Demidchik Vadim, Tyutereva Elena V, Voitsekhovskaja Olga V
Laboratory of Plant Ecological Physiology, Komarov Botanical Institute, Russian Academy of Sciences, ul. Professora Popova 2, 197376St Petersburg, Russia.
Funct Plant Biol. 2018 Jan;45(2):28-46. doi: 10.1071/FP16380.
Environmental stresses such as salinity, drought, oxidants, heavy metals, hypoxia, extreme temperatures and others can induce autophagy and necrosis-type programmed cell death (PCD) in plant roots. These reactions are accompanied by the generation of reactive oxygen species (ROS) and ion disequilibrium, which is induced by electrolyte/K+ leakage through ROS-activated ion channels, such as the outwardly-rectifying K+ channel GORK and non-selective cation channels. Here, we discuss mechanisms of the stress-induced ion disequilibrium and relate it with ROS generation and onset of morphological, biochemical and genetic symptoms of autophagy and PCD in roots. Based on our own data and that in the literature, we propose a hypothesis on the induction of autophagy and PCD in roots by loss of cytosolic K+. To support this, we present data showing that in conditions of salt stress-induced autophagy, gork1-1 plants lacking root K+ efflux channel have fewer autophagosomes compared with the wild type. Overall, literature analyses and presented data strongly suggest that stress-induced root autophagy and PCD are controlled by the level of cytosolic potassium and ROS.
盐度、干旱、氧化剂、重金属、缺氧、极端温度等环境胁迫可诱导植物根系发生自噬和坏死型程序性细胞死亡（PCD）。这些反应伴随着活性氧（ROS）的产生和离子失衡，而离子失衡是由ROS激活的离子通道（如外向整流钾通道GORK和非选择性阳离子通道）导致电解质/K+泄漏所引起的。在此，我们讨论胁迫诱导的离子失衡机制，并将其与ROS生成以及根系自噬和PCD的形态、生化和遗传症状的发生联系起来。基于我们自己的数据以及文献中的数据，我们提出了一个关于细胞质K+流失诱导根系自噬和PCD的假说。为支持这一假说，我们展示的数据表明，在盐胁迫诱导自噬的条件下，缺乏根系K+外流通道的gork1-1植物与野生型相比，自噬体数量更少。总体而言，文献分析和所展示的数据有力地表明，胁迫诱导的根系自噬和PCD受细胞质钾和ROS水平的控制。
