在前一基金的支持下，我们发现生长素（IAA）作为一氧化氮的上游信号分子调控了机理I植物耐缺铁响应的增强。然而对于IAA的上游信号过程仍不清楚。一些研究发现缺铁显著增加根系中蔗糖的积累，而我们最近研究发现外源蔗糖处理可增强缺铁根系的高铁还原酶活性。另有研究指出蔗糖也能增强拟南芥硝酸盐转运体（NRT）基因AtNRT1.1表达的作用，而AtNRT1.1转运体最近被证实具有转运IAA分子的功能。基于上述前期研究，本申请项目拟以番茄植物为材料，从缺铁诱导根系蔗糖积累的途径、蔗糖对缺铁根系各种耐缺铁响应的增强性调控作用、NRT主导的IAA转运在蔗糖调控的耐缺铁响应增强中的作用等几个方面深入研究缺铁诱导的蔗糖积累对番茄根系耐缺铁响应的调控作用及其内在的分子生理机制。

Based on our previous Natural Science Foundation of China, we demonstrated that auxin (IAA) acts the upstream signal of nitric oxide in the regulation of resisting responses of strategy I plants to iron deficiency. However, the upstream signal of IAA still remains unknown. Some studies observed that iron deficiency significantly increases the sucrose accumulation in roots, while our recent study found that exogenous sucrose obviously enhances Fe-deficiency-induced ferric chelate reductase in tomato roots. In another hand, other researchers have also observed an enhancement of AtNRT1.1 expression by sucrose in Arabidopsis plants, while the AtNRT1.1 was recently demonstrated to have a function of IAA transport. Taking all above together, this applying project will be aimed to study the molecular and physiological mechanisms of iron-deficiency-induced sucrose accumulation in regulating iron-deficiency-induced resistant responses in roots by using tomato plants, and studies are mainly include: the pathway of iron-deficiency-induced sucrose accumulation in roots; the positive regulation of sucrose in enhancing iron-deficiency-induced resistant responses; Role of NRT mediated IAA transport in the above regulating process.