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β-amino-butyric acid-induced resistance against necrotrophic pathogens is based on ABA-dependent priming for callose
Auteur(s)
Ton, Jurriaan
Date de parution
2004
In
The Plant Journal, Blackwell, 2004/38/1/119-130
Résumé
The non-protein amino acid β-amino-butyric acid (BABA) protects plants against a wide range of pathogens. We have examined the effectiveness and mode of action of BABA on resistance against two necrotrophic pathogens. Treatment of <i>Arabidopsis</i> with BABA induced resistance against <i>Alternaria brassicicola</i> and <i>Plectosphaerella cucumerina</i> to a similar level by jasmonic acid (JA). Conversely, treatment with benzothiadiazole (BTH), a functional analogue of salicylic acid (SA), had no significant effect on the resistance against both pathogens. BABA-induced resistance against <i>A. brassicicola</i> and <i>P. cucumerina</i> was unaffected in the JA-insensitive mutant <i>coi1-1</i> and the camalexin-deficient mutant <i>pad3-1</i>. Moreover, the expression of BABA-induced resistance was not associated with enhanced accumulation of camalexin or enhanced transcription of the JA-inducible <i>PDF1.2</i> gene. The expression of BABA-induced resistance against <i>P. cucumerina</i> was unaffected in mutants impaired in ethylene (ET) and SA signalling, but was blocked in the abscisic acid (ABA)-deficient mutant <i>aba1-5</i>, the ABA-insensitive mutant <i>abi4-1</i> and the callose-deficient mutant <i>pmr4-1</i>. Upon infection by both pathogens, BABA-treated plants showed an earlier and more pronounced accumulation of callose. Treatment with the callose-inhibitor 2-deoxy-D-glucose (2-DDG) reversed the BABA-induced resistance against <i>A. brassicicola</i>. Furthermore, primed callose deposition was absent in BABA-treated <i>abi4-1</i> and <i>pmr4-1</i> plants upon infection by <i>P. cucumerina</i>. Although the expression of BABA-induced resistance was not associated with enhanced transcription of the ABA-inducible <i>RAB18</i> gene, application of ABA mimicked the effect of BABA on the level of callose accumulation and resistance. Hence, BABA-induced resistance against necrotrophic pathogens is based on primed callose accumulation, which is controlled by an ABA-dependent defence pathway.
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Resource Types::text::journal::journal article
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