期刊
FEBS LETTERS
卷 587, 期 14, 页码 2164-2172出版社
WILEY
DOI: 10.1016/j.febslet.2013.05.034
关键词
Chloroplast dysfunction; Fumonisin B1; Programmed cell death; Phenylalanine ammonia lyase; Reactive oxygen species; Salicylic acid
资金
- Program for Changjiang Scholars and Innovative Research Team in University [IRT0829]
- Key Program of NSFC-Guangdong Joint Funds of China [U0931005]
- National High Technology Research and Development Program of China (863 Program) [2007AA10Z204]
We report a novel regulatory mechanism by which reactive oxygen species (ROS) regulate fumonisin B1 (FB1)-induced cell death. We found that FB1 induction of light-dependent ROS production promoted the degradation of GFP-labeled chloroplast proteins and increased phenylalanine ammonia lyase (PAL) activity, PAL1 gene expression and SA content, while pretreatment with ROS manipulators reversed these trends. Moreover, treatment with H2O2 or 3-amino-1,2,4-triazole increased PAL activity, PAL1 gene expression and SA content. PAL inhibitor significantly blocked FB1-induced lesion formation and SA increase. Our results demonstrate that light-dependent ROS accumulation stimulates the degradation of chloroplastic proteins and up-regulates PAL-mediated SA synthesis, thus promoting FB1-induced light-dependent cell death. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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