Cell and Developmental Biology Section, Division of Biological Sciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0116, USA.
Ann Bot. 2012 Jan;109(1):5-17. doi: 10.1093/aob/mcr252. Epub 2011 Oct 12.
Stomatal guard cells are the regulators of gas exchange between plants and the atmosphere. Ca(2+)-dependent and Ca(2+)-independent mechanisms function in these responses. Key stomatal regulation mechanisms, including plasma membrane and vacuolar ion channels have been identified and are regulated by the free cytosolic Ca(2+) concentration (Ca(2+)).
Here we show that CO(2)-induced stomatal closing is strongly impaired under conditions that prevent intracellular Ca(2+) elevations. Moreover, Ca(2+) oscillation-induced stomatal closing is partially impaired in knock-out mutations in several guard cell-expressed Ca(2+)-dependent protein kinases (CDPKs) here, including the cpk4cpk11 double and cpk10 mutants; however, abscisic acid-regulated stomatal movements remain relatively intact in the cpk4cpk11 and cpk10 mutants. We further discuss diverse studies of Ca(2+) signalling in guard cells, discuss apparent peculiarities, and pose novel open questions. The recently proposed Ca(2+) sensitivity priming model could account for many of the findings in the field. Recent research shows that the stomatal closing stimuli abscisic acid and CO(2) enhance the sensitivity of stomatal closing mechanisms to intracellular Ca(2+), which has been termed 'calcium sensitivity priming'. The genome of the reference plant Arabidopsis thaliana encodes for over 250 Ca(2+)-sensing proteins, giving rise to the question, how can specificity in Ca(2+) responses be achieved? Calcium sensitivity priming could provide a key mechanism contributing to specificity in eukaryotic Ca(2+) signal transduction, a topic of central interest in cell signalling research. In this article we further propose an individual stomatal tracking method for improved analyses of stimulus-regulated stomatal movements in Arabidopsis guard cells that reduces noise and increases fidelity in stimulus-regulated stomatal aperture responses ( Box 1). This method is recommended for stomatal response research, in parallel to previously adopted blind analyses, due to the relatively small and diverse sizes of stomatal apertures in the reference plant Arabidopsis thaliana.
保卫细胞是植物与大气之间气体交换的调节者。Ca(2+)依赖性和非依赖性机制在这些反应中起作用。已鉴定出关键的气孔调节机制，包括质膜和液泡离子通道，并受细胞质游离 Ca(2+)浓度(Ca(2+))调节。
在这里，我们表明，在阻止细胞内 Ca(2+)升高的条件下，CO(2)诱导的气孔关闭受到严重损害。此外，在几种保卫细胞表达的 Ca(2+)依赖性蛋白激酶（CDPKs）的敲除突变体中，Ca(2+)振荡诱导的气孔关闭部分受损，包括 cpk4cpk11 双突变体和 cpk10 突变体；然而，在 cpk4cpk11 和 cpk10 突变体中，脱落酸调节的气孔运动仍然相对完整。我们进一步讨论了保卫细胞中 Ca(2+)信号转导的不同研究，讨论了明显的特殊性，并提出了新的开放性问题。最近提出的 Ca(2+)敏感性启动模型可以解释该领域的许多发现。最近的研究表明，气孔关闭刺激物脱落酸和 CO(2)增强了气孔关闭机制对细胞内 Ca(2+)的敏感性，这被称为“钙敏感性启动”。参考植物拟南芥的基因组编码了超过 250 种 Ca(2+)感应蛋白，这就提出了一个问题，即如何实现 Ca(2+)反应的特异性？钙敏感性启动可以提供一种关键机制，有助于真核生物 Ca(2+)信号转导的特异性，这是细胞信号研究的一个核心问题。在本文中，我们进一步提出了一种单独的气孔跟踪方法，用于改进拟南芥保卫细胞中刺激调节的气孔运动分析，该方法减少了噪声并提高了刺激调节的气孔孔径响应的保真度（框 1）。由于参考植物拟南芥的气孔孔径相对较小且多样化，因此该方法建议与之前采用的盲目分析方法一起用于气孔反应研究。
