Oligogalacturonic acid and chitosan reduce stomatal aperture by inducing the evolution of reactive oxygen species from guard cells of tomato and Commelina communis

Stomatal opening provides access to inner leaf tissues for many plant patho gens, so narrowing stomatal apertures may be advantageous for plant defense . We investigated how guard cells respond to elicitors that can be generate d from cell walls of plants or pathogens during pathogen infection. The eff ect of oligogalacturonic acid (OGA), a degradation product of the plant cel l wall, and chitosan (beta-1,4-linked glucosamine), a component of the fung al cell wall, on stomatal movements were examined in leaf epidermis of toma to (Lycopersicon esculentum L.) and Commelina communis L. These elicitors r educed the size of the stomatal aperture. OGA not only inhibited light-indu ced stomatal opening, but also accelerated stomatal closing in both species ; chitosan inhibited light-induced stomatal opening in tomato epidermis. Th e effects of OGA and chitosan were suppressed when ECTA, catalase, or ascor bic acid was present in the medium, suggesting that Ca2+ and H2O2 mediate t he elicitor-induced decrease of stomatal apertures. We show that the H2O2 t hat is involved in this process is produced by guard cells in response to e licitors. Our results suggest that guard cells infected by pathogens may cl ose their stomata via a pathway involving H2O2 production, thus interfering with the continuous invasion of pathogens through the stomatal pores.