OsGT-4a基因在水稻盐胁迫应答中的功能和分子机制研究

项目名称： OsGT-4a基因在水稻盐胁迫应答中的功能和分子机制研究

项目编号： No.31501239

项目类型： 青年科学基金项目

立项/批准年度： 2016

项目学科： 食品科学、农学基础与作物学

项目作者： 秦瑞英

作者单位： 安徽省农业科学院

项目金额： 20万元

中文摘要： 盐胁迫是水稻生产面临的重要环境问题，水稻的盐应答机理也一直是农学和植物学研究的热点问题。盐胁迫可在转录水平上调控多种基因，但其分子机制尚不完全清楚。在前期研究中，项目组发现水稻OsRAV7基因可特异性受盐胁迫而不受其他非生物逆境胁迫诱导，且其盐响应可能由一个同样受盐诱导的GT转录因子家族成员OsGT-4a控制。本项目拟以前期创制的OsGT-4a过表达和CRISPR/Cas9靶向突变体为主要材料，通过生理学、生物化学和功能基因组学分析，阐明OsGT-4a在水稻盐胁迫反应中的功能及其作用机制；同时通过细致分析OsGT-4a的表达模式及相应表达机制，明确盐应答相关的OsGT-4a上游调控模式。通过上述研究，本项目试图揭示OsGT-4a参与水稻盐胁迫响应转录调控的分子机理，从而围绕OsGT-4a构建水稻盐胁迫应答的调控模型，并初步阐明盐特异性响应在耐逆反应中的生物学意义。

中文关键词： 非生物逆境；盐胁迫；转录因子；应答；基因编辑

英文摘要： Salt stress is an important challenge in rice production. The mechanism of salt tolerance has been focused by agriculture and plant biology research. Mounts of studies indicated that many tolerance-related genes were transcriptionally regulated by salt stress. However, the underlying mechanism has not been fully identified yet. In previous research, we found a rice gene OsRAV7 is specifically induced by salt stress but not by other regular abiotic stresses including osmotic stress and cold stress. Further study indicated that the salt induction was dependent on a salt-inducible GT gene family member, OsGT-4a. Based on these data, we plan to analyze the function and possible mechanism of OsGT-4a in rice salt tolerance by physiological, biochemical and functional genomic experiments using the existing OsGT-4a overexpression and CRISPR/Cas9-induced target mutation lines. Meanwhile, detailed expression pattern of OsGT-4a and molecular mechanism of salt induction of OsGT-4a itself will also investigated to elucidate the upstream regulation of OsGT-4a. Taken together, our project will reveal the molecular mechanism of the OsGT-4a-participated rice salt response, and will establish the regulation model of salt-specific plant gene regulation. The result of our project might help to better understand the biological role of salt-specific gene regulation in plant salt tolerance.

英文关键词： Abiotic stress;Salt stress;Transcription factor;Stress response;Gene editing