Wang Xuening, Lv Shuo, Han Xiangyu, Guan Xiongjuan, Shi Xiong, Kang Jingke, Zhang Luosha, Cao Bing, Li Chen, Zhang Wei, Wang Guodong, Zhang Yonghong
National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, Key Laboratory of Medicinal Resources and Natural Pharmaceutical Chemistry, Ministry of Education, College of Life Sciences, Shaanxi Normal University, Xi'an, China.
Laboratory of Medicinal Plant, Institute of Basic Medical Sciences, School of Basic Medicine, Biomedical Research Institute, Hubei Key Laboratory of Wudang Local Chinese Medicine Research, Hubei University of Medicine, Shiyan, China.
Front Plant Sci. 2019 Dec 17;10:1630. doi: 10.3389/fpls.2019.01630. eCollection 2019.
Strigolactones (SLs) are known to mediate plant acclimation to environmental stress. We recently reported that SLs acted as prominent regulators in promotion of stomatal closure. However, the detailed mechanism by which SLs induce stomatal closure requires further investigation. Here we studied the essential role of the calcium (Ca) signal mediating by the calcium-dependent protein kinase (CPK) in SL-induced stomatal closure. SL-induced stomatal closure was strongly inhibited by a Ca chelator and Ca channel blockers, indicating that Ca functions in SL promotion of stomatal closure. Through examining a collection of mutants, we identified CPK33, potentially acting as a Ca transducer, which is implicated in guard cell SL signaling. SL- and Ca-induced stomatal closure were impaired in mutants. CPK33 kinase activity is essential for SL induction of stomatal closure as SL-induced stomatal closure is blocked in the dead kinase mutant of CPK33. The mutant is impaired in HO-induced stomatal closure, but not in SL-mediated HO production. Our study thus uncovers an important player CPK33 which functions as an essential Ca signals mediator in guard cell SL signaling.
独脚金内酯（SLs）已知可介导植物对环境胁迫的适应性。我们最近报道，SLs在促进气孔关闭方面起着重要的调节作用。然而，SLs诱导气孔关闭的详细机制仍需进一步研究。在这里，我们研究了钙依赖蛋白激酶（CPK）介导的钙（Ca）信号在SL诱导气孔关闭中的关键作用。Ca螯合剂和Ca通道阻滞剂强烈抑制SL诱导的气孔关闭，表明Ca在SL促进气孔关闭中发挥作用。通过检测一系列突变体，我们鉴定出CPK33可能作为Ca传感器，参与保卫细胞SL信号传导。在突变体中，SL和Ca诱导的气孔关闭受到损害。CPK33激酶活性对于SL诱导的气孔关闭至关重要，因为在CPK33的失活激酶突变体中，SL诱导的气孔关闭被阻断。该突变体在过氧化氢（HO）诱导的气孔关闭中受损，但在SL介导的HO产生中未受损。因此，我们的研究揭示了一个重要的参与者CPK33，它在保卫细胞SL信号传导中作为必需的Ca信号介质发挥作用。
