SALICYLIC-ACID POTENTIATES DEFENSE GENE-EXPRESSION IN TISSUE EXHIBITING ACQUIRED-RESISTANCE TO PATHOGEN ATTACK

Citation
Laj. Mur et al., SALICYLIC-ACID POTENTIATES DEFENSE GENE-EXPRESSION IN TISSUE EXHIBITING ACQUIRED-RESISTANCE TO PATHOGEN ATTACK, Plant journal, 9(4), 1996, pp. 559-571
Citations number
46
Categorie Soggetti
Plant Sciences",Biology
Journal title
ISSN journal
09607412
Volume
9
Issue
4
Year of publication
1996
Pages
559 - 571
Database
ISI
SICI code
0960-7412(1996)9:4<559:SPDGIT>2.0.ZU;2-S
Abstract
Salicylic acid (SA) is absolutely required for establishment of acquir ed resistance in non-infected tissues following localized challenge of other leaves with a necrotizing pathogen. Although not directly respo nsive to SA, or induced systemically following pathogen challenge, the expression of defence gene promoter fusions AoPR1-GUS and PAL-3-GUS a fter wounding or pathogen challenge could be enhanced by pre-treating tobacco plants hydroponically with SA, a phenomenon designated 'potent iation'. Potentiation of AoPR1-GUS wound-responsiveness was also demon strated locally, but not systemically, in tobacco tissue exhibiting ac quired resistance following infection with either viral or bacterial p athogens. Potentiation of wound-responsive expression by prior woundin g could not be demonstrated. In contrast, potentiation of pathogen-res ponsive AoPR1-GUS expression was exhibited both locally and systemical ly in non-infected tissue. The spatial and temporal exhibition of defe nce gene potentiation correlated directly with the acquisition of resi stance in non-infected tissue. Pathogen-responsive potentiation was ob tained at about 10-fold lower levels of salicylic acid than wounding-r esponsive potentiation in AoPR1-GUS tobacco plants prefed with salicyl ate. These results may explain the failure to observe systemic potenti ation of the wound-responsive defence gene expression. The data sugges t a dual role for SA in terms of gene induction in acquired immunity: a direct one by induction of genes such as pathogenesis-related protei ns, and an indirect one by potentiation of expression of other local d efence genes (such as PAL and AoPR1) which do not respond directly to SA but become induced on pathogen attack or wounding.