Priming as a mechanism in induced systemic resistance of plants

Citation
U. Conrath et al., Priming as a mechanism in induced systemic resistance of plants, EUR J PL P, 107(1), 2001, pp. 113-119
Citations number
52
Categorie Soggetti
Plant Sciences
Journal title
EUROPEAN JOURNAL OF PLANT PATHOLOGY
ISSN journal
09291873 → ACNP
Volume
107
Issue
1
Year of publication
2001
Pages
113 - 119
Database
ISI
SICI code
0929-1873(200101)107:1<113:PAAMII>2.0.ZU;2-Y
Abstract
Induced systemic resistance is a plant defence state that is associated wit h an enhanced ability - the so-called priming - to resist pathogen attack b y stronger activation of cellular defence responses. So far, however, primi ng has not been widely appreciated when studying induced plant disease resi stance. During the past several years, it has been demonstrated that pre-tr eatment of cultured parsley cells with inducers of systemic resistance, sal icylic acid or a benzothiadiazole, leads to the direct activation of a set of defence-related genes and also primes the cells for stronger elicitation of another set of defence genes including those encoding phenylalanine amm onia-lyase. From these results, it was concluded that the resistance induce rs have at least a dual role in plant defence-gene activation. When elucida ting whether priming plays a role in induced systemic resistance of Arabido psis, pre-treating plants with benzothiadiazole was found to augment the su bsequent activation of phenylalanine ammonia-lyase genes by Pseudomonas inf ection, wounding and osmotic stress and also to enhance wound/osmotic stres s-induced callose production. The augmentation of phenylalanine ammonia-lya se gene activation or/and callose deposition was not seen in the Arabidopsi s non-expresser of pathogenesis-related genes1 mutant which is compromised in induced resistance, while it was present, without benzothiadiazole pre-t reatment, in the constitutive expresser of pr genes1 and 5 mutants in which induced resistance is constitutive. Together these studies point to primin g as an important cellular mechanism in induced systemic resistance of plan ts which requires the intact non-expresser of pathogenesis-related genes1 g ene.