State Key Laboratory of Crop Biology, Shandong Key Laboratory of Crop Biology, Shandong Agricultural University, Tai'an 271018, Shandong, China.
Physiol Plant. 2011 Feb;141(2):117-29. doi: 10.1111/j.1399-3054.2010.01422.x. Epub 2010 Nov 4.
Alternaria alternata has received considerable attention in current literature and most of the studies are focused on its pathogenic effects on plant chloroplasts, but little is known about the characteristics of programmed cell death (PCD) induced by metabolic products (MP) of A. alternata, the effects of the MP on mitochondrial respiration and its relation to PCD. The purpose of this study was to explore the mechanism of MP-induced PCD in non-green tobacco BY-2 cells and to explore the role of mitochondrial inhibitory processes in the PCD of tobacco BY-2 cells. MP treatment led to significant cell death that was proven to be PCD by the concurrent cytoplasm shrinkage, chromatin condensation and DNA laddering observed in the cells. Moreover, MP treatment resulted in the overproduction of reactive oxygen species (ROS), rapid ATP depletion and a respiratory decline in the tobacco BY-2 cells. It was concluded that the direct inhibition of the mitochondrial electron transport chain (ETC), alternative pathway (AOX) capacity and catalase (CAT) activity by the MP might be the main contributors to the MP-induced ROS burst observed in tobacco BY-2 cells. The addition of adenosine together with the MP significantly inhibited ATP depletion without preventing PCD; however, when the cells were treated with the MP plus CAT, ROS overproduction was blocked and PCD did not occur. The data presented here demonstrate that the ROS burst played an important role in MP-induced PCD in the tobacco BY-2 cells.
链格孢Alternaria alternata 在当前文献中受到了相当多的关注，大多数研究都集中在其对植物叶绿体的致病作用上，但对代谢产物（MP）诱导的程序性细胞死亡（PCD）的特征、MP 对线粒体呼吸的影响及其与 PCD 的关系知之甚少。本研究旨在探索 MP 诱导非绿色烟草 BY-2 细胞 PCD 的机制，并探讨线粒体抑制过程在烟草 BY-2 细胞 PCD 中的作用。MP 处理导致明显的细胞死亡，通过观察到的细胞质收缩、染色质浓缩和 DNA 梯状，证明这是 PCD。此外，MP 处理导致烟草 BY-2 细胞中活性氧（ROS）的过度产生、ATP 的快速耗竭和呼吸下降。研究结论认为，MP 对线粒体电子传递链（ETC）、替代途径（AOX）能力和过氧化氢酶（CAT）活性的直接抑制可能是 MP 诱导烟草 BY-2 细胞中观察到的 ROS 爆发的主要原因。添加腺苷与 MP 一起显著抑制了 ATP 的耗竭，而不会阻止 PCD；然而，当用 MP 加 CAT 处理细胞时，ROS 的过度产生被阻断，PCD 不会发生。这里呈现的数据表明，ROS 爆发在 MP 诱导的烟草 BY-2 细胞 PCD 中起重要作用。
