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Plant Physiol. 2002 Mar;128(3):1046-56.

Benzothiadiazole-induced priming for potentiated responses to pathogen infection, wounding, and infiltration of water into leaves requires the NPR1/NIM1 gene in Arabidopsis.

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Department of Biology, University of Kaiserslautern, D-67653 Kaiserslautern, Germany.


Systemic acquired resistance (SAR) is a plant defense state that is induced, for example, after previous pathogen infection or by chemicals that mimic natural signaling compounds. SAR is associated with the ability to induce cellular defense responses more rapidly and to a greater degree than in noninduced plants, a process called "priming." Arabidopsis plants were treated with the synthetic SAR inducer benzothiadiazole (BTH) before stimulating two prominent cellular defense responses, namely Phe AMMONIA-LYASE (PAL) gene activation and callose deposition. Although BTH itself was essentially inactive at the immediate induction of these two responses, the pretreatment with BTH greatly augmented the subsequent PAL gene expression induced by Pseudomonas syringae pv. tomato infection, wounding, or infiltrating the leaves with water. The BTH pretreatment also enhanced the production of callose, which was induced by wounding or infiltrating the leaves with water. It is interesting that the potentiation by BTH pretreatment of PAL gene activation and callose deposition was not seen in the Arabidopsis nonexpresser of PR genes 1/noninducible immunity 1 mutant, which is compromised in SAR. In a converse manner, augmented PAL gene activation and enhanced callose biosynthesis were found, without BTH pretreatment, in the Arabidopsis constitutive expresser of pathogenesis-related genes (cpr)1 and constitutive expresser of pathogenesis-related genes 5 mutants, in which SAR is constitutive. Moreover, priming for potentiated defense gene activation was also found in pathogen-induced SAR. In sum, the results suggest that priming is an important cellular mechanism in acquired disease resistance of plants that requires the nonexpresser of PR genes 1/noninducible immunity 1 gene.

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