Myo-Inositol Metabolism and Osmotic Stress Tolerance

简森这项工作解决了高等植物耐盐性的机制。以往的研究结果表明，肌醇生物合成的激活是植物对过量钠内流做出适应性反应的一个重要方面。研究人员集中在两个方面，即该途径的酶的生化特征和胁迫植物中通过该途径的通量和肌醇的运输。他们将获得对代谢通量的完整描述，这是维持足够高的肌醇浓度以合成膜磷脂和利用肌醇的信号分子所必需的。将继续研究最近检测到的钠/肌醇同向转运蛋白的特性、其表达特征以及对盐胁迫信号的响应。数据表明，钠-肌醇共运输可能是同步光合作用(固碳)、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，认为钠/质子逆向运输是一种耐受机制。叶片对钠的依赖于肌醇的吸收是耐盐性的控制因素。

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.