Autophagy is a highly conserved recycling system in eukaryotes for bulk degradation of intracellular components. Plant autophagy has been shown to function in various abiotic stress responses, pathogen defense, and senescence. Ethylene is a very important hormone that regulates growth, development and senescence process in plant, and it also involved in responsing to various of biotic and abiotic stresses. Previous studies showed that ATG genes were induced by ethylene which indicates that ethylene may be involved in autophagy regulation. Over the past decade, our molecular and physiological understanding of plant autophagy has greatly increased. However, little is known about the mechanism of hormone-related autophagy initiation. Our preliminary data show that autophagy was induced by ACC treatment. The autophagosome numbers were much more in ethylene-overproducing mutants, but less in ethylene-insensitive mutants. These results indicated that ethylene signaling positive regulates autophagy pathway. Further, ethylene related genes were down-regulated in autophagy-deficient mutants, and ethylene signaling was enhanced in autophagy-induced condition. That suggests that there is a feedback regulation between autophagy and ethylene pathway. Based on previous work, we further intend to elucidate the mechanism of how ethylene signaling regulate autophagy pathway and the feedback regulation. Results from this study may further strengthen our understanding of the biological function of ethylene and provide theoretical basis for regulatory mechanism of autophagy in plants.
自噬是真核生物中重要的物质循环再利用过程,它参与植物中许多重要的生命活动,如非生物胁迫应答、病原菌侵染和衰老等。乙烯是调节植物生长、发育和衰老的激素,也参与植物对多种生物和非生物胁迫的应答。研究表明乙烯处理能够诱导自噬基因表达,暗示着乙烯可能参与调控自噬途径。随着自噬在植物中的研究逐渐深入,我们对自噬形成分子机制的认识逐渐清楚,但对于植物激素参与调控自噬起始的分子机制还不清楚。前期研究结果显示ACC诱导自噬发生,自噬体数目在乙烯信号突变体中很少,而在乙烯过量表达突变体中更多,说明乙烯正调控自噬发生。在自噬缺失条件下,乙烯相关基因表达显著下调;而在自噬诱导的条件下,乙烯信号明显增强,暗示着自噬可能反馈调节乙烯通路。本项目拟在已有工作基础上,深入研究植物乙烯调控自噬发生的分子机理以及自噬对乙烯通路的反馈调节机制。研究结果将拓展植物激素乙烯的生理功能以及为植物自噬的调控机理提供新的理论依据。
项目背景: 自噬是真核生物中重要的物质循环再利用过程,参与植物中许多重要的生命活动。乙烯是一种重要的植物激素,参与调节植物生长发育和逆境胁迫应答。研究表明乙烯能够诱导自噬基因表达,暗示着乙烯可能参与调控自噬途径,但对于乙烯参与调控自噬起始的分子机制还不清楚。.研究内容:本项目深入研究了乙烯信号调控植物细胞自噬参与低氧胁迫的生物学功能和乙烯通路转录因子EIN3转录调控自噬基因ATG13a的分子机制。.重要结果:研究发现乙烯信号缺失导致拟南芥对低氧胁迫敏感;乙烯信号能够诱导自噬相关基因的表达;乙烯信号转录因子EIN3影响低氧胁迫下自噬基因表达。进一步研究发现,EIN3能够结合ATG13a启动子并激活ATG13a基因表达,进而提高细胞自噬活性。.科学意义:该工作首次揭示了EIN3参与调控植物细胞自噬,从而影响植物低氧胁迫耐受性,进一步丰富了对植物乙烯信号调控植物非生物逆境应答功能及作用机理的认识。
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数据更新时间:2023-05-31
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