UV-B辐射诱导拟南芥气孔关闭过程中UVR8信号通路成员和乙烯信号转导组分之间的相互关系的研究

In recent years, although much progress has been made in the ultraviolet B (UV-B) receptor UVR8-dependent UV-B-specific signaling pathway, the role of this signaling pathway in UV-B-induced synthesis of phytohormone ethylene and the interrelationships and their interacted mechanisms among the elements of the UVR8-dependent signaling pathway and the ethylene signaling pathway are poorly understood. Based on the previous results that the UVR8-dependent signaling pathway elements UVR8, COP1 and HY5/HYH as well as the ethylene receptors and signaling elements all participate in the signal transduction network of UV-B-induced stomatal closure in Arabidopsis, we will continually use the model plant Arabidopsis as the research material in this project, and combine various research methods and means in genetics, biochemistry and molecular biology to study the following three main questions: First, whether and how the UVR8-dependent signaling pathway mediates the UV-B-induced production of ethylene; Second, what are the interrelationships among the components of the UVR8-dependent signaling pathway and the ethylene signaling pathway in the signal transduction network of UV-B-induced stomatal closure. Finally, how the key players of the two signaling pathways interact at gene expression and protein levels. The study will not only help us to gain further insight into the signal transduction mechanisms of the UV-B-regulated stomatal movement, but also benefit us to further understand the interactions of UVR8-dependent signaling pathway and the ethylene signaling pathway under UV-B radiation.

近年来，紫外线B（UV-B）受体UVR8介导的UV-B专一信号通路的研究已取得很大进展，但对该信号通路在UV-B调控植物激素乙烯生成中的作用以及该信号通路成员与乙烯信号转导组分之间的相互关系及其作用机制却知之甚少。本项目在前期研究已表明UVR8信号通路主要成员UVR8、COP1和HY5/HYH以及乙烯受体和乙烯信号转导元件均参与UV-B诱导拟南芥气孔关闭的基础上，以拟南芥为材料，结合遗传学、生物化学和分子生物学的研究方法和手段，首先研究UVR8信号通路在UV-B调控乙烯生成中的作用，然后解析在UV-B诱导气孔关闭的信号转导网络中UVR8信号通路成员和乙烯信号转导组分之间的相互关系，最后在基因表达和蛋白水平揭示两种信号转导途径组分之间互作的机制。该研究不仅可以深化UV-B辐射调控气孔运动的信号转导机制，而且也有助于人们进一步认识UV-B辐射下UVR8信号通路与乙烯信号转导途径之间的相互关系。

尽管前人研究已表明UVR8-COP1-HY5信号通路、乙烯、过氧化氢(H2O2)和一氧化氮(NO)均参与了紫外线B(UV-B)诱导气孔关闭的信号转导过程，但对它们之间的相互关系却并不清楚。本项目以拟南芥为材料，结合生物化学、遗传学和分子生物学的研究方法和技术，对这一问题进行了深入的研究。结果表明：UV-B辐射能诱导拟南芥野生型乙烯生物合成限速酶ACC合酶基因ACS2/6/11的表达、乙烯、H2O2和NO的生成以及气孔关闭，但这些UV-B效应均能被uvr8、cop1和hy5突变体显著抑制；其次，抑制乙烯生成能显著抑制UV-B诱导的保卫细胞H2O2和NO生成以及气孔关闭，乙烯信号转导组分ETR1,EIN2和EIN3的突变也能抑制UV-B诱导保卫细胞NO形成和气孔关闭，ETR1突变也抑制了UV-B诱导的保卫细胞H2O2的生成，但EIN2和EIN3的突变不能抑制UV-B诱导的保卫细胞H2O2的生成；在可见光和UV-B辐射下，外源乙烯能诱导uvr8突变体保卫细胞H2O2和NO生成以及气孔关闭，也能诱导cop1和hy5突变体H2O2的产生，但不能诱导cop1和hy5突变体NO的产生和气孔关闭；外源NO能诱导uvr8、cop1和hy5突变体气孔关闭，但外源H2O2只能诱导uvr8突变体的气孔关闭，而不能诱导cop1和hy5突变体的气孔关闭；在拟南芥野生型背景下过表达EIN2、EIN3、COP1和HY5以及在EIN2和EIN3突变体背景下过表达COP1和HY5均能诱导保卫细胞NO的形成和气孔关闭，但在COP1和HY5突变体背景下过表达EIN2和EIN3却不能诱导保卫细胞NO的形成和气孔关闭。这些结果表明UV-B诱导气孔关闭的信号转导途径是：UV-B依赖于UVR8-COP1-HY5信号通路诱导了ACS基因表达并导致乙烯产生，乙烯通过其受体诱导了保卫细胞H2O2形成，然后H2O2通过依赖于EIN2、EIN3、COP1和HY5的方式诱导了保卫细胞NO的形成并导致了气孔关闭。

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