Lipid Peroxide-Derived Short-Chain Carbonyls Mediate Hydrogen Peroxide-Induced and Salt-Induced Programmed Cell Death in Plants
Lipid Peroxide-Derived Short-Chain Carbonyls Mediate Hydrogen Peroxide-Induced and Salt-Induced Programmed Cell Death in Plants
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DOI：
10.1104/pp.115.256834
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发表时间：
2015-07-01
期刊：
影响因子：
7.4
通讯作者：
Mano, Jun'ichi
中科院分区：
文献类型：
--
作者：
Biswas, Md. Sanaullah;Mano, Jun'ichi
脂质过氧化物衍生的有毒羰基化合物（oxylipin carbonyls），下游产生的活性氧（ROS），最近被发现介导非生物胁迫诱导的植物损伤。在这里，我们研究了氧脂素羰基如何导致细胞死亡。当烟草（Nicotiana tabacum）亮黄-2（BY-2）细胞暴露于过氧化氢时，几种短链氧脂素羰基化合物[即4-羟基-（E）-2-壬烯醛和丙烯醛]积累，细胞发生程序性细胞死亡（PCD），根据DNA片段化、末端脱氧核苷酸转移酶dUTP缺口末端标记阳性细胞核增加和细胞质回缩判断。这些氧脂素羰基在烟草和拟南芥的BY-2细胞和根中引起PCD。为了测试氧脂素羰基介导氧化信号导致PCD的可能性，我们进行了药理学和遗传学实验。肌肽和肼苯哒嗪，具有不同的化学清除羰基，显着抑制氧化脂质羰基的增加，并阻止PCD在BY-2细胞和拟南芥根，但他们没有影响ROS和脂质过氧化物的水平。过量产生2-烯醛还原酶（一种拟南芥酶，用于解毒α，β-不饱和羰基）的转基因烟草品系在过氧化氢或盐处理后根表皮中的PCD比野生型少，而由于胁迫处理导致的ROS水平增加在品系之间没有差异。从这些结果，我们得出结论，氧脂素羰基参与的PCD过程中的氧化应激细胞。我们比较了不同羰基化合物在BY-2细胞中诱导PCD的能力，发现丙烯醛和4-羟基-（E）-2-壬烯醛是最有效的羰基化合物。羰基诱导的PCD的生理相关性和可能的机制进行了讨论。
Lipid peroxide-derived toxic carbonyl compounds (oxylipin carbonyls), produced downstream of reactive oxygen species (ROS), were recently revealed to mediate abiotic stress-induced damage of plants. Here, we investigated how oxylipin carbonyls cause cell death. When tobacco (Nicotiana tabacum) Bright Yellow-2 (BY-2) cells were exposed to hydrogen peroxide, several species of short-chain oxylipin carbonyls [i.e. 4-hydroxy-(E)-2-nonenal and acrolein] accumulated and the cells underwent programmed cell death (PCD), as judged based on DNA fragmentation, an increase in terminal deoxynucleotidyl transferase dUTP nick end labeling-positive nuclei, and cytoplasm retraction. These oxylipin carbonyls caused PCD in BY-2 cells and roots of tobacco and Arabidopsis (Arabidopsis thaliana). To test the possibility that oxylipin carbonyls mediate an oxidative signal to cause PCD, we performed pharmacological and genetic experiments. Carnosine and hydralazine, having distinct chemistry for scavenging carbonyls, significantly suppressed the increase in oxylipin carbonyls and blocked PCD in BY-2 cells and Arabidopsis roots, but they did not affect the levels of ROS and lipid peroxides. A transgenic tobacco line that overproduces 2-alkenal reductase, an Arabidopsis enzyme to detoxify alpha,beta-unsaturated carbonyls, suffered less PCD in root epidermis after hydrogen peroxide or salt treatment than did the wild type, whereas the ROS level increases due to the stress treatments were not different between the lines. From these results, we conclude that oxylipin carbonyls are involved in the PCD process in oxidatively stressed cells. Our comparison of the ability of distinct carbonyls to induce PCD in BY-2 cells revealed that acrolein and 4-hydroxy-(E)-2-nonenal are the most potent carbonyls. The physiological relevance and possible mechanisms of the carbonyl-induced PCD are discussed.