水稻UAP1和UAP2基因协同参与叶早衰和防御反应过程的功能及代谢通路研究

Inactivation of enzymatic function of UDP-N-acetylglucosamine pyrophosphorylase 1 (UAP1), makes the leaves of uap1 mutant exhibiting phenotypes of early leaf senescence and defence responses after a short period’s normal growth. However, the molecular mechanisms involved in these processes still need to be further studied. Based on our results of previous studies, this project proposes hypotheses: (1) the function of UAP2 gene is probably the key factor to ensure the uap1 mutant leaves grow normally for a short time; (2) there possibly exists a metabolic pathway associated with UAP genes to function during the processes of early leaf senescence and defence responses of uap1 mutant. This project plans to confirm the functions of UAP1 and UAP2 genes cooperatively involved in the processes of early leaf senescence and defence responses, from the molecular, cellular, tissue, and plant levels. Using uap1 mutant, and its transgenic plants by UAP1 gene functional complementation and UAP2 gene functional rescue, this project is to reveal the key points of the UAP-involved metabolic pathway and their change regulation during the processes of early leaf senescence and defence responses. Meanwhile, this project hopes to discover novel genes encoding specific glycosylated proteins involved in early leaf senescence and defence responses. This project will lay the foundation to deeply elucidate the function and molecular pathway of UAP genes, and bring new insight into the scientific field of early leaf senescence and defence responses.

水稻UDP-N-乙酰氨基葡萄糖焦磷酸化酶1（UAP1）的酶学功能丧失，导致uap1突变体的叶片在短时间正常生长后出现叶早衰和防御反应表型，但其所涉及的分子机制，还有待深入研究。本项目根据前期研究结果提出假设：（1）UAP2基因的功能可能是保证uap1突变体叶片能够正常生长一段时间的关键性因素；（2）在uap1突变体的叶早衰和防御反应发生过程中，可能存在一条UAP基因参与的代谢通路在发挥作用。本项目拟从分子、细胞、组织以及植株水平等多层次明确UAP1和UAP2基因协同参与叶早衰和防御反应过程的功能；欲利用uap1突变体、及其UAP1基因互补和UAP2基因补救转基因材料，探明在叶早衰和防御反应发生过程中，UAP基因参与的代谢通路的关键环节及其变化规律，同时挖掘参与该过程的编码特异糖基化蛋白的新基因。本项目将为深入阐释UAP基因的功能和分子途径奠定基础，给叶早衰和防御反应的科研领域带来新的认识。

水稻UDP-N-乙酰氨基葡萄糖焦磷酸化酶1（UAP1）的酶学功能丧失，导致突变体uap1的叶片在短时间正常生长后出现叶早衰和防御反应表型。但是uap1的叶片能先正常生长的机制，uap1叶表型变化过程中UAP基因参与的代谢通路及其变化规律等，还有待深入研究。本项目从表型、生理、生信、分子、细胞、植株个体等方面多层次探明并证实UAP2基因的功能是uap1的叶片能先正常生长的原因，即UDP-N-乙酰氨基葡萄糖焦磷酸化酶2（UAP2）和1（UAP1）基因协同发挥功能参与水稻叶早衰和防御反应过程。利用uap1突变体及其UAP基因补救转基因材料探明UAP基因下游的内质网胁迫激发未折叠蛋白质应答途径参与了叶早衰和防御反应过程，并明确了该途径的变化规律。利用转基因技术明确了UAP1基因调控叶衰老和防御反应过程的负调控模式。利用水稻衰老剑叶中N-糖基化修饰蛋白组的定性研究揭示了蛋白质糖基化修饰可能在叶衰老过程中发挥重要功能，并发掘了一系列参与叶衰老的关键的候选糖基化蛋白质。对UAP基因所在的植物UDP葡萄糖焦磷酸化酶(UDPGP)基因家族进行了全面分析，揭示了它们保守的演化参与细胞死亡的潜在功能机制。.本项目支持项目主持人以第一作者或通讯作者身份在“Frontiers in Plant Science”、“Plant Molecular Biology”、“Planta”、“Plant Growth Regulation”、“Genes”、“核农学报”等国内外权威学术期刊上发表研究论文8篇（第一、二标注基金资助），包括SCI论文6篇、北大中文核心期刊论文2篇，其中，中科院2区SCI论文4篇、中科院3区SCI论文2篇，具有重要的学术影响。培养了项目主持人成为江西农业大学校聘“青年教授”和江西省“青年井冈学者”；培养了博士2名、硕士3名完成毕业，取得良好的社会效益。

内容获取失败，请点击重试