蛋白激酶PKS5通過阻斷質膜H+-ATP酶與14-3-3蛋白的相互作用抑制其活性
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| 蛋白激酶PKS5通過阻斷質膜H+-ATP酶與14-3-3蛋白的相互作用抑制其活性
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如何調控細胞的pH梯度對植物響應激素和環(huán)境非常重要，例如生長素、藍光和真菌的分泌物。然而，這個調控過程中的信號是什么依然知之甚少。丹麥Copenhagen 大學的Fuglsang和中國科學家郭巖等報道了PKS5（一種擬南芥絲氨酸/蘇氨酸蛋白激酶）是質膜質子泵（PM H+-ATPase）的負調控因子。 Fuglsang和郭巖等科學家采用“非損傷微測技術（MIFE）”檢測了不同pH條件下擬南芥pks5突變體根中凈質子流量的變化情況，發(fā)現(xiàn)在根部成熟區(qū)測得的H+流野生型和突變體沒有明顯差異，而在根尖處，野生型內的H+外流遠遠高于突變體，pks5突變體植株把質子排出胞外因而能夠忍耐外部更高的pH。PKS5在C端調控區(qū)域的Ser931位點磷酸化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與Ca2+結合蛋白SCaBP1相互作用，引起胞外高pH促進胞內Ca2+的增加。 |
 上圖：使用非損傷微測技術檢測到的擬南芥野 生型和pks5根部尖端和成熟根部質子流。正值為外流。 | ||
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PKS5是新的Ca2+信號途徑的調控者，控制PM H+-ATPase的活性和胞外的酸化。這一發(fā)現(xiàn)支持了在pks5-1中PM H+-ATPase的活性較高這一觀點，這也為翻譯后修飾控制離子通過質膜的運輸提供了一個新的實例 。 | |||
關 鍵 詞：PKS5；質膜質子泵（PM H+-ATPase）；非損傷微測技術(MIFE)
參考文獻：Anja T.Fuglsang, et al. The Plant Cell, 2007, 19:1617-1634
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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.
