Factors Contributing to Abscisic Acid-Mediated Predisposition to Disease Caused by Phytophthora capsici.

다국어 초록 (Multilingual Abstract)

Plants respond to changes in the environment with complex signaling networks, often under the control of phytohormones that generate positive and negative crosstalk among downstream effectors of the response. Brief dehydration stresses such as salinity and water deficit, which induce a rapid and transient systemic increase in levels of abscisic acid (ABA), can influence disease response pathways. Plant defense responses to pathogens are mediated in part by the phytohormones salicylic acid (SA), jasmonic acid (JA) and ethylene (ET). ABA has been associated with susceptibility of plants to bacteria, fungi, and oomycetes but relatively little attention has been directed at its role in abiotic stress predisposition to root pathogens. Plant roots exposed to a brief episode of salt (sodium chloride) stress prior to infection are severely diseased relative to non-stressed plants. This study examines the impact of salinity stress on infection of tomato roots by Phytophthora capsici. An increase in root ABA levels in tomato preceded or temporally paralleled the onset of stress-induced susceptibility. ABA-deficient tomato mutants were shown to have a reduced predisposition response, which could be restored by complementation of the mutant with exogenous ABA. ABA related gene expression did not appear to be altered by P. capsici infection. Pathogenesis-related gene expression was induced in non-stressed plants during P. capsici infection. However, these genes were strongly suppressed in plants that had been salt-stressed prior to inoculation. SA- and JA-mediated responses in tomato roots are impacted by exposure to salinity as evidenced by the suppression of hallmark defense gene expression. Interference with SA or ET network functions does not significantly alter the predisposing effect of salt on disease severity. Rather, it appears that elevated ABA induced by salinity confers the dominant impact on the disease phenotype observed. This impact, which does not preclude effects on other phytohormone networks, is sufficient to predispose tomato to Phytophthora root and crown rot.
In a second study, the plant activators Actigard (1,2,3-benzothiadiazole-7-thiocarboxylic acid-s-methyl-ester, BTH) and Tiadinil (N-(3-chloro-4-methylphenyl)-4- methyl-1,2,3-thiadiazole-5-carboxamide, TDL) were examined for their effects on disease and their impact on ABA-mediated, salinity-induced predisposition in hydroponically-grown tomato seedlings. An episode of salt stress to roots significantly increased the severity of disease caused by the bacterial speck pathogen Pseudomonas syringae pv. tomato (Pst) relative to non-stressed plants. In spite of the protection afforded by BTH and TDL to Pst, root treatment with these SAR activators increased the levels of ABA in roots and shoots similar to levels observed in salt-stressed plants. The results indicate that plant activators can protect tomato plants from bacterial speck disease under predisposing salt stress, and suggest that some SA-mediated defense responses may function sufficiently in plants with elevated levels of ABA.