uORF翻译调控因子在植物抗病反应中的功能研究
批准号:
32070284
项目类别:
面上项目
资助金额:
58.0 万元
负责人:
胥国勇
依托单位:
学科分类:
植物与环境互作
结题年份:
2024
批准年份:
2020
项目状态:
已结题
项目参与者:
胥国勇
中文摘要
翻译调控是控制植物免疫活性的重要途经,上游阅读框uORF是介导该调控的重要RNA元件,但目前对控制uORF功能的基因知之甚少。在病原微生物效应因子引起的免疫激活过程中,uORFs的翻译抑制作用被解除,使得转录因子TBF1积累帮助宿主建立免疫系统。我们已获得含有翻译报告基因uORFs-LUC植株,证明了其荧光水平的变化受到免疫信号调控,并在该遗传背景下通过化学诱变筛选得到了12株荧光增强的突变体。本研究将对其中dst7突变体进行系统研究。该突变体失去了响应免疫激活的翻译调控功能,无法帮助宿主建立免疫系统,我们将进一步利用分子生物学、遗传学、生物化学等手段分析该目标基因DST7参与翻译调控的信号通路。通过以上研究,我们将更加深入理解蛋白质翻译调控机制,并利用该调控机制改良作物的抗病害能力。
英文摘要
Global translational reprogramming is a fundamental layer of immune regulation in plants. It is mediated by the collaborative action between cis-RNA element and trans-acting factors. Upstream open reading frame (uORF) represents as one of the prevalent regulator mRNA cis-element, but the underlying trans-acting factors or the regulators are poorly understood. TBF1, a key transcription factor in plant growth-defense transition, is tightly controlled by uORFs at the translation level. However, this suppression control is alleviated upon the recognition of.pathogen effectors for the establishment of effector-triggered immunity (ETI). This information inspires us to identify uORF regulators which may control immunity through translational reprogramming. With the utilization of translation reporter uORFsTBF1-LUC, we have identified 12 mutants displaying increased LUC fluorescence, indicating the loss of uORF-mediated translational suppression. We will focus on dst7 mutant as it also compromises ETI responses. We propose to perform mass-spectrum to find out the interactors of DST7 and further to illustrate how those interactors participate in uORF-mediated translational control during ETI response. Our results will advance our understanding of translational control mechanisms during immune responses and provide another important layer of immune regulation for engineering disease resistant plants.
植物病害对农业生产构成严重威胁,研究植物免疫机制对培育抗病作物至关重要。本项目聚焦于翻译调控在植物免疫中的作用,特别是免疫基因TBF1的5′LS(5′ leader sequence)作为翻译调控的关键分子开关。研究通过转基因拟南芥和正向遗传筛选,鉴定出HEM1为调控蛋白质翻译的关键成员,发现HEM1在ETI(Effector Triggered Immunity,效应子触发免疫)免疫激活时与翻译因子互作形成团聚体,抑制免疫基因过度翻译,维持细胞存活和组织健康。..主要发现包括:(1)HEM1是ETI细胞死亡的负调控因子,其缺失导致全局性翻译紊乱,解除了促死亡免疫基因的翻译限制。(2)HEM1是一个相变蛋白,其相变依赖于LCD,响应免疫信号刺激与翻译因子形成团聚体,调控翻译重编程。(3)HEM1的LCD介导翻译调控和ETI引起的细胞死亡,精确敲除LCD的突变体表现出与完全缺失突变体相同的表型。研究结果表明,HEM1通过其LCD结构域与翻译因子互作形成团聚体,在植物ETI免疫中发挥重要作用,有效抑制免疫基因过度翻译,平衡抗病性与组织健康,为未来培育抗病高产优质作物提供理论指导。
国内基金
海外基金