Driedonks Nicky, Xu Jiemeng, Peters Janny L, Park Sunghun, Rieu Ivo
Department of Molecular Plant Physiology, Institute for Water and Wetland Research, Radboud University , Nijmegen, Netherlands.
Department of Horticulture, Forestry and Recreation Resources, Kansas State University , Manhattan, KS, USA.
Front Plant Sci. 2015 Nov 17;6:999. doi: 10.3389/fpls.2015.00999. eCollection 2015.
High temperature has become a global concern because it seriously affects the growth and reproduction of plants. Exposure of plant cells to high temperatures result in cellular damage and can even lead to cell death. Part of the damage can be ascribed to the action of reactive oxygen species (ROS), which accumulate during abiotic stresses such as heat stress. ROS are toxic and can modify other biomacromolecules including membrane lipids, DNA, and proteins. In order to protect the cells, ROS scavenging is essential. In contrast with their inherent harms, ROS also function as signaling molecules, inducing stress tolerance mechanisms. This review examines the evidence for crosstalk between the classical heat stress response, which consists of heat shock factors (HSFs) and heat shock proteins (HSPs), with the ROS network at multiple levels in the heat response process. Heat stimulates HSF activity directly, but also indirectly via ROS. HSFs in turn stimulate the expression of HSP chaperones and also affect ROS scavenger gene expression. In the short term, HSFs repress expression of superoxide dismutase scavenger genes via induction of miRNA398, while they also activate scavenger gene expression and stabilize scavenger protein activity via HSP induction. We propose that these contrasting effects allow for the boosting of the heat stress response at the very onset of the stress, while preventing subsequent oxidative damage. The described model on HSFs, HSPs, ROS, and ROS scavenger interactions seems applicable to responses to stresses other than heat and may explain the phenomenon of crossacclimation.
高温已成为全球关注的问题，因为它严重影响植物的生长和繁殖。植物细胞暴露于高温会导致细胞损伤，甚至可能导致细胞死亡。部分损伤可归因于活性氧（ROS）的作用，ROS在诸如热胁迫等非生物胁迫期间积累。ROS具有毒性，可修饰包括膜脂、DNA和蛋白质在内的其他生物大分子。为了保护细胞，清除ROS至关重要。与它们固有的危害相反，ROS还作为信号分子发挥作用，诱导胁迫耐受机制。本综述研究了经典热应激反应（由热休克因子（HSFs）和热休克蛋白（HSPs）组成）与热反应过程中多个水平的ROS网络之间相互作用的证据。热直接刺激HSF活性，但也通过ROS间接刺激。HSFs反过来刺激HSP伴侣蛋白的表达，也影响ROS清除基因的表达。短期内，HSFs通过诱导miRNA398抑制超氧化物歧化酶清除基因的表达，同时它们也通过HSP诱导激活清除基因的表达并稳定清除蛋白的活性。我们提出，这些相反的作用使得在胁迫刚开始时热应激反应得以增强，同时防止随后的氧化损伤。所描述的关于HSFs、HSPs、ROS和ROS清除剂相互作用的模型似乎适用于对除热以外的其他胁迫的反应，并且可能解释交叉适应现象。
