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.