Salicylic acid potentiates defence gene expression in tissue exhibiting acquired resistance to pathogen attack

Abstract

Salicylic acid (SA) is absolutely required for establishment of acquired resistance in non‐infected tissues following localized challenge of other leaves with a necrotizing pathogen. Although not directly responsive to SA, or induced systemically following pathogen challenge, the expression of defence gene promoter fusions AoPR1—GUS and PAL‐3—GUS after wounding or pathogen challenge could be enhanced by pre‐treating tobacco plants hydroponically with SA, a phenomenon designated ‘potentiation’. Potentiation of AoPR1—GUS wound‐responsiveness was also demonstrated locally, but not systemically, in tobacco tissue exhibiting acquired resistance following infection with either viral or bacterial pathogens. Potentiation of wound‐responsive expression by prior wounding could not be demonstrated. In contrast, potentiation of pathogen‐responsive AoPR1—GUS expression was exhibited both locally and systemically in non‐infected tissue. The spatial and temporal exhibition of defence gene potentiation correlated directly with the acquisition of resistance in non‐infected tissue. Pathogen‐responsive potentiation was obtained at about 10‐fold lower levels of salicylic acid than wounding‐responsive potentiation in AoPR1—GUS tobacco plants prefed with salicylate. These results may explain the failure to observe systemic potentiation of the wound‐responsive defence gene expression. The data suggest a dual role for SA in terms of gene induction in acquired immunity: a direct one by induction of genes such as pathogenesis‐related proteins, and an indirect one by potentiation of expression of other local defence genes (such as PAL and AoPR1) which do not respond directly to SA but become induced on pathogen attack or wounding.

Death Don't Have No Mercy: Cell Death Programs in Plant-Microbe Interactions.

“…Because it is thought that 2,6-dichloroisonicotinic acid acts at the same point as or downstream of SA in this pathway (Delaney et al, 1995), one conclusion is that these mutants define steps in a feedback loop operating to interpret SA-dependent signals. These genetic results are consistent with other results implicating a feedback role for SA during the defense response (Kauss et al, 1992;Kauss and Jeblick, 1995;Mauch-Mani and Slusarenko, 1996;Mur et al, 1996; see also Ryals et al, 1996, in this issue). It will also be informative to combine the cell death control mutants with other mutants required for R gene function, such as ndr (Century et al, 1995), whose position in the scheme shown in Figure 2 is tentative.…”

Rhizobacteria-mediated induced systemic resistance (ISR) in Arabidopsis requires sensitivity to jasmonate and ethylene but is not accompanied by an increase in their production

“…A plausible explanation is that ISR-expressing plants are potentiated for the expression of JA-inducible, defense-related genes, leading to a faster and greater gene activation after infection with a challenging pathogen. Potentiation of defense-related gene activation has been demonstrated for SA-inducible PR genes in SAR-expressing tobacco [33] and Arabidopsis plants [52]. Recently, we demonstrated that the expression of the JA-inducible Atvsp gene is potentiated in ISRexpressing plants [52], leading to a higher Atvsp transcript accumulation after challenge inoculation.…”

Accumulation of Salicylic Acid and 4-Hydroxybenzoic Acid in Phloem Fluids of Cucumber during Systemic Acquired Resistance Is Preceded by a Transient Increase in Phenylalanine Ammonia-Lyase Activity in Petioles and Stems1

“…syringae system, PAL expression may be amplified in vascular tissue by a product of the phenylpropanoid pathway. For example, SA has been reported to potentiate the expression of PAL and other defense-related genes, allowing higher levels of expression in response to elicitors (Mur et al, 1996;Shirasu et al, 1997).…”