Myo-Inositol Metabolism and Osmotic Stress Tolerance

肌醇代谢和渗透应激耐受性

• 批准号: 9808932
• 负责人: Richard Jensen
• 金额: $ 33.5万
• 依托单位: University of Arizona
• 依托单位国家: 美国
• 项目类别: Continuing Grant
• 财政年份: 1998
• 资助国家: 美国
• 起止时间: 1998-09-01 至 2002-08-31
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=9808932&HistoricalAwards=false
• 关键词: Myo; Inositol; Metabolism; Osmotic; Stress

JensenThe work addresses mechanisms of salinity tolerance in higher plants. Previous results showed that activation of inositol biosynthesis constitutes one essential aspect of a plant's adaptive response to excess sodium influx. The investigators concentrate on two aspects, of biochemical characterization of the enzymes of the pathway and the flux through the pathway in stressed plants and inositol transport. They will obtain a complete description of the metabolic flux that is necessary to sustain inositol concentrations high enough for the synthesis of membrane phospholipids and signaling molecules which utilize inositol. The characterization of a recently detected sodium/inositol symporter protein, its expression characteristics and response to salt stress signaling, will be pursued. Data indicate that sodium-inositol co-transport might be the mechanism that synchronizes photosynthesis (carbon fixation), growth and sodium uptake. This aspect of work has the potential of changing a dogma held by plant physiologists, assuming sodium/proton antiport as a tolerance mechanism. That the inositol-dependent uptake of sodium into the leaves is the controlling factor in salt stress tolerance.

詹森的工作解决了高等植物耐盐性的机制。先前的研究结果表明，肌醇生物合成的激活构成了植物对过量钠离子流入的适应性反应的一个重要方面。研究人员集中在两个方面，生化表征的酶的途径和通量通过途径在胁迫植物和肌醇运输。他们将获得代谢通量的完整描述，代谢通量是维持肌醇浓度足够高以合成膜磷脂和利用肌醇的信号分子所必需的。最近检测到的钠/肌醇同向转运蛋白，其表达特性和响应盐胁迫信号的表征，将被追求。数据表明，钠-肌醇共运输可能是抑制光合作用（碳固定）、生长和钠吸收的机制。这方面的工作有可能改变植物生理学家的教条，假设钠/质子反向转运作为一种耐受机制。 肌醇依赖性钠吸收是盐胁迫耐性的控制因素。