Dihydrosphingosine-lnduced Programmed Cell Death in Tobacco BY-2 Cells Is Independent of H2O2 Production

作     者：Christophe Lachaud 

作者机构：Universite de Toulouse UPS UMR 5546 Surfaces Cellulaires et Signalisation chez les Vegetaux BP 42617 F-31326 Castanet-Tolosan France CNRS UMR 5546 BP 42617 F-31326 Castanet-Tolosan France 

出 版 物：《Molecular Plant》 (分子植物（英文版）)

年 卷 期：2011年第4卷第2期

页      面：310-318页

核心收录：

学科分类：0710[理学-生物学] 081702[工学-化学工艺] 07[理学] 08[工学] 0817[工学-化学工程与技术] 071009[理学-细胞生物学] 09[农学] 0901[农学-作物学] 0902[农学-园艺学] 090102[农学-作物遗传育种] 

基　　金：Université de Toulouse Centre National de la Recherche Scientifique, CNRS 

主　　题：Tobacco BY-2 cells calcium signaling cytosolic calcium aequorin sphingolipids LCBs dihydrosphingosine sphinganine apoptosis Programmed Cell Death (PCD) Reactive Oxygen Species (ROS) H2O2 oxidative burst. 

摘      要：Sphinganine or dihydrosphingosine （d18：0, DHS）, one of the most abundant free sphingoid Long Chain Base （LCB） in plants, has been recently shown to induce both cytosolic and nuclear calcium transient increases and a correlated Programmed Cell Death （PCD） in tobacco BY-2 cells. In this study, in order to get deeper insight into the LCB signaling pathway leading to cell death, the putative role of Reactive Oxygen Species （ROS） has been investigated. We show that DHS triggers a rapid dose-dependent production of H2O2 that is blocked by diphenyleniodonium （DPI）, indicating the involvement of NADPH oxidase（s） in the process. In addition, while DPI does not block DHS-induced calcium increases, the ROS production is inhibited by the broad spectrum calcium channel blocker lanthanum （La^3＋）. Therefore, ROS production occurs downstream of DHS-induced Ca^2＋ transients. Interestingly, DHS activates expression of defense-related genes that is inhibited by both La^3＋ and DPI. Since DPI does not prevent DHS-induced cell death, these results strongly indicate that DHS-induced H2O2 production is not implicated in PCD mechanisms but rather would be associated to basal cell defense mechanisms.