Multi-Level Interactions Between Heat Shock Factors, Heat Shock Proteins, and the Redox System Regulate Acclimation to Heat.
Multi-Level Interactions Between Heat Shock Factors, Heat Shock Proteins, and the Redox System Regulate Acclimation to Heat.
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DOI：
10.3389/fpls.2015.00999
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发表时间：
2015
影响因子：
5.6
通讯作者：
Rieu I
中科院分区：
文献类型：
--
作者：
Driedonks N;Xu J;Peters JL;Park S;Rieu I
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。植物细胞暴露在高温下会导致细胞损伤，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，活性氧在热应激等非生物应激过程中积累。活性氧是有毒的，可以修饰其他生物大分子，包括膜脂、DNA和蛋白质。为了保护细胞，清除活性氧是必不可少的。与其固有的危害相反，ROS还可以作为信号分子，诱导胁迫耐受机制。本文综述了经典热应激反应（由热休克因子（hsf）和热休克蛋白（HSPs）组成）与热反应过程中多个水平的ROS网络之间串扰的证据。热直接刺激HSF活动，但也通过ROS间接刺激。hsf反过来刺激HSP伴侣的表达，也影响ROS清道夫基因的表达。在短期内，hsf通过诱导miRNA398抑制超氧化物歧化酶清除率基因的表达，同时通过HSP诱导激活清除率基因表达，稳定清除率蛋白活性。我们认为，这些对比效应允许在应激开始时促进热应激反应，同时防止随后的氧化损伤。所描述的hsf、hsp、ROS和ROS清除剂相互作用的模型似乎适用于对除热以外的胁迫的反应，并可能解释交叉驯化现象。
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.