蛋白激酶PKS5通过阻断质膜H+-ATP酶与14-3-3蛋白的相互作用抑制其活性
2009-08-25 来源:本站 点击次数:3886
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| 蛋白激酶PKS5通过阻断质膜H+-ATP酶与14-3-3蛋白的相互作用抑制其活性
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如何调控细胞的pH梯度对植物响应激素和环境非常重要，例如生长素、蓝光和真菌的分泌物。然而，这个调控过程中的信号是什么依然知之甚少。丹麦Copenhagen 大学的Fuglsang和中国科学家郭岩等报道了PKS5（一种拟南芥丝氨酸/苏氨酸蛋白激酶）是质膜质子泵（PM H+-ATPase）的负调控因子。 Fuglsang和郭岩等科学家采用“非损伤微测技术（MIFE）”检测了不同pH条件下拟南芥pks5突变体根中净质子流量的变化情况，发现在根部成熟区测得的H+流野生型和突变体没有明显差异，而在根尖处，野生型内的H+外流远远高于突变体，pks5突变体植株把质子排出胞外因而能够忍耐外部更高的pH。PKS5在C端调控区域的Ser931位点磷酸化PM H+-ATPase AHA2，磷酸化抑制PM H+-ATPase和有活性的14-3-3蛋白的相互作用。PKS5与Ca2+结合蛋白SCaBP1相互作用，引起胞外高pH促进胞内Ca2+的增加。 |
 上图：使用非损伤微测技术检测到的拟南芥野 生型和pks5根部尖端和成熟根部质子流。正值为外流。 | ||
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PKS5是新的Ca2+信号途径的调控者，控制PM H+-ATPase的活性和胞外的酸化。这一发现支持了在pks5-1中PM H+-ATPase的活性较高这一观点，这也为翻译后修饰控制离子通过质膜的运输提供了一个新的实例 。 | |||
关 键 词：PKS5；质膜质子泵（PM H+-ATPase）；非损伤微测技术(MIFE)
参考文献：Anja T.Fuglsang, et al. The Plant Cell, 2007, 19:1617-1634
abstract:
Regulation of the trans-plasma membrane pH gradient is an important part of plant responses to several hormonal and environmental cues, including auxin, blue light, and fungal elicitors. However, little is known about the signaling components that mediate this regulation. Here, we report that an Arabidopsis thaliana Ser/Thr protein kinase, PKS5, is a negative regulator of the plasma membrane proton pump (PM H+-ATPase). Loss-of-function pks5 mutant plants are more tolerant of high external pH due to extrusion of protons to the extracellular space. PKS5 phosphorylates the PM H+-ATPase AHA2 at a novel site, Ser-931, in the C-terminal regulatory domain. Phosphorylation at this site inhibits interaction between the PM H+-ATPase and an activating 14-3-3 protein in a yeast expression system. We show that PKS5 interacts with the calcium binding protein SCaBP1 and that high external pH can trigger an increase in the concentration of cytosolic-free calcium. These results suggest that PKS5 is part of a calcium-signaling pathway mediating PM H+-ATPase regulation.
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