4.7 Article

Reactive oxygen species from chloroplasts contribute to 3-acetyl-5-isopropyltetramic acid-induced leaf necrosis of Arabidopsis thaliana

期刊

PLANT PHYSIOLOGY AND BIOCHEMISTRY
卷 52, 期 -, 页码 38-51

出版社

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.plaphy.2011.11.004

关键词

3-AIPTA (3-acetyl-5-isopropyltetramic acid); ROS (reactive oxygen species); Cell death; Photosynthesis inhibitor; Chlorophyll a fluorescence transient; OJIP

资金

  1. National Natural Science Foundation of China [31000834]
  2. New Teacher Foundation of Doctoral Program of Education Ministry of China [200803071004]
  3. Education Ministry of China [200900 97110018]
  4. China 863 Program [2011AA10A206]
  5. 111 Project [B07030]
  6. Jiangsu Higher Education Institutions

向作者/读者索取更多资源

3-Acetyl-5-isopropyltetramic acid (3-AIPTA), a derivate of tetramic acid, is responsible for brown leaf-spot disease in many plants and often kills seedlings of both mono- and dicotyledonous plants. To further elucidate the mode of action of 3-AIPTA, during 3-AIPTA-induced cell necrosis, a series of experiments were performed to assess the role of reactive oxygen species (ROS) in this process. when Arabidopsis thaliana leaves were incubated with 3-AIPTA, photosystem II (PSII) electron transport beyond Q(A) (the primary plastoquinone acceptor of PSII) and the reduction of the end acceptors at the PSI acceptor side were inhibited; this was followed by increase in charge recombination and electron leakage to O-2, resulting in chloroplast-derived oxidative burst. Furthermore, the main antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX) lost their activity. Excess ROS molecules directly attacked a variety of cellular components and subsequently caused electrolyte leakage, lipid peroxidation and cell membrane disruption. Finally, this led to cell destruction and leaf tissue necrosis. Thus, 3-AIPTA-triggered leaf necrosis of Arabidopsis was found to be a result of direct oxidative injury from the chloroplast-originated ROS burst initiated by the inhibition of normal photosynthetic electron transport. (C) 2011 Elsevier Masson SAS. All rights reserved.

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