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Reactive oxygen species promote chloroplast dysfunction and salicylic acid accumulation in fumonisin B1‐induced cell death
Author(s) -
Xing Fuqiang,
Li Zhe,
Sun Aizhen,
Xing Da
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.05.034
Subject(s) - fumonisin b1 , reactive oxygen species , phenylalanine ammonia lyase , programmed cell death , chemistry , phenylalanine , chloroplast , salicylic acid , biochemistry , microbiology and biotechnology , apoptosis , biology , amino acid , gene , mycotoxin , food science
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 H 2 O 2 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.