Fusaric acid induction of programmed cell death modulated through nitric oxide signalling in tobacco suspension cells

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• 作者：Jiao Jiao (1)
  Benguo Zhou (2)
  Xiaoping Zhu (1)
  Zhengliang Gao (2)
  Yuancun Liang (1)
  
• 关键词：Tobacco suspension cells ; Fusaric acid ; Programmed cell death ; Nitric oxide ; Caspase ; 3 ; like protease
• 刊名：Planta
• 出版年：2013
• 出版时间：October 2013
• 年：2013
• 卷：238
• 期：4
• 页码：727-737
• 全文大小：
• 作者单位：Jiao Jiao (1)
  Benguo Zhou (2)
  Xiaoping Zhu (1)
  Zhengliang Gao (2)
  Yuancun Liang (1)
  
  1. Department of Plant Pathology, Shandong Agricultural University, Taian, 271018, China
  2. Tobacco Research Institute, Anhui Academy of Agricultural Sciences, Hefei, 230031, China
  
• ISSN：1432-2048

文摘

Fusaric acid (FA) is a nonhost-selective toxin mainly produced by Fusarium oxysporum, the causal agent of plant wilt diseases. We demonstrate that FA can induce programmed cell death (PCD) in tobacco suspension cells and the FA-induced PCD is modulated by nitric oxide (NO) signalling. Cells undergoing cell death induced by FA treatment exhibited typical characteristics of PCD including cytoplasmic shrinkage, chromatin condensation, DNA fragmentation, membrane plasmolysis, and formation of small cytoplasmic vacuoles. In addition, caspase-3-like activity was activated upon the FA treatment. The process of FA-induced PCD was accompanied by a rapid accumulation of NO in a FA dose-dependent manner. Pre-treatment of cells with NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) or NO synthase inhibitor N G-monomethyl-arginine monoacetate (L-NMMA) significantly reduced the rate of FA-induced cell death. Furthermore, the caspase-3-like activity and the expression of PAL and Hsr203J genes were alleviated by application of cPTIO or L-NMMA to FA-treated tobacco cells. This indicates that NO is an important factor involved in the FA-induced PCD. Our results also show that pre-treatment of tobacco cells with a caspase-3-specific inhibitor, Ac-DEVD-CHO, can reduce the rate of FA-induced cell death. These results demonstrate that the FA-induced cell death is a PCD and is modulated by NO signalling through caspase-3-like activation.