Analysis of priming mechanisms marking chitosan-induced resistance
We tested whether induced resistance triggered by chitosan is mediated by priming mechanisms through the assessment of its capacity to induced long-lasting resistance in distal parts of the plants. Treatments with 1% chitosan induced long-lasting resistance against B. cinereaof up to 2 weeks after initial treatment of tomato plants (Fig 2a).
In order to assess whether treatments with chitosan directly affects plant development, we tested plant growth one week after treatment with 1% chitosan. These experiments revealed that chitosan treatment triggers a statistically significant growth promotion, therefore indicating that induced resistance by chitosan does not negatively impact plant development (Fig S3a).
To study whether chitosan induced resistance (IR) was based on known mechanisms of priming, callose and hormone profiling analysis were performed after subsequent infection. Treatment with chitosan resulted in the accumulation of approximately twice the callose deposited at the site of attack compared to plants treated with water (Fig 2b,c). In addition, mass spectrometry profiling of defence-dependent hormones demonstrated that chitosan-induced resistance is mediated specifically by accumulation of jasmonic acid (JA) (Fig 2d) and its amino acid conjugate JA- isoleucine (JA-Ile, Fig S3b). In contrast, no other impacts were found in the concentration of other defence hormones such as salicylic acid (SA) and abscisic acid (ABA) (Fig 2d). Thus, chitosan-IR is based on priming of callose at the infection site and accumulation of JA and its conjugate JA-Ile.