Protein phosphatase 1 positively regulates stomatal opening in response to blue light in Vicia faba
Protein phosphatase 1 positively regulates stomatal opening in response to blue light in Vicia faba
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DOI：
10.1073/pnas.0602503103
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发表时间：
2006-09-05
影响因子：
11.1
通讯作者：
Shimazaki, Ken-ichiro
中科院分区：
文献类型：
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作者：
Takemiya, Atsushi;Kinoshita, Toshinori;Shimazaki, Ken-ichiro
植物蓝光受体类植物光敏素通过激活质膜H+-ATPase来调节气孔的开放，其机制尚不清楚。本文报道了在蚕豆保卫细胞中，1型蛋白磷酸酶(PP1)正向调节向光素和H+-ATPase之间的蓝光信号。我们从保卫细胞中克隆了PP1的四个催化亚基(PP1c)，并测定了其亚型在不同组织中的表达。用一个氨基酸突变失去酶活性的PP1c亚型转化蚕豆保卫细胞，或用PP1c的特异性抑制蛋白人抑制物-2转化蚕豆保卫细胞，可抑制蓝光诱导的气孔开放。在这些转化的保卫细胞中加入质膜H+-ATPase激活剂褐霉素，可诱导正常的气孔开放，表明转化不影响气孔开放的基本机制。PP1的抑制剂TAutomycin抑制蓝光诱导的H+泵、保卫细胞原生质体质膜H+-ATPase的磷酸化和气孔的开放。然而，他托霉素并不抑制蓝光依赖的趋光素的磷酸化。我们认为，PP1在保卫细胞的蓝光信号通路中位于趋光素的下游和H+-ATPase的上游。
Phototropins, plant blue light receptors, mediate stomatal opening through the activation of the plasma membrane H+-ATPase by unknown mechanisms. Here we report that type 1 protein phosphatase (PP1) positively regulates the blue light signaling between phototropins and the H+-ATPase in guard cells of Vicia taba. We cloned the four catalytic subunits of PP1 (PP1c) from guard cells and determined the expression of the isoforms in various tissues. Transformation of Vicia guard cells with PP1c isoforms that had lost enzymatic activity by one amino acid mutation, or with human inhibitor-2, a specific inhibitor protein of PP1c, suppressed blue light-induced stomatal opening. Addition of fusicoccin, an activator of the plasma membrane H+-ATPase, to these transformed guard cells induced normal stomatal opening, suggesting that the transformations did not affect the basic mechanisms for stomatal opening. Tautomycin, an inhibitor of PP1, inhibited blue light-induced H+ pumping, phosphorylation of the plasma membrane H+-ATPase in guard cell protoplasts, and stomatal opening. However, tautomycin did not inhibit the blue light-dependent phosphorylation of phototropins. We conclude that PP1 functions downstream of phototropins and upstream of the H+-ATPase in the blue light signaling pathway of guard cells.