干旱胁迫不仅影响豆科植物的生长发育，也影响了共生固氮。然而，对于豆科在水分缺失条件下怎样调节C/N平衡和共生固氮却知之甚少。脱水素在植物抗旱中发挥了重要作用，关于其分子机制却知之甚少。在前期研究中，我们以拟南芥为材料揭示了脱水素MtCAS31调节气孔密度抵抗干旱的分子机制。我们通过深入研究发现MtCAS31在截型苜蓿中能够通过系统降低失水量和保护共生固氮来抵抗干旱，本项目拟阐明MtCAS31在豆科植物的抗旱机制。通过研究MtCAS31和水通道蛋白MtPIP2;7的互作位点，结合二者的表达特征、体内外生理生化功能，阐明这种互作对MtPIP2;7功能的影响，揭示脱水素系统降低苜蓿失水量的分子机制；研究MtCAS31和豆血红蛋白MtLb120的互作的生物学意义，探究脱水素在体内外对豆血红蛋白的保护作用，揭示干旱大量诱导表达的脱水素保护共生固氮的分子机制。本课题对豆科作物抗旱育种具有重要价值。

Drought stress negatively affects plant growth、development and symbiotic nitrogen fixation (SNF) in legumes. However it is still unknown how internal C:N balance and SNF impact on plant response to water limitation. Dehydrins play important roles in drought response, but the function of dehydrins in SNF under drought stress has not been studied. Here, we show a dehydrin protein, MtCAS31 (cold-acclimation-specific 31 protein), plays roles in water maintenance and SNF regulation in Medicago truncatula. This project intends to further study the molecular mechanisms of MtCAS31 under drought stress in legumes. Reveal the molecular mechanism of dehydrin reducing the water loss in M. truncatula through studying the interaction sites of MtCAS31 and aquaporin MtPIP2;7, combining the physiological and biochemical functions. Reveal the molecular mechanism of drought induced dehydrin MtCAS31 protecting SNF through studying the interaction sites and protective effect between MtCAS31 and leghemoglobin MtLb120.The results have important value on leguminous crops drought-resistant breeding.