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Systemic acquired resistance (SAR) in Carica papaya L. is induced by benzothiadiazole (BTH). The response is manifested by increased tolerance to infection by the virulent pathogen Phytophthora palmivora, by increased β-1,3-glucanase and chitinase activities, and by increased accumulation of a PR1 mRNA. Infection of untreated papaya by P. palmivora also induced β-1,3-glucanase and chitinase activities but at much lower levels. This response to P. palmivora is characteristic of a compatible interaction. Papaya has at least four members of the PR-1 gene family; BTH reduces mRNA accumulation for two of these and increases it in the other two. One of these, PR-1d, is induced over 20-fold; mRNA accumulation for this gene increased for at least 14 days after BTH treatment. In contrast, both chitinase and β-1,3-glucanase activities peaked after 1–2 days then returned to base levels at approximately 10 days. Papaya has an NPR1 gene that contains structural domains conserved with arabidopsis; these domains are involved in protein–protein interactions and nuclear localization, which are essential for function in SAR of arabidopsis. The papaya NPR1 gene is expressed constitutively and is slightly induced by BTH treatment. Overall, these findings indicate the basic elements of papaya SAR resemble the pathway as described in arabidopsis and tobacco. |
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