CIPK23 regulates blue light-dependent stomatal opening in Arabidopsis thaliana.
CIPK23 regulates blue light-dependent stomatal opening in Arabidopsis thaliana.
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DOI：
10.1111/tpj.14955
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发表时间：
2020-11
期刊：
影响因子：
--
通讯作者：
Shimazaki KI
中科院分区：
文献类型：
--
作者：
Inoue SI;Kaiserli E;Zhao X;Waksman T;Takemiya A;Okumura M;Takahashi H;Seki M;Shinozaki K;Endo Y;Sawasaki T;Kinoshita T;Zhang X;Christie JM;Shimazaki KI
这项研究表明 CIPK23 是一种向光素相互作用的蛋白激酶，可促进拟南芥中蓝光和向光素依赖性气孔的打开。我们认为 CIPK23 不介导质膜 H+-ATP 酶激活，但介导气孔开放中的内向整流 K+ 通道激活。 向光素（phot1 和 phot2）是植物蓝光受体激酶，在拟南芥中发挥介导向光性、叶绿体运动、叶片扁平化和气孔开放的作用。在理解与光激活促光素受体相关的机制方面已经取得了相当大的进展。然而，相比之下，人们对促光素信号成分的身份了解较少。在这项研究中，我们通过使用体外筛选方法 (AlphaScreen) 来分析与拟南芥蛋白激酶库的相互作用，专门寻找与向光素相互作用的蛋白激酶。我们发现 CBL 相互作用蛋白激酶 23 (CIPK23) 与 phot1 和 phot2 相互作用。尽管这些相互作用通过体外 Pull-down 和体内双分子荧光互补测定得到验证，但 CIPK23 并未被 phot1 磷酸化，至少在体外是这样。发现缺乏 CIPK23 的突变体对蓝光的反应表现出气孔开放受损，但在其他向光素介导的反应中没有缺陷。我们进一步发现，在 cipk23 突变体的保卫细胞中，蓝光激活的内向整流 K+ (K+ in) 通道受到损害，而质膜 H+-ATP 酶的激活则没有受到损害。 BLUS1 突变体中 K+ 通道中的蓝光激活也受到损害，BLUS1 是保卫细胞中的向光素底物之一。因此，我们得出结论，CIPK23 通过激活通道中的 K+ 促进气孔开放，很可能与 BLUS1 一致，但通过的机制不是激活 H+-ATP 酶。讨论了 CIPK23 作为气孔保卫细胞中新发现的向光素信号传导成分的作用。
This study indicates that CIPK23 is a phototropin‐interacting protein kinase that promotes blue light‐ and phototropin‐dependent stomatal opening in Arabidopsis thaliana. We propose that CIPK23 does not mediate plasma membrane H+‐ATPase activation but mediates inward‐rectifying K+ channel activation in stomatal opening. Phototropins (phot1 and phot2) are plant blue light receptor kinases that function to mediate phototropism, chloroplast movement, leaf flattening, and stomatal opening in Arabidopsis. Considerable progress has been made in understanding the mechanisms associated with phototropin receptor activation by light. However, the identities of phototropin signaling components are less well understood by comparison. In this study, we specifically searched for protein kinases that interact with phototropins by using an in vitro screening method (AlphaScreen) to profile interactions against an Arabidopsis protein kinase library. We found that CBL‐interacting protein kinase 23 (CIPK23) interacts with both phot1 and phot2. Although these interactions were verified by in vitro pull‐down and in vivo bimolecular fluorescence complementation assays, CIPK23 was not phosphorylated by phot1, as least in vitro. Mutants lacking CIPK23 were found to exhibit impaired stomatal opening in response to blue light but no deficits in other phototropin‐mediated responses. We further found that blue light activation of inward‐rectifying K+ (K+ in) channels was impaired in the guard cells of cipk23 mutants, whereas activation of the plasma membrane H+‐ATPase was not. The blue light activation of K+ in channels was also impaired in the mutant of BLUS1, which is one of the phototropin substrates in guard cells. We therefore conclude that CIPK23 promotes stomatal opening through activation of K+ in channels most likely in concert with BLUS1, but through a mechanism other than activation of the H+‐ATPase. The role of CIPK23 as a newly identified component of phototropin signaling in stomatal guard cells is discussed.
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影响因子：
16.6
作者：
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7.4
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