Induction of defence gene expression by oligogalacturonic acid requires in- creases in both cytosolic calcium and hydrogen peroxide in Arabidopsis thaliana

作     者：Steven J NEILL Xiang Yang HU, Steven J NEILL, Wei Ming CAI, Zhang Cheng TANG Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200032, China. Centre for Research in Plant Science, University of the West of England, Bristol, Coldharbour Lane, Bristol BS16 1QY, UK

作者机构：Centre for Research in Plant Science University of the West of England Bristol Coldharbour Lane Bristol BS16 1QY UK 

出 版 物：《Cell Research》 (细胞研究(英文版))

年 卷 期：2004年第14卷第3期

页      面：234-240页

核心收录：

学科分类：0710[理学-生物学] 0831[工学-生物医学工程（可授工学、理学、医学学位）] 07[理学] 09[农学] 071007[理学-遗传学] 0901[农学-作物学] 090102[农学-作物遗传育种] 

基　　金：国家自然科学基金(39870050) 中国科学院资助项目(GrantKSCX2-SW-322) GST antibodies were obtained from Professor IE Somssich Professor S Kauffmann (Université Louis Pasteur, 67084 Strasbourg cedex,France) 

主　　题：Arabidopsis thaliana cytosolic calcium defence gene expression hydrogen peroxide OGA. 

摘      要：Responses to oligogalacturonic acid （OGA） were determined in transgenic Arabidopsis thaliana seedlings expressing the calcium reporter protein aequorin. OGA stimulated a rapid, substantial and transient increase in the concentration of cytosolic calcium （[Ca2+]cyt） that peaked after ca. 15 s. This increase was dose-dependent, saturating at ca. 50 μg Gal equiv/ml of OGA. OGA also stimulated a rapid generation of H2O2. A small, rapid increase in H2O2 content was followed by a much larger oxidative burst, with H2O2 content peaking after ca. 60 min and declining thereafter. Induction of the oxidative burst by OGA was also dose-dependent, with a maximum response again being achieved at ca. 50 μg Gal equiv/mL. Inhibitors of calcium fluxes inhibited both increases in [Ca2+]cyt and [H2O2], whereas inhibitors of NADPH oxidase blocked only the oxidative burst. OGA increased strongly the expression of the defence-related genes CHS, GST, PAL and PR-1. This induction was suppressed by inhibitors of calcium flux or