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Oligogalacturonic Acid and Chitosan Reduce Stomatal Aperture by Inducing the Evolution of Reactive Oxygen Species from Guard Cells of Tomato and Commelina communis1

Sumin Lee, Hyunjung Choi, SuJeoung Suh, In-Suk Doo, Ki-Young Oh, Eun Jeong Choi, Ann T. Schroeder Taylor, Philip S. Low, and Youngsook Lee*

Department of Life Science, Pohang University of Science and Technology, Pohang 790-784, Korea (S.L., H.C., S.S., I.-S.D., K.-Y.O., E.J.C., Y.L.); and Department of Chemistry, Purdue University, West Lafayette, Indiana 47907 (A.T.S.T., P.S.L.)

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 (beta -1,4-linked glucosamine), a component of the fungal cell wall, on stomatal movements were examined in leaf epidermis of tomato (Lycopersicon esculentum L.) and Commelina 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.

1   This work was supported by a Korea-United States cooperative research grant from the Korea Science and Engineering Foundation (no. 966-0500-007-2 awarded to Y.L.) and by a grant from the National Science Foundation of the United States (nos. INT-9600183 and MCB-9725934 awarded to P.S.L.).
*   Corresponding author; e-mail ylee{at}postech.ac.kr; fax 82-562-279-2199.

Plant Physiol. (1999) 121: 147-152
Copyright Clearance Center:   0032-0889/99/121//06
© 1999 American Society of Plant Physiologists




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