We have demonstrated that root treatment with
hexanoic acid protects tomato plants against Botrytis cinerea.
Hexanoic acid-induced resistance (Hx-IR) was blocked in the
jasmonic acid (JA)-insensitive mutant jai1 (a coi1 homolog) and in the
abscisic acid (ABA)-deficient mutant flacca (flc). Upon
infection, the LoxD gene as well as the
oxylipin 12-oxo-phytodienoic acid and the bioactive molecule
JA-Ile were clearly induced in treated plants. However, the basal ABA levels were not altered.
Hexanoic acid primed
callose deposition against B. cinerea in a cultivar-dependent manner. Treated plants from Ailsa Craig, Moneymaker, and Rheinlands Ruhm showed increased
callose deposition but not from Castlemart.
Hexanoic acid did not prime
callose accumulation in flc plants upon B. cinerea
infection; therefore, ABA could act as a positive regulator of Hx-IR by enhancing
callose deposition. Furthermore, although
hexanoic acid protected the JA-deficient mutant defensless1 (def1), the priming for
callose was higher than in the wild type. This suggests a link between JA and
callose deposition in tomato. Hence, the obtained results support the idea that
callose,
oxylipins, and the JA-signaling pathway are involved in Hx-IR against B. cinerea. Moreover our data support the relevance of JA-signaling for basal defense against this necrotroph in tomato.
Hexanoic acid also protected against Pseudomonas syringae, indicating a broad-spectrum effect for this new inducer.