The Heat Shock Response in Moss Plants Is Regulated by Specific Calcium-Permeable Channels in the Plasma Membrane
The Heat Shock Response in Moss Plants Is Regulated by Specific Calcium-Permeable Channels in the Plasma Membrane
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DOI：
10.1105/tpc.108.065318
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发表时间：
2009-09-01
期刊：
影响因子：
11.6
通讯作者：
Goloubinoff, Pierre
中科院分区：
文献类型：
--
作者：
Saidi, Younousse;Finka, Andrija;Goloubinoff, Pierre
陆地植物容易受到强烈的温度变化的影响，因此必须感知早期适度的温度增量，以诱导适当的细胞防御，如分子伴侣，以应对即将到来的有害温度。为了研究植物如何感知环境温度的温和变化，我们在重组系的藓小立碗藓监测热诱导型启动子的激活，不耐热酶的完整性，和细胞质钙的波动。温和的温度增量，或等温处理与膜流化剂或热休克蛋白90抑制剂，诱导的热休克反应（HSR），严重依赖于前Ca2+瞬态通过质膜。电生理学实验表明，存在的Ca2+渗透通道的质膜，是短暂激活温和的温度增量或化学扰动膜流动性。在第一分钟的温度应力的钙离子流入的幅度调制的强度的HSR，和Ca2+通道阻滞剂防止HSR和耐热性的发病。我们的数据表明，温和的温度增量的早期感知发生在植物细胞质膜独立于胞质蛋白展开。热信号通过特定的膜调节的Ca2+内流转化为有效的HSR，导致耐热性。
Land plants are prone to strong thermal variations and must therefore sense early moderate temperature increments to induce appropriate cellular defenses, such as molecular chaperones, in anticipation of upcoming noxious temperatures. To investigate how plants perceive mild changes in ambient temperature, we monitored in recombinant lines of the moss Physcomitrella patens the activation of a heat-inducible promoter, the integrity of a thermolabile enzyme, and the fluctuations of cytoplasmic calcium. Mild temperature increments, or isothermal treatments with membrane fluidizers or Hsp90 inhibitors, induced a heat shock response (HSR) that critically depended on a preceding Ca2+ transient through the plasma membrane. Electrophysiological experiments revealed the presence of a Ca2+-permeable channel in the plasma membrane that is transiently activated by mild temperature increments or chemical perturbations of membrane fluidity. The amplitude of the Ca2+ influx during the first minutes of a temperature stress modulated the intensity of the HSR, and Ca2+ channel blockers prevented HSR and the onset of thermotolerance. Our data suggest that early sensing of mild temperature increments occurs at the plasma membrane of plant cells independently from cytosolic protein unfolding. The heat signal is translated into an effective HSR by way of a specific membrane-regulated Ca2+ influx, leading to thermotolerance.