GDSL脂酶CDI6参与保卫细胞CO2信号转导的分子机制

Stomata are the main valve of gas exhange, uptaking CO2 for photosynthesis and also losing water for transpiration. Elevated concentrations of CO2 induce stomatal closing via rapid physiological responses and also reduce stomatal density by long-time exposure,thus further reducing CO2 assimilation rate, water use efficiency and affecting plants development and production. On the other hand, reducing stomatal aperture adequatly is an important way to improve water use effieciency and drought resistance. However, the the whole signaling tranduction pathway and the mechanism by which CO2 controls stomatal movements have remained largely unknown. Our previous work showed that Arabidopsis GDSL-lipase CDI6 regualtes CO2-induced stomatal movement and drought resistance.Howerever the mechanism is unkown and there was no reports showing that GDSL lipases paly roles in stoamtal movement.The proposed project will conduct an in-depth investigation that CDI6 regulates CO2-induced stomatal closure pathway, to ellucidate the the molecular and physiological mechanisms. We will expore biochemical activity of CDI6 and whether phosphalipids components changes affect the CO2-induced stomatal closing, to further elucidate the molecular network that regulated by CDI6. These investigations will further deepen the mechanisms and network of CO2-induced stomatal movements and explore methods to improve drought resistance in plants,and also will provide knowledge to understand the biological funtions of GDSL lipases.

气孔是植物吸收CO2和散失蒸腾水分的阀门，在调控植物固碳效率和水分利用率中起重要作用。环境中高浓度CO2促进气孔关闭，同时也降低气孔密度，从而影响植物碳同化效率和水分利用率，并进一步影响植物的生长和产量。另一方面，在水分短缺下，适当的减小气孔的孔径是提高植物水分利用率和抗旱性的重要途径。我们前期研究发现拟南芥GDSL脂酶CDI6参与调控CO2诱导的气孔运动和抗旱性，但是具体调控机制还不清楚，同时GDSL脂酶参与调控气孔运动还未见被报道。本项目将深入研究GDSL脂酶CDI6在CO2诱导的气孔关闭信号转导途径中的功能，阐明分子调控机制；探究CDI6的酶活是否影响CO2诱导的气孔关闭;并初步鉴定CDI6的生化活性。该研究不仅能深入解析CO2信号转导途径的分子机制，为作物抗逆遗传改良提供思路和理论依据，还助于理解GDSL的功能。

气孔是植物吸收CO2和散失蒸腾水分的阀门，在调控植物固碳效率和水分利用率中起重要作用。环境中高浓度CO2促进气孔关闭，同时也降低气孔密度，从而影响植物碳同化效率和水分利用率，并进一步影响植物的生长和产量。另一方面，在水分短缺下，适当的减小气孔的孔径是提高植物水分利用率和抗旱性的重要途径。我们前期研究发现拟南芥GDSL脂酶CDI6参与调控CO2诱导的气孔运动和抗旱性，但是具体调控机制还不清楚，同时GDSL脂酶参与调控气孔运动还未见被报道。本项目研究发现：1）CDI6调控CO2诱导的气孔关闭处于经典的途径中。2）解析了CDI6的酶活是其介导CO2调控气孔关闭的主要机制，并且氨基酸S35是CDI6酶活必需的。3）通过与MPK12和HT1的遗传互作分析阐明了CDI6在经典的CO2信号途径中可能位于MPK12的上游。4）体外酶活实验发现CDI6是一个硫酯酶，可以将体内的细胞内产生的VLC acyl-CoA催化生成超长链脂肪酸VLCFAs。5）说明了VLC acyl-CoA有可能是一种信号可以促进气孔的关闭。6）开发了一种无损伤检测气孔运动的新方法。本项目研究更新和进一步完善了保卫细胞CO2信号传导途径的模式，并且提出VLC acyl-CoA可能作为第二信使在CO2信号传导途径中起作用，为后续研究和进一步解析保卫细胞CO2信号传导的机制提供基础。