草莓PME38和PME39基因调控非呼吸跃变型果实软化的机制研究

Fruit softening, which is a major determinant of fruit quality and shelf life, is the consequence of multiple cellular processes, including extensive remodeling of cell wall structure. Abscisic acid regulates cell-wall remodeling and is the main hormone that controls ripening in non-climacteric fruit. However, there is only limited knowledge of the molecular mechanisms underlying that abscisic acid regulates softening in non-climacteric fruit. Here, we show that PME38 and PME39 from pectin methylesterase (PME) gene family take part in softening during fruit development of strawberry which is a kind of non-climacteric fruit, and the expression level of PME genes are induced in colour turning fruits with abscisic acid transitory-treatment. Furthermore, PME38 and PME39 are shown to be co-expressed with some transcription factor genes during strawberry fruit development. So, we speculated that abscisic acid signal activates the expression of PME genes via those transcription factors. Based on the foundation of research, this project plan to advance our understanding of regulation of softening and explore the different molecular mechanisms of softening between climacteric and non-climacteric fruit with a series of experiment and multi-analyzing of genome, transcriptome and epigenome. It will provide useful molecular genetic information for improving fruit quality.

果实的软硬程度决定了口感品质和贮藏期，细胞壁结构的改变是导致果实软化的主要因素。脱落酸参与调控细胞壁的重塑过程，同时也是促进非呼吸跃变型果实成熟的主要激素，但其对非呼吸跃变型果实软化的调控机制仍不清楚。本实验室前期研究发现，果胶甲酯酶（PME）家族的PME38、39基因参与非呼吸跃变型果实草莓的软化过程，并且其表达水平受脱落酸信号的诱导。经过共表达网络分析，我们发现了与PME38、39表达模式一致的转录因子。并推测，脱落酸可能通过激活转录因子调节PME基因的表达，参与草莓果实软化。本项目据此将设计一系列生理生化及基因功能验证试验，并联合多组学分析。目的是深入研究脱落酸调控PME38、39参与果实软化的分子机制，并探索PME介导的调控网络在呼吸跃变型与非呼吸跃变型果实软化中的机制差异。为果实的品质改良提供宝贵的基因资源及理论基础。

果实的软硬程度决定了口感品质和贮藏期，细胞壁结构的改变是导致果实软化的主要因素。脱落酸调控细胞壁的重塑过程，同时也是促进非呼吸跃变型果实成熟的主要激素，但其对非呼吸跃变型果实软化的调控机制仍不清楚。本研究发现，果胶甲酯酶（PME）家族的FvPME38和FvPME39基因参与非呼吸跃变型果实草莓的软化过程，并且其表达水平受脱落酸信号的诱导。为了进一步探究脱落酸信号调控草莓果实软化的分子机制，我们通过分析表观遗传数据获取FvPME38和FvPME39基因转录开放位点，并结合转录组数据共表达网络，筛选到一个未知功能的MYB家族基因FvMYB79，其表达模式与FvPME38基因高度一致。并通过一系列生理生化及基因功能试验，验证了FvMYB79基因响应激素信号，通过结合FvPME38基因启动子并激活FvPME38降解细胞壁主要组分果胶，正向调控草莓果实软化过程。研究结果为揭示脱落酸信号调控草莓果实软化该关键科学问题提供重要的理论依据。同时，本项目还联合多组学分析，进一步探究FvMYB79-PME介导的果实软化调控模型在呼吸跃变型和非呼吸跃变型果实中的差异，同时获得参与呼吸跃变型果实软化的重要候选基因。总共发表SCI期刊论文3篇，其中一区论文1篇，二区论文2篇；FvMYB79作为重要的基因资源已申请国家发明专利1项。以上研究成果将为果实品质改良提供宝贵的基因资源及理论基础。