Abstract
Some unexplored mechanisms of chitosan (CHT)-induced resistance have been investigated by using the pathosystem Tobacco necrosis virus (TNV) – Phaseolus vulgaris L. In particular, it was shown that CHT does not exert a direct antiviral activity and that stomatal uptake of the compound is determinant for the induction of plant defence mechanisms against TNV. By a chemical approach, using ethylene inhibitors or donors, it was also demonstrated that these defence mechanisms do not involve ethylene pathway. Conversely, the infection with TNV stimulated the production of this hormone in leaf tissues, associated with the development of necrotic lesions. Finally, in open field trials, CHT treatments did not incur fitness costs in bean plants, probably due to the activation of priming mechanisms as opposed to the direct resistance induction.
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