Elevated CO2-Induced Responses in Stomata Require ABA and ABA Signaling.
Elevated CO2-Induced Responses in Stomata Require ABA and ABA Signaling.
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CO2 诱导的气孔反应升高需要 ABA 和 ABA 信号传导
DOI：
10.1016/j.cub.2015.09.013
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发表时间：
2015-10-19
期刊：
影响因子：
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通讯作者：
Hetherington AM
中科院分区：
文献类型：
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作者：
Chater C;Peng K;Movahedi M;Dunn JA;Walker HJ;Liang YK;McLachlan DH;Casson S;Isner JC;Wilson I;Neill SJ;Hedrich R;Gray JE;Hetherington AM
全球环境变化的一个组成部分是大气中CO2 （[CO2]）浓度的增加。增加的[CO2]减少了叶片气孔的开度和气孔的密度，从而减少了蒸散发。令人惊讶的是，考虑到蒸腾作用对控制陆地水分通量和植物养分获取的重要性，我们对[CO2]控制气孔发育和功能的细胞内信号通路所涉及的分子成分知之甚少。在这里，我们报道了[CO2]诱导的关闭和气孔密度的降低需要活性氧（ROS）的产生，从而为这些信号通路增加了一个新的共同元素。我们还表明，这两种反应都需要ABA受体的PYR/RCAR家族和ABA本身。利用遗传方法，我们发现保护细胞或其前体中的ABA足以介导[CO2]诱导的气孔密度响应。综上所述，我们的研究结果表明，气孔对[CO2]增加的响应是通过ABA的中介作用进行的。在[CO2]诱导气孔孔径减少的情况下，这是通过进入保护细胞ABA信号通路发生的。在这两种[CO2]介导的反应中，我们的数据与ABA增加系统对[CO2]敏感性的机制一致，但也可以解释为需要二氧化碳诱导的ABA生物合成增加，特别是在保护细胞谱系中。此外，气孔[CO2]信号对ABA的依赖性表明，从进化角度来看，ABA通路可能来自祖先。CO2诱导的气孔关闭和密度降低需要活性氧，CO2诱导的气孔关闭和密度降低需要ABA和ABA受体，保护细胞/前体ABA足以介导关闭和密度降低，通过ABA操作的气孔CO2响应解释了这些途径之间的重叠。Chater等人描述了在CO2诱导的气孔关闭升高和CO2诱导的气孔密度降低升高中对ABA和ABA信号的需求。这表明ABA本身在气孔CO2感知的下游，ABA信号可能早于CO2诱导的气孔响应的起源。
An integral part of global environment change is an increase in the atmospheric concentration of CO2 ([CO2]). Increased [CO2] reduces leaf stomatal apertures and density of stomata that plays out as reductions in evapotranspiration. Surprisingly, given the importance of transpiration to the control of terrestrial water fluxes and plant nutrient acquisition, we know comparatively little about the molecular components involved in the intracellular signaling pathways by which [CO2] controls stomatal development and function. Here, we report that elevated [CO2]-induced closure and reductions in stomatal density require the generation of reactive oxygen species (ROS), thereby adding a new common element to these signaling pathways. We also show that the PYR/RCAR family of ABA receptors and ABA itself are required in both responses. Using genetic approaches, we show that ABA in guard cells or their precursors is sufficient to mediate the [CO2]-induced stomatal density response. Taken together, our results suggest that stomatal responses to increased [CO2] operate through the intermediacy of ABA. In the case of [CO2]-induced reductions in stomatal aperture, this occurs by accessing the guard cell ABA signaling pathway. In both [CO2]-mediated responses, our data are consistent with a mechanism in which ABA increases the sensitivity of the system to [CO2] but could also be explained by requirement for a CO2-induced increase in ABA biosynthesis specifically in the guard cell lineage. Furthermore, the dependency of stomatal [CO2] signaling on ABA suggests that the ABA pathway is, in evolutionary terms, likely to be ancestral. CO2-induced stomatal closure and density reduction require reactive oxygen species CO2-induced stomatal closure and density reduction require ABA and ABA receptors Guard cell/precursor ABA is sufficient to mediate closure and density reduction Stomatal CO2 responses operating via ABA explains overlap between these pathways Chater et al. describe the requirement for ABA and ABA signaling in both elevated CO2-induced stomatal closure and elevated CO2-induced reductions in stomatal density, suggesting that ABA itself is downstream of stomatal CO2 perception and that ABA signaling is likely to predate the origin of CO2-induced stomatal responses.