Department of Plant Biology, University of Szeged, Középfasor 52, 6701 Szeged, PO Box 654, Hungary.
Protoplasma. 2013 Feb;250(1):273-84. doi: 10.1007/s00709-012-0408-4. Epub 2012 Apr 26.
Salt stress- and salicylic acid (SA)-induced cell death can be activated by various signaling pathways including ethylene (ET) signaling in intact tomato plants. In tomato suspension cultures, a treatment with 250 mM NaCl increased the production of reactive oxygen species (ROS), nitric oxide (NO), and ET. The 10(-3) M SA-induced cell death was also accompanied by ROS and NO production, but ET emanation, the most characteristic difference between the two cell death programs, did not change. ET synthesis was enhanced by addition of ET precursor 1-aminocyclopropane-1-carboxylic acid, which, after 2 h, increased the ROS production in the case of both stressors and accelerated cell death under salt stress. However, it did not change the viability and NO levels in SA-treated samples. The effect of ET induced by salt stress could be blocked with silver thiosulfate (STS), an inhibitor of ET action. STS reduced the death of cells which is in accordance with the decrease in ROS production of cells exposed to high salinity. Unexpectedly, application of STS together with SA resulted in increasing ROS and reduced NO accumulation which led to a faster cell death. NaCl- and SA-induced cell death was blocked by Ca(2+) chelator EGTA and calmodulin inhibitor W-7, or with the inhibitors of ROS. The inhibitor of MAPKs, PD98059, and the cysteine protease inhibitor E-64 reduced cell death in both cases. These results show that NaCl induces cell death mainly by ET-induced ROS production, but ROS generated by SA was not controlled by ET in tomato cell suspension.
盐胁迫和水杨酸（SA）诱导的细胞死亡可以通过多种信号通路激活，包括完整番茄植株中的乙烯（ET）信号通路。在番茄悬浮培养物中，用 250 mM NaCl 处理会增加活性氧（ROS）、一氧化氮（NO）和 ET 的产生。10(-3) M SA 诱导的细胞死亡也伴随着 ROS 和 NO 的产生，但 ET 释放，这是两种细胞死亡程序之间最显著的差异，并没有改变。ET 合成通过添加 ET 前体 1-氨基环丙烷-1-羧酸（1-aminocyclopropane-1-carboxylic acid）得到增强，在这两种胁迫源的情况下，2 小时后，ROS 的产生增加，并加速盐胁迫下的细胞死亡。然而，它并没有改变 SA 处理样品的活力和 NO 水平。盐胁迫诱导的 ET 作用可以被 ET 作用抑制剂硫酸银（STS）阻断。STS 减少了细胞死亡，这与暴露在高盐环境下的细胞 ROS 产生减少是一致的。出乎意料的是，STS 与 SA 一起应用会导致 ROS 增加和 NO 积累减少，从而导致更快的细胞死亡。Ca(2+)螯合剂 EGTA 和钙调蛋白抑制剂 W-7，或 ROS 抑制剂可以阻断 NaCl 和 SA 诱导的细胞死亡。MAPKs 抑制剂 PD98059 和半胱氨酸蛋白酶抑制剂 E-64 减少了两种情况下的细胞死亡。这些结果表明，NaCl 主要通过 ET 诱导的 ROS 产生诱导细胞死亡，但番茄悬浮细胞中 SA 产生的 ROS 不受 ET 控制。
