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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >CO2 signaling in guard cells: Calcium sensitivity response modulation, a Ca2+-independent phase, and CO2 insensitivity of the gca2 mutant
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CO2 signaling in guard cells: Calcium sensitivity response modulation, a Ca2+-independent phase, and CO2 insensitivity of the gca2 mutant

机译：保卫细胞中的CO2信号传递：钙敏感性响应调节，Ca2 +独立相和gca2突变体的CO2不敏感性

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摘要

Leaf stomata close in response to high carbon dioxide levels and open at low CO2. CO2 concentrations in leaves are altered by daily dark/light cycles, as well as the continuing rise in atmospheric CO2. Relative to abscisic acid and blue light signaling, little is known about the molecular, cellular, and genetic mechanisms of CO2 signaling in guard cells. Interestingly, we report that repetitive Ca2+ transients were observed during the stomatal opening stimulus, low [CO2]. Furthermore, low/high [CO2] transitions modulated the cytosolic Ca2+ transient pattern in Arabidopsis guard cells (Landsberg erecta). Inhibition of cytosolic Ca2+ transients, achieved by loading guard cells with the calcium chelator 1,2-bis(2-amino-phenoxy)ethane-N,N,N',N'-tetraacetic acid and not adding external Ca2+, attenuated both high CO2-induced stomatal closing and low CO2-induced stomatal opening, and also revealed a Ca2+-independent phase of the CO2 response. Furthermore, the mutant, growth controlled by abscisic acid (gca2) shows impairment in [CO2] modulation of the cytosolic Ca2+ transient rate and strong impairment in high CO2-induced stomatal closing. Our findings provide insights into guard cell CO2 signaling mechanisms, reveal Ca2+-independent events, and demonstrate that calcium elevations can participate in opposed signaling events during stomatal opening and closing. A model is proposed in which CO2 concentrations prime Ca2+ sensors, which could mediate specificity in Ca2+ signaling.
机译：叶片气孔在高二氧化碳水平下关闭，在低二氧化碳下打开。每天的暗/亮周期以及大气中CO2的持续增加都会改变叶片中的CO2浓度。相对于脱落酸和蓝光信号，关于保卫细胞中CO2信号传导的分子，细胞和遗传机制知之甚少。有趣的是，我们报道在气孔开放刺激期间观察到重复的Ca2 +瞬变，低[CO2]。此外，低/高[CO2]过渡调节了拟南芥保卫细胞（兰兹勃罗直立细胞）中胞质Ca2 +瞬态模式。通过向保卫细胞中加入钙螯合剂1,2-双（2-氨基-苯氧基）乙烷-N，N，N'，N'-四乙酸而不加外部Ca2 +来实现抑制胞质Ca2 +瞬变的作用CO2诱导的气孔关闭和低的CO2诱导的气孔打开，并且还揭示了CO2响应的Ca2 +独立相。此外，由脱落酸（gca2）控制的突变体生长显示胞质Ca2 +瞬时速率的[CO2]调节受损，而高CO2诱导的气孔关闭则严重受损。我们的发现提供了对保卫细胞CO2信号传导机制的见解，揭示了Ca2 +非依赖性事件，并证明了钙升高可以参与气孔打开和关闭过程中相反的信号事件。提出了一个模型，其中CO2浓度会激发Ca2 +传感器，从而可以介导Ca2 +信号传导的特异性。

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