赤桉ICE1调控低温胁迫响应的分子机理研究

项目名称： 赤桉ICE1调控低温胁迫响应的分子机理研究

项目编号： No.31470673

项目类型： 面上项目

立项/批准年度： 2015

项目学科： 农业科学

项目作者： 林元震

作者单位： 华南农业大学

项目金额： 85万元

中文摘要： 本项目拟以选育出耐寒性强的赤桉103为主要试材，在已初步分析转录因子EcaICE1基因的分子功能基础上，进一 步研究EcaICE1调控低温胁迫应答的基因网络及其功能分析。运用分子细胞生物学、分子生物学等理论和技术体系，研究目的基因EcaICE1在赤桉中的时空表达和基因定位以及功能互作，明确EcaICE1蛋白的表达和功能特性。同时利用赤桉超表达、amiRNA干扰表达等手段，从野生型、超表达、缺失突变体赤桉的形态结构、生理生化及分子变化等角度入手，结合mRNA、基因芯片分析，研究EcaICE1调控植物低温胁迫应答的基因网络及其功能，从中探讨EcaICE1的抗寒功能及其调控机理。上述这些研究的目的是从细胞及分子水平上弄清转录因子EcaICE1在植物低温胁迫中的调控基因网络，建立EcaICE1调控低温胁迫基因应答途径的理论模型，为研究桉树抗寒机制及遗传改良奠定基础，具有重要的理论意义。

中文关键词： 赤桉；转录因子；调控机制；低温胁迫

英文摘要： ICE1 (inducer of CBF expression 1) encodes a MYC-like bHLH transcriptional activator, can bind to CBF3 promoter, and induces the expression of CBF3 and its downstream genes during cold acclimation. Therefore ICE1 plays important roles in the response of plants under cold stress.On the basis of former molecular analysis of Eucalyptus ICE1 gene(EcaICE1) from cold-resistant E. camaldulensis clone 103, we will further discover the gene regulatory network and its molecular function of EcaICE1 under low temperature stress.The expressional and structural character of EcaICE1 will be confirmed from expression pattern, gene localization and protein interaction by the methods of molecular biology. The gene regulatory network and its molecular function of EcaICE1 will be studied from the phenotype, physiotype and trascript expression profiles of plants of wild, overexpression and RNAi expression, to discuss the gene regulation under cold stress and molecular mechanism of cold tolerance, with the methods of mRNA blot and DNA chip. The purpose of this study is to discover the gene regulatory network and its control by EcaICE1 and to present one model of EcaICE1 regulation of cold signaling and tolerance from the cell and molecular levels, which may provide important information not only for the molecular biological research of cold resistance but also for the genetic improvement of cold resistance in Eucalyptus and other forest trees.

英文关键词： Eucalyptus;transcription factor;regulation;cold stress