Mori Izumi C, Murata Yoshiyuki, Yang Yingzhen, Munemasa Shintaro, Wang Yong-Fei, Andreoli Shannon, Tiriac Hervé, Alonso Jose M, Harper Jeffery F, Ecker Joseph R, Kwak June M, Schroeder Julian I
Cell and Developmental Biology Section, Division of Biological Sciences and Center for Molecular Genetics, University of California San Diego, La Jolla, California, USA.
PLoS Biol. 2006 Oct;4(10):e327. doi: 10.1371/journal.pbio.0040327.
Abscisic acid (ABA) signal transduction has been proposed to utilize cytosolic Ca(2+) in guard cell ion channel regulation. However, genetic mutants in Ca(2+) sensors that impair guard cell or plant ion channel signaling responses have not been identified, and whether Ca(2+)-independent ABA signaling mechanisms suffice for a full response remains unclear. Calcium-dependent protein kinases (CDPKs) have been proposed to contribute to central signal transduction responses in plants. However, no Arabidopsis CDPK gene disruption mutant phenotype has been reported to date, likely due to overlapping redundancies in CDPKs. Two Arabidopsis guard cell-expressed CDPK genes, CPK3 and CPK6, showed gene disruption phenotypes. ABA and Ca(2+) activation of slow-type anion channels and, interestingly, ABA activation of plasma membrane Ca(2+)-permeable channels were impaired in independent alleles of single and double cpk3cpk6 mutant guard cells. Furthermore, ABA- and Ca(2+)-induced stomatal closing were partially impaired in these cpk3cpk6 mutant alleles. However, rapid-type anion channel current activity was not affected, consistent with the partial stomatal closing response in double mutants via a proposed branched signaling network. Imposed Ca(2+) oscillation experiments revealed that Ca(2+)-reactive stomatal closure was reduced in CDPK double mutant plants. However, long-lasting Ca(2+)-programmed stomatal closure was not impaired, providing genetic evidence for a functional separation of these two modes of Ca(2+)-induced stomatal closing. Our findings show important functions of the CPK6 and CPK3 CDPKs in guard cell ion channel regulation and provide genetic evidence for calcium sensors that transduce stomatal ABA signaling.
脱落酸（ABA）信号转导被认为在保卫细胞离子通道调节中利用胞质Ca²⁺。然而，尚未鉴定出损害保卫细胞或植物离子通道信号反应的Ca²⁺传感器基因变体，并且Ca²⁺非依赖型ABA信号机制是否足以产生完整反应仍不清楚。钙依赖蛋白激酶（CDPKs）被认为有助于植物的核心信号转导反应。然而，迄今为止尚未报道拟南芥CDPK基因破坏突变体表型，这可能是由于CDPKs存在重叠冗余。两个在拟南芥保卫细胞中表达的CDPK基因CPK3和CPK6表现出基因破坏表型。在单突变和双突变cpk3cpk6保卫细胞的独立等位基因中，ABA和Ca²⁺对慢型阴离子通道的激活，有趣的是，ABA对质膜Ca²⁺渗透通道的激活均受损。此外，这些cpk3cpk6突变等位基因中ABA和Ca²⁺诱导的气孔关闭部分受损。然而，快型阴离子通道电流活性未受影响，这与通过提出的分支信号网络在双突变体中部分气孔关闭反应一致。施加Ca²⁺振荡实验表明，CDPK双突变体植物中Ca²⁺反应性气孔关闭减少。然而，持久的Ca²⁺编程气孔关闭未受损，为这两种Ca²⁺诱导气孔关闭模式的功能分离提供了遗传学证据。我们的研究结果表明CPK6和CPK3 CDPKs在保卫细胞离子通道调节中具有重要功能，并为转导气孔ABA信号的钙传感器提供了遗传学证据。
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