Plant responses to high temperature
Plant responses to high temperature
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DOI：
10.1002/9780470988503.ch5
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发表时间：
2005-01-01
期刊：
影响因子：
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通讯作者：
Vierling, Elizabeth
中科院分区：
文献类型：
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作者：
Larkindale, Jane;Mishkind, Michael;Vierling, Elizabeth
植物以许多不同的方式经历高温，对高温的适应或驯化发生在不同的时间尺度和植物组织水平上。暴露于高温可以是慢性或长期的，如在较热的栖息地所经历的，或者由于季节性或每日极端温度而更加急性。同样清楚的是，不同的植物组织和器官以及处于不同生长阶段的植物将以不同的方式受到损害，这取决于在胁迫时活跃的主要细胞过程的热敏感性。总而言之，这意味着“热应激”（因此，“耐热性”）不是一个单一的现象，而是生物体内平衡的一系列复杂扰动。在细胞水平上，热影响广泛的结构和功能。高温改变脂质性质，导致膜变得更加流动，从而破坏膜过程。所有蛋白质都有一个最佳的活性温度窗口，因此温度升高会改变酶的活性，导致代谢途径的不平衡，最终在高温下蛋白质变性。膜和蛋白质的损伤导致活性氧物质（AOS）的产生。这可能无法通过高温下的抗氧化剂有效控制，导致除了加热的直接影响外，还导致热诱导的氧化损伤。在生理水平上，这种损害转化为光合作用效率降低，同化物转运受损和碳增益损失。这些因素反过来又联合收割机导致物候改变、繁殖失败和加速衰老（Hall，2001）。因此，可以预期，植物对热的反应涉及许多不同的过程，涉及许多基因。同样重要的是要认识到，在自然环境中，植物经常暴露在高温和其他压力下。高温和干旱胁迫尤其如此，这两种胁迫往往同时发生。热胁迫也可能伴随着高辐照胁迫。其他环境应力也会导致与热引起的类似类型的损伤。因此，预计植物对不同胁迫的反应可能重叠，暴露于任何一种胁迫可能影响随后对另一种胁迫的反应。因此，来自不同压力的信号和保护途径可能会交叉，共享共同的组件。
Plants experience high temperature in many different ways and adaptation or acclimation to high temperature occurs over different time scales and levels of plant organization. Exposure to high temperature can be chronic or long term, as experienced in hotter habitats, or it can be more acute, as a result of seasonal or daily temperature extremes. It is also clear that different plant tissues and organs, and plants at different growth stages will be damaged in different ways depending on the heat susceptibility of the dominant cellular processes that are active at the time of the stress. Altogether, this means that ‘heat stress’(and therefore,‘heat tolerance’) is not a single phenomenon, but rather a varying set of complex perturbations of organismal homeostasis. At the cellular level, heat affects a wide range of structures and functions. High temperatures alter lipid properties, causing membranes to become more fluid and thereby disrupting membrane processes. All proteins have an optimal temperature window for activity, so increased temperatures alter enzyme activity leading to imbalance in metabolic pathways, and eventually at high temperature proteins denature. Membrane and protein damage leads to the production of active oxygen species (AOS). This may not be effectively controlled through antioxidants at high temperatures, resulting in heat-induced oxidative damage in addition to the direct effects of heating. At the physiological level, this damage translates into reduced efficiency of photosynthesis, impaired translocation of assimilates and loss of carbon gain. These factors in turn combine to cause altered phenology, reproductive failure and accelerated senescence (Hall, 2001). Thus, it is to be expected that many different processes, involving many genes, are involved in plant responses to heat. It is also important to recognize that, in the natural environment, plants are often exposed to heat in conjunction with other stresses. This is especially true of heat and drought stress, which often co-occur. Heat stress may also be accompanied by high irradiance stress. Other environmental stresses also result in similar types of damage as those caused by heat. Therefore, it is expected that the responses of plants to different stresses might overlap, and that exposure to any one stress may affect subsequent reactions to another stress. Signaling and protective pathways from different stresses are therefore likely to intersect, sharing common components.