Heat stress activates phospholipase D and triggers PIP2 accumulation at the plasma membrane and nucleus
Heat stress activates phospholipase D and triggers PIP2 accumulation at the plasma membrane and nucleus
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DOI：
10.1111/j.1365-313x.2009.03933.x
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发表时间：
2009-10-01
期刊：
影响因子：
7.2
通讯作者：
Munnik, Teun
中科院分区：
文献类型：
--
作者：
Mishkind, Michael;Vermeer, Joop E. M.;Munnik, Teun
热应激诱导一系列生理调节，促进持续的稳态和生存期间的温度升高。在这里，我们报告说，在温度突然升高的几分钟内，植物将特定的磷脂部署到特定的细胞内位置：磷脂酶D（PLD）和磷脂酰肌醇磷酸激酶（PIPK）被激活，磷脂酸（PA）和磷脂酰肌醇4，5-二磷酸（PIP 2）迅速积累，热诱导的PIP 2定位于质膜，核膜，核仁和点状细胞质结构。PA和PIP 2的稳态水平的增加发生在温度从20-25摄氏度的环境水平增加到35摄氏度及以上的几分钟内。在热胁迫的拟南芥幼苗和水稻叶片中观察到类似的模式。PA的积累，在响应温度升高的结果，在很大程度上从PLD的激活，而不是磷脂酶C和甘油二酯激酶，用于产生这种脂质的替代途径的顺序作用。脉冲标记分析表明，PIP 2响应是由于PIPK的激活，而不是脂肪酶或PIP 2磷酸酶的抑制。抑制剂实验表明，PIP 2反应需要通过G蛋白的信号传导，因为氟化铝阻断热诱导的PIP 2增加。这些结果的背景下，PIP 2和PA，包括离子通道和细胞骨架的调节所发挥的不同的细胞作用进行了讨论。
Heat stress induces an array of physiological adjustments that facilitate continued homeostasis and survival during periods of elevated temperatures. Here, we report that within minutes of a sudden temperature increase, plants deploy specific phospholipids to specific intracellular locations: phospholipase D (PLD) and a phosphatidylinositolphosphate kinase (PIPK) are activated, and phosphatidic acid (PA) and phosphatidylinositol 4,5-bisphosphate (PIP2) rapidly accumulate, with the heat-induced PIP2 localized to the plasma membrane, nuclear envelope, nucleolus and punctate cytoplasmic structures. Increases in the steady-state levels of PA and PIP2 occur within several minutes of temperature increases from ambient levels of 20-25 degrees C to 35 degrees C and above. Similar patterns were observed in heat-stressed Arabidopsis seedlings and rice leaves. The PA that accumulates in response to temperature increases results in large part from the activation of PLD rather than the sequential action of phospholipase C and diacylglycerol kinase, the alternative pathway used to produce this lipid. Pulse-labelling analysis revealed that the PIP2 response is due to the activation of a PIPK rather than inhibition of a lipase or a PIP2 phosphatase. Inhibitor experiments suggest that the PIP2 response requires signalling through a G-protein, as aluminium fluoride blocks heat-induced PIP2 increases. These results are discussed in the context of the diverse cellular roles played by PIP2 and PA, including regulation of ion channels and the cytoskeleton.