远红光和红光下拟南芥光敏色素抑制SPA2活性的分子机制

SPA (SUPPRESSOR OF PHYA-105) gene family (SPA1-SPA4), forms E3 ubiquitin ligase complexs with CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1), which are responsible for the degradation of various photomorphogenesis promoting factors, resulting in desensitization to light signaling. SPA2 is one of important members of the SPA gene family. It has been reported that SPA2 promotes skotomorphogenesis in darkness. However, the unique roles of SPA2 in suppressing photomorphogenesis under different light conditions are largely unknown. Recently, our lab found that seedlings of SPA2 overexpression lines display extremely etiolation phenotype in red light，but they show insensitive to far-red light treatments. This result not only suggests that SPA2 takes different roles in seedling de-etiolation in response to red or far-red light treatment, but also suggest both red light receptor (phytochrome B) and far-red light receptor (phytochorme A) dissimilarly modulate SPA2 activities in response to various light treatments. We will constructe over-expressing lines of SPA2 full length, different domain deletions and point mutants of phosphorylation sites to explore SPA2 functions in seedling etiolation under red and far-red light. We will also demonstrate light specific interactions between phytochormes and SPA2 through yeast two-hybrid analysis and in vivo co-IP assay. Our results will contribute that activity modulation of the COP1-SPA E3 complex by light-activated phytochromes is an effective and pivotal regulatory step in light signaling.

SPA基因家族（SPA1-SPA4）由四个成员组成，在蛋白水平它们与COP1形成COP1-SPAs E3泛素连接酶复合体，共同抑制植物光形态建成的发育。SPA2是SPA基因家族中的重要成员，已报道其在黑暗中促进暗形态建成，而对其在光下抑制光形态建成的功能却知之甚少。本研究发现SPA2过量表达在红光下引起显著的黄化反应，然而这些SPA2转基因植株却对远红光不敏感，不仅暗示着SPA2在红光和远红光的功能不同，而且暗示红光和远红光主要受体光敏色素B和光敏色素A对SPA2活性的调节也存在差异。在该研究基础上，我们将通过SPA2蛋白全长、功能区段缺失和磷酸化位点突变的转基因表型分析，证明各区段和磷酸化位点对SPA2活性的贡献；通过光敏色素A和光敏色素B与SPA2的光质特异互作机制分析、光敏色素对SPA2磷酸化和核转运调控，进一步明确光敏色素通过互作直接抑制SPA2的活性，进而促进植物的光形态建成。