RT Journal Article SR Electronic T1 Oligogalacturonic Acid and Chitosan Reduce Stomatal Aperture by Inducing the Evolution of Reactive Oxygen Species from Guard Cells of Tomato and Commelina communis JF Plant Physiology JO Plant Physiol. FD American Society of Plant Biologists SP 147 OP 152 DO 10.1104/pp.121.1.147 VO 121 IS 1 A1 Lee, Sumin A1 Choi, Hyunjung A1 Suh, SuJeoung A1 Doo, In-Suk A1 Oh, Ki-Young A1 Jeong Choi, Eun A1 Schroeder Taylor, Ann T. A1 Low, Philip S. A1 Lee, Youngsook YR 1999 UL http://www.plantphysiol.org/content/121/1/147.abstract AB Stomatal opening provides access to inner leaf tissues for many plant pathogens, so narrowing stomatal apertures may be advantageous for plant defense. We investigated how guard cells respond to elicitors that can be generated from cell walls of plants or pathogens during pathogen infection. The effect of oligogalacturonic acid (OGA), a degradation product of the plant cell wall, and chitosan (β-1,4-linked glucosamine), a component of the fungal cell wall, on stomatal movements were examined in leaf epidermis of tomato (Lycopersicon esculentum L.) andCommelina communis L. These elicitors reduced the size of the stomatal aperture. OGA not only inhibited light-induced stomatal opening, but also accelerated stomatal closing in both species; chitosan inhibited light-induced stomatal opening in tomato epidermis. The effects of OGA and chitosan were suppressed when EGTA, catalase, or ascorbic acid was present in the medium, suggesting that Ca2+ and H2O2 mediate the elicitor-induced decrease of stomatal apertures. We show that the H2O2 that is involved in this process is produced by guard cells in response to elicitors. Our results suggest that guard cells infected by pathogens may close their stomata via a pathway involving H2O2 production, thus interfering with the continuous invasion of pathogens through the stomatal pores.