漆酶基因家族扩张与林木木质素积累之间的相关性研究

Copy number variation of gene family plays important roles in the key traits and new adaptation of forestry trees. Lignin contents in forestry trees are higher than that in herbs. In the lignin biosynthesis, laccase is the key enzyme to catalyze lignin polymerization. Our previous study found that laccase gene family had significantly expanded in Populus genome after divergence of Populus and Arabidopsis. But the functions of the expanded laccase genes and whether this expansion affects the lignin accumulation of forestry trees remain unclear. To address these questions, this study will focus on Populus laccase gene family. First, we will identify all the laccase genes in the Populus genome and investigate the evolutionary patterns of this family in plants. Second, the expression patterns and the subcellular localization of Populus laccases will be examined. Third, the enzyme activities of Populus laccase proteins will be investigated. Fourth, we will transform the expanded Populus laccase genes into Arabidopsis mutants and test their functions. Finally, by integrating all the results of molecular evolution, gene expressions and protein functions, this study investigate the internal connection between laccase gene expansion and accumulation of lignin in poplar. This study will provide a typical model about how copy number variation of gene family shapes natural variation in forestry trees.

基因家族拷贝数变异是塑造不同物种表型和适应性性状的一个重要机制。与草本植物相比，林木中木质素有显著积累，我们的前期研究发现木质素合成代谢途径重要基因家族“漆酶家族”在杨树中发生了显著扩张，这种扩张是否贡献于杨树木质素的高度积累呢？为了回答这一科学问题，本项目以杨树漆酶基因家族为研究对象，从比较功能基因组学层面，揭示杨树漆酶基因家族特异性扩张的分子机制，阐明扩张后的功能分化模式，以及漆酶家族的扩张与杨树木质素高度积累之间的联系，从而逐步揭示基因家族拷贝数变异与林木表型和适应性性状之间的内在联系。本项目的研究为林木遗传改良提供候选基因资源和新的理论依据。

林木关键性状形成的遗传机制解析是林木定向改良的理论基础。本项目以杨树为研究材料，针对林木木质素合成的分子机制及杨树缺铁响应机制开展研究。以木质素合成代谢途径重要基因家族漆酶家族（laccase）为研究对象，分析了LAC基因家族在基因组中的分布特点、成员组成和基因谱系关系以及该基因家族在杨树中发生特异性扩张之后的功能进化特点。对缺铁条件下，杨树生理，生化和转录组特征进行分析。发现缺铁条件下，叶绿素合成和光合作用途径受到极大抑制。这些途径的抑制导致萎黄和枝条生长受阻。尽管两种光合系统（PSI和PSII）在缺Fe条件下都受到抑制，但PSI受到的影响比PSII更严重、更早。缺铁还导致根的生长和根中二价金属离子的积累增加。在Fe缺乏反应的晚期，NRAMP1被诱导以促进Fe2+摄取。这表明杨树缺铁晚期，NRAMP1可能取代了我们熟知的IRT1，成为主要的Fe2+转运蛋白。结果已投稿并返回修改中。

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