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KMID : 0368419980410010043
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Journal of Plant Biology
1998 Volume.41 No. 1 p.43 ~ p.49
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Generation of Active Oxygen Species(AOS) and Induction of β-Glucanase Activity by Fungal Elicitor Xylanase in the Suspension Cultured Cells of Tobacco
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Kim, Su Jin
Ko, Jae Heung/Park, Ky Young/Lee, Sun Hi
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Abstract
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It was investigated that active oxygen species (AOS) involved in the plant defense responses induced by fungal elicitor xylanase. When xylanase from the fungus Trichoderma viridae was treated to tobacco suspension cultured cells as an elicitor, β-glucanase activity was increased markedly. Lignin biosynthesis was also increased and peaked at 72 h after the treatment with xylanase. The treatment of H_2O_2 also dramatically increased β-glucanase activity at 24 h, which was much earlier than that of xylanase did. Using Iucigenin- and Iuminol-dependent chemiluminescence, the effects of xylanase on oxidative burst were examined. Superoxide anion (O_2) production was peaked at 40h and 52 h after xylanase treatment and hydrogen peroxide (H_2O_2) release was peaked at 44 h and 56 h, suggesting H_2O_2 burst was followed by O_2 generation. The scavengers of AOS, n-propyl gallate (PG) and mannitol, inhibited xylanase-induced β-glucanase activity by 85% and 50%, respectively. The activity of superoxide dismutase (SOD), which catalyzes the dismutation of O_2 to H_2O_2, began to increase from 24 h and reached to maximum at 48 h after xylanase treatment. Pretreatment of N,N,-diethyldithiocarbamate (DDC), known as a SOD inhibitor, caused the inhibition of H_2O_2 generation by 80% and reduced the β-glucanase activity by 60%. Treatment of 2,5-nor-bonadiene (NBD), a specific ethylene-action inhibitor, did not have any significant effect on xylanase-induced β-glucanase activity. This result suggested that ethylene did not involve in xylanase-induced response. Our results strongly suggest that the AOS generation is an essential component in plant defense response, in which cell wall degrading enzyme, glucanase, contributes to remove the necrotic tissue induced by pathogens.
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