The high-affinity K⁺ transporter HAK5 is the major contributor to root K⁺ uptake from dilute solutions in K⁺-starved Arabidopsis plants. Its functionality is tightly regulated and its activity is enhanced under K⁺ starvation by the transcriptional induction of the AtHAK5 gene, and by the activation of the transporter via the AtCBL1–AtCIPK23 complex. In the present study, the 26 members of the Arabidopsis CIPK protein kinase family were screened in yeast for their capacity to activate HAK5-mediated K⁺ uptake. Among them, AtCIPK1 was the most efficient activator of AtHAK5. In addition, AtCIPK9, previously reported to participate in K⁺ homeostasis, also activated the transporter. In roots, the genes encoding AtCIPK1 and AtCIPK9 were induced by K⁺ deprivation and atcipk1 and atcipk9 Arabidopsis KO mutants showed a reduced AtHAK5-mediated Rb⁺ uptake. Activation of AtHAK5 by AtCIPK1 did not occur under hyperosmotic stress conditions, where AtCIPK1 function has been shown to be required to maintain plant growth. Taken together, our data contribute to the identification of the complex regulatory networks that control the high-affinity K⁺ transporter AtHAK5 and root K⁺ uptake.

中文翻译：

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拟南芥 K+ 转运蛋白 HAK5 介导的高亲和力根 K+ 摄取受蛋白激酶 CIPK1 和 CIPK9 调节。

高亲和力的 K ⁺转运蛋白 HAK5 是K ⁺饥饿的拟南芥植物从稀溶液中吸收K ^{+的主要贡献者。}通过AtHAK5基因的转录诱导和通过 AtCBL1-AtCIPK23 复合物激活转运蛋白，其功能受到严格调节，并且在 K ⁺饥饿下其活性得到增强。在本研究中，在酵母中筛选了拟南芥 CIPK 蛋白激酶家族的 26 个成员激活 HAK5 介导的 K ⁺摄取的能力。其中，AtCIPK1 是 AtHAK5 最有效的激活剂。另外，AtCIPK9，此前报道过参加K ⁺体内平衡，也激活了转运蛋白。在根中，编码 AtCIPK1 和 AtCIPK9 的基因被 K ⁺剥夺诱导，并且atcipk1和atcipk9拟南芥 KO 突变体显示出 AtHAK5 介导的 Rb ⁺摄取减少。AtCIPK1 对 AtHAK5 的激活在高渗胁迫条件下不会发生，其中 AtCIPK1 功能已被证明是维持植物生长所必需的。总之，我们的数据有助于识别控制高亲和力 K ⁺转运蛋白 AtHAK5 和根 K ⁺吸收的复杂调控网络。