarly in transgenic NahG plants that overproduce a salicylate hydroxylase and cannot accumulate SA and in nontransformed control plants. The lack of SA requirement for the induced resistance against E. carotovora subsp. carotovora suggests the presence of a different signal transduction pathway involved in this plant-pathogen interaction
ISSN:0894-0282
1943-7706
DOI:10.1094/mpmi.1998.11.1.23