Silicon does not mitigate cell death in cultured tobacco BY-2 cells subjected to salinity without ethylene emission
Silicon does not mitigate cell death in cultured tobacco BY-2 cells subjected to salinity without ethylene emission
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DOI：
10.1007/s00299-014-1712-6
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发表时间：
2015-02-01
影响因子：
6.2
通讯作者：
Bi, Yurong
中科院分区：
文献类型：
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作者：
Liang, Xiaolei;Wang, Huahua;Bi, Yurong
当培养的烟草 BY-2 细胞中乙烯受到抑制时，硅会诱导细胞死亡。 Si 和乙烯信号传导之间存在串扰。硅 (Si) 有利于植物生长。它可以减轻植物的生物和非生物胁迫。硅在植物中的作用仍然是个谜。本研究探讨了当乙烯受到抑制时，硅在烟草 BY-2 细胞培养物中诱导细胞死亡的机制。结果表明，K2SiO3减轻了NaCl应力的损害。 Si处理迅速增加乙烯排放和乙烯生物合成基因的表达。用 Si + Ag 和 Si + 氨基氧乙酸（AOA，乙烯生物合成抑制剂）处理会减少细胞生长并增加细胞损伤。 Si + Ag 处理诱导过氧化氢 (H2O2) 产生并最终导致细胞死亡。用Si+Ag处理的BY-2细胞的一些细胞核出现TUNEL阳性。 H2O2 和一氧化氮 (NO) 产生的抑制降低了 Si + Ag 处理引起的细胞死亡率。 Si消除了Ag对旁路途径的上调。这些数据表明乙烯在植物的硅功能中起着重要作用。如果没有乙烯，Si不仅不能增强植物的抗性，而且还会增加H2O2的产生，并进一步诱导烟草BY-2细胞的细胞死亡。
Silicon induces cell death when ethylene is suppressed in cultured tobacco BY-2 cells. There is a crosstalk between Si and ethylene signaling.Silicon (Si) is beneficial for plant growth. It alleviates both biotic and abiotic stresses in plants. How Si works in plants is still mysterious. This study investigates the mechanism of Si-induced cell death in tobacco BY-2 cell cultures when ethylene is suppressed. Results showed that K2SiO3 alleviated the damage of NaCl stress. Si treatment rapidly increased ethylene emission and the expression of ethylene biosynthesis genes. Treatments with Si + Ag and Si + aminooxyacetic acid (AOA, ethylene biosynthesis inhibitor) reduced the cell growth and increased cell damage. The treatment with Si + Ag induced hydrogen peroxide (H2O2) generation and ultimately cell death. Some nucleus of BY-2 cells treated with Si + Ag appeared TUNEL positive. The inhibition of H2O2 and nitric oxide (NO) production reduced the cell death rate induced by Si + Ag treatment. Si eliminated the up-regulation of alternative pathway by Ag. These data suggest that ethylene plays an important role in Si function in plants. Without ethylene, Si not only failed to enhance plant resistance, but also elevated H2O2 generation and further induced cell death in tobacco BY-2 cells.