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1-Butanol triggers programmed cell death in Populus euphratica cell cultures
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  • 作者:Jing Zhang (1)
    Yicheng Yu (1)
    Zongyun Li (1)
    Cunhua Sun (1)
    Jian Zhang (1)
    Meiyan Liu (1)
    Aimin Wang (1)
    Jian Sun (1)
  • 关键词:Populus euphratica cells ; 1 ; Butanol ; Programmed cell death ; PA ; NO ; Mitochondria H2O2
  • 刊名:Plant Growth Regulation
  • 出版年:2014
  • 出版时间:September 2014
  • 年:2014
  • 卷:74
  • 期:1
  • 页码:33-45
  • 全文大小:2,208 KB
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  • 作者单位:Jing Zhang (1)
    Yicheng Yu (1)
    Zongyun Li (1)
    Cunhua Sun (1)
    Jian Zhang (1)
    Meiyan Liu (1)
    Aimin Wang (1)
    Jian Sun (1)

    1. Institute of Integrative Plant Biology, School of Life Science, Jiangsu Normal University, Xuzhou, 221116, Jiangsu Province, People’s Republic of China
  • ISSN:1573-5087
文摘
1-Butanol, which is a specific inhibitor of phospholipase D, usually inhibits phosphatidic acid (PA) production and blocks the PA-dependent signaling pathway under stress conditions. However, the effects of 1-butanol on plant cells under non-stress condition are still unclear. In this study, we report that 1-butanol induced a dose dependent cell death in poplar (Populus euphratica) cell cultures. In contrast, the control 2-butanol and ethanol had no effects on cell viability. 1-Butanol-treated cells displayed hallmark features of programmed cell death (PCD), such as shrinkage of the cytoplasm, DNA fragmentation, condensed or stretched chromatin and the activation of caspase-3-like protease. Exogenous application of PA markedly inhibited the 1-butanol-induced PCD. 1-Butanol also caused a burst of mitochondrial H2O2 ([H2O2]mit) that was usually accompanied by a loss of mitochondrial membrane potential (?em class="a-plus-plus">Ψm). Supplement of PA, antioxidant enzyme (catalase) and antioxidant (ascorbic acid) reversed this effect. Moreover, a significant increase of nitric oxide (NO) was observed in 1-butanol-treated poplar cells. This NO burst was suppressed by PA or inhibitors of NO synthesis. Further pharmacological experiments indicate that the burst of NO contributed to the 1-butanol-induced inhibition of antioxidant enzymes and subsequent H2O2-dependent PCD. In conclusion, we propose that 1-butanol is a potent inducer of PCD in plants and this process is regulated by the PA, NO and H2O2.

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