LPR2蛋白调控拟南芥根系铵毒害的作用机制研究

铵态氮是植物可利用的主要氮源之一，但以铵态氮为主要氮源或唯一氮源时，植物生长会表现出严重的毒害现象，其中根系生长抑制是典型铵毒症状。目前，国内外学者已提出多种可能的铵毒产生机制，但其确切机制仍不清晰。本申请项目基于前期发现的亚铁氧化酶LPR2介导韧皮部铁沉积在铵胁迫抑制根系生长中起关键作用的现象，利用现有LPR2相关的拟南芥遗传材料为主要研究对象，从铵胁迫调控根系组织中LPR2的表达特征及其与韧皮部铁沉积的耦合关系入手，重点研究LPR2介导的铁沉积过程在诱导氧自由基产生和胼胝质积累中的作用，以及由此引发的韧皮部蔗糖运输-卸载阻抑对根系生长发育的影响，以期系统解析LPR2在植物铵胁迫抑制根系生长中的作用机制，进而为农业生产或生态保护中解决铵毒问题提供相关理论依据。

Ammonium is one of the main forms of plant-available nitrogen sources. Nevertheless, when ammonium is the predominant or the only source of nitrogen, ammonium is notorious for its toxic effects in most plants, including stunting root growth. Although several possible mechanisms for ammonium toxicity have been proposed previously, the exact mechanisms underlying ammonium toxicity in plants remain elusive. On the basis of our recent finding that LPR2-dependent iron deposition in phloem plays an important role in root growth arrest under ammonium stress, the present project will be aimed to investigate the underlying mechanisms for ammonium toxicity by using LPR2-related Arabidopsis genotypes. Firstly, we will analyze the spatiotemporal expression pattern of LPR2 response to ammonium stress and its coupling relationship with iron deposition in the phloem. Afterward, we will clarify the role of iron deposition in ROS (Reactive Oxygen Species) burst and callose accumulation in the phloem. Finally, we will focus on investigating the relationship between the inhibition of sucrose transporting due to callose deposition in phloem and the root growth arrest under ammonium stress. The studies of this project will provide a theoretical basis for coping with ammonium toxicity in agriculture and ecosystems.