锌作为一种重要的微量元素参与了植物体内广泛的生理和生化过程,本文详细介绍了涉及Zn2+吸收转运的Z IP基因家族(ZRT/IRT相关蛋白)和CDF(C ation d iffus ion fac ilitator)家族。Z IP家族转运蛋白主要负责将Zn2+等二价阳离子跨膜转运...锌作为一种重要的微量元素参与了植物体内广泛的生理和生化过程,本文详细介绍了涉及Zn2+吸收转运的Z IP基因家族(ZRT/IRT相关蛋白)和CDF(C ation d iffus ion fac ilitator)家族。Z IP家族转运蛋白主要负责将Zn2+等二价阳离子跨膜转运进细胞内,以完成细胞内多种生理生化反应。CDF家族转运蛋白主要负责将过量的Zn2+运出细胞,或者将细胞内过量Zn2+进行区室化隔离,降低Zn2+对细胞的危害作用。Z IP家族转运蛋白和CDF家族转运蛋白的相互协调使得Zn2+在细胞和有机体水平上维持着稳态,进而为细胞内各种生理生化反应的进行提供一种保障机制。展开更多
Zn^(2+)is required for the activity of many mitochondrial proteins,which regulate mitochondrial dynamics,apoptosis and mitophagy.However,it is not understood how the proper mitochondrial Zn^(2+)level is achieved to ma...Zn^(2+)is required for the activity of many mitochondrial proteins,which regulate mitochondrial dynamics,apoptosis and mitophagy.However,it is not understood how the proper mitochondrial Zn^(2+)level is achieved to maintain mitochondrial homeostasis.Using Caenorhabditis elegans,we reveal here that a pair of mitochondrion-localized transporters controls the mitochondrial level of Zn^(2+).We demonstrate that SLC-30A9/ZnT9 is a mitochondrial Zn^(2+)exporter.Loss of SLC-30A9 leads to mitochondrial Zn^(2+)accumulation,which damages mitochondria,impairs animal development and shortens the life span.We further identify SLC-25A25/SCaMC-2 as an important regulator of mitochondrial Zn^(2+)import.Loss of SLC-25A25 suppresses the abnormal mitochondrial Zn^(2+)accumulation and defective mitochondrial structure and functions caused by loss of SLC-30A9.Moreover,we reveal that the endoplasmic reticulum contains the Zn^(2+)pool from which mitochondrial Zn^(2+)is imported.These findings establish the molecular basis for controlling the correct mitochondrial levels for normal mitochondrial structure and functions.展开更多
文摘锌作为一种重要的微量元素参与了植物体内广泛的生理和生化过程,本文详细介绍了涉及Zn2+吸收转运的Z IP基因家族(ZRT/IRT相关蛋白)和CDF(C ation d iffus ion fac ilitator)家族。Z IP家族转运蛋白主要负责将Zn2+等二价阳离子跨膜转运进细胞内,以完成细胞内多种生理生化反应。CDF家族转运蛋白主要负责将过量的Zn2+运出细胞,或者将细胞内过量Zn2+进行区室化隔离,降低Zn2+对细胞的危害作用。Z IP家族转运蛋白和CDF家族转运蛋白的相互协调使得Zn2+在细胞和有机体水平上维持着稳态,进而为细胞内各种生理生化反应的进行提供一种保障机制。
基金This work was supported by grants from the National Science Foundation of China(91954204 and 31730053)the National Basic Research Program of China(2017YFA0503403)Yunnan Province Science and Technology Department(#202001BB050077 and#202105AB160003).
文摘Zn^(2+)is required for the activity of many mitochondrial proteins,which regulate mitochondrial dynamics,apoptosis and mitophagy.However,it is not understood how the proper mitochondrial Zn^(2+)level is achieved to maintain mitochondrial homeostasis.Using Caenorhabditis elegans,we reveal here that a pair of mitochondrion-localized transporters controls the mitochondrial level of Zn^(2+).We demonstrate that SLC-30A9/ZnT9 is a mitochondrial Zn^(2+)exporter.Loss of SLC-30A9 leads to mitochondrial Zn^(2+)accumulation,which damages mitochondria,impairs animal development and shortens the life span.We further identify SLC-25A25/SCaMC-2 as an important regulator of mitochondrial Zn^(2+)import.Loss of SLC-25A25 suppresses the abnormal mitochondrial Zn^(2+)accumulation and defective mitochondrial structure and functions caused by loss of SLC-30A9.Moreover,we reveal that the endoplasmic reticulum contains the Zn^(2+)pool from which mitochondrial Zn^(2+)is imported.These findings establish the molecular basis for controlling the correct mitochondrial levels for normal mitochondrial structure and functions.
