کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2047915 | 1074045 | 2013 | 9 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Reactive oxygen species promote chloroplast dysfunction and salicylic acid accumulation in fumonisin B1-induced cell death Reactive oxygen species promote chloroplast dysfunction and salicylic acid accumulation in fumonisin B1-induced cell death](/preview/png/2047915.png)
• Light-dependent ROS production is associated with FB1-induced cell death.
• ROS cause chloroplast dysfunction in response to FB1 treatment.
• ROS promote SA synthesis via PAL-mediated signaling pathway in FB1-induced cell death.
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.
Journal: FEBS Letters - Volume 587, Issue 14, 11 July 2013, Pages 2164–2172