植物自噬相关基因在响应逆境胁迫中的功能和作用机制
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国家自然科学基金(32360483,32160466);甘肃省自然科学基金重点项目(23JRRA764)


Functions and mechanisms of autophagy-related genes in plant responses to adversity stresses
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    摘要:

    自噬是真核生物中进化保守的自我降解机制,植物细胞自噬不仅在其生长发育过程中发挥重要作用,而且参与应对各种生物和非生物逆境胁迫。植物可通过自噬降解多余或受损的细胞质物质和细胞器来抵御逆境胁迫。自噬的发生依赖于自噬相关基因(autophagy-related genes,ATGs),转录因子能够直接结合ATGs启动子,从而激活自噬并调节其转录水平和翻译后修饰。ATGs还与激素直接或间接互作,调控植物逆境胁迫应答反应。当受到盐分、干旱、极端温度、营养亏缺和病原菌等胁迫时,植物ATGs被显著诱导,自噬活性增强,降解变性和未折叠蛋白质,从而提高植物抗逆性。本文对植物ATGs发现、结构、分类及其在逆境胁迫响应中的作用等方面研究成果进行了综述,并对其未来研究方向进行展望,为农作物抗逆性遗传改良提供了基因资源和理论依据。

    Abstract:

    Autophagy is an evolutionarily conserved self-degradation process in eukaryotes. It not only plays a role in plant growth and development but also is involved in plant responses to biotic and abiotic stresses. Plants can initiate autophagy to degrade the surplus or damaged cytoplasmic materials and organelles, thus coping with abiotic and biotic stresses. The initiation of autophagy depends on autophagy-related genes (ATGs). The transcription factors can directly bind to the promoters of ATGs to activate autophagy and regulate their transcriptional levels and post-translational modifications. Furthermore, ATGs can directly or indirectly interact with plant hormones to regulate plant responses to stresses. When plants are exposed to salinity, drought, extreme temperatures, nutrient deficiencies, and pathogen stress, ATGs are significantly induced, which enhances the autophagy activity to facilitate the degradation of the denatured and misfolded proteins, thereby enhancing plant tolerance to adversity stresses. This article summarizes the discovery, structures, and classification of plant ATGs, reviews the research progress in the mechanisms of ATGs in plant responses to abiotic and biotic stresses, and prospects the future research directions. This review is expected to provide the genetic resources and a theoretical foundation for the genetic improvement of crops in responses to stress tolerance.

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任云儿,伍国强,魏明. 植物自噬相关基因在响应逆境胁迫中的功能和作用机制[J]. 生物工程学报, 2025, 41(2): 510-529

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  • 收稿日期:2024-08-15
  • 最后修改日期:2024-09-09
  • 在线发布日期: 2025-02-11
  • 出版日期: 2025-02-25
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