Abstract

Chitosan is a partially deacetylated linear polysaccharide composed of β-1,4-linked units of D-glucosamine and N-acetyl glucosamine. As well as acting as a structural component of fungal cell walls, chitosan can be applied as a potent antifungal agent. However, the mode-of-action of chitosan in fungal pathogens is poorly understood. Here, we report that chitosan is effective for control of rice blast disease. Chitosan application impairs growth of the blast fungus Magnaporthe oryzae and has a pronounced effect on appressorium-mediated plant infection. Chitosan inhibits septin-mediated F-actin re-modelling at the appressorium pore, thereby preventing re-polarisation of the infection cell and rice leaf cuticle penetration. We found that chitosan causes plasma membrane permeabilization of M. oryzae and affects NADPH oxidase-dependent synthesis of reactive oxygen species, essential for septin ring formation and fungal pathogenicity. Our data further show that the toxicity of chitosan to M. oryzae requires the protein kinase C-dependent cell wall integrity pathway and the Nox1 NADPH oxidase. A conditionally lethal, analogue (PP1)-sensitive mutant of Pkc1 is partially remediated for growth in the presence of chitosan and PP1, while Δnox1 mutants increase their glucan/chitin cell wall ratio, rendering them resistant to chitosan. Taken together, our data show that chitosan is a potent fungicide for control of the rice blast fungus which involves the cell wall integrity pathway, disrupts plasma membrane and inhibits septin-mediated plant infection.