Mitochondria, the main energy transducers in plant cells, require the proper assembly of respiratory chain complexes Ⅰ–Ⅴ for their function. The NADH dehydrogenase4(nad4) gene encodes mitochondrial respiratory chai...Mitochondria, the main energy transducers in plant cells, require the proper assembly of respiratory chain complexes Ⅰ–Ⅴ for their function. The NADH dehydrogenase4(nad4) gene encodes mitochondrial respiratory chain complex Ⅰ subunit Ⅳ, but the mechanism underlying nad4 transcript splicing is unclear. Here, we report that the P-type pentatricopeptide repeat(PPR) protein DEFECTIVE KERNEL 43(DEK43) is responsible for cis-splicing of the nad4 transcript in maize. We demonstrate that DEK43 localizes to both the nucleus and mitochondria. The mutation of Dek43 resulted in embryo-lethal and light-colored defective kernels. Among the 22 mitochondrial group Ⅱ introns, the splicing efficiency of nad4 introns 1 and 3 was reduced by up to 50% compared to the wild type. The levels of complex Ⅰ and supercomplex Ⅰ+Ⅲ2 were also reduced in dek43. Furthermore, in-gel NADH dehydrogenase assays indicated that the activities of these complexes were significantly reduced in dek43. Further, the mitochondrial ultrastructure was altered in the mutant. Together, our findings indicate that DEK43, a dual-localized PPR protein,plays an important role in maintaining mitochondrial function and maize kernel development.展开更多
SIRT1(Sirtuin type 1)是依赖NAD+的组蛋白去乙酰化酶,对作用底物组蛋白赖氨酸残基进行去乙酰化修饰而发挥多种生理功能.SIRT1通过增加脂肪分解,减少脂肪堆积;增加糖异生,维持正常血糖水平;增加胰岛素敏感性,改善胰岛素抵抗;抑制蛋白水...SIRT1(Sirtuin type 1)是依赖NAD+的组蛋白去乙酰化酶,对作用底物组蛋白赖氨酸残基进行去乙酰化修饰而发挥多种生理功能.SIRT1通过增加脂肪分解,减少脂肪堆积;增加糖异生,维持正常血糖水平;增加胰岛素敏感性,改善胰岛素抵抗;抑制蛋白水解酶活性,减少骨骼肌质量丢失等多种途径调节机体物质代谢,改善代谢的失衡.因此,提高SIRT1活性已成为治疗多种疾病的方法之一.运动是刺激SIRT1表达的有效因素,小分子多酚类是SIRT1的激活剂,低强度激光照射可改善SIRT1活性,这些方法均已广泛用于多种疾病的防治.展开更多
基金funded by the National Natural Science Foundation of China(91735301 and 91535109)the National Plant Transgenic Program(2016ZX08003-003)+2 种基金Taishan Scholars Project(ts201712024)Funds of Shandong“Double Tops”Program(SYL2017YSTD03)a project(dxkt201707)from the State Key Laboratory of Crop Biology。
文摘Mitochondria, the main energy transducers in plant cells, require the proper assembly of respiratory chain complexes Ⅰ–Ⅴ for their function. The NADH dehydrogenase4(nad4) gene encodes mitochondrial respiratory chain complex Ⅰ subunit Ⅳ, but the mechanism underlying nad4 transcript splicing is unclear. Here, we report that the P-type pentatricopeptide repeat(PPR) protein DEFECTIVE KERNEL 43(DEK43) is responsible for cis-splicing of the nad4 transcript in maize. We demonstrate that DEK43 localizes to both the nucleus and mitochondria. The mutation of Dek43 resulted in embryo-lethal and light-colored defective kernels. Among the 22 mitochondrial group Ⅱ introns, the splicing efficiency of nad4 introns 1 and 3 was reduced by up to 50% compared to the wild type. The levels of complex Ⅰ and supercomplex Ⅰ+Ⅲ2 were also reduced in dek43. Furthermore, in-gel NADH dehydrogenase assays indicated that the activities of these complexes were significantly reduced in dek43. Further, the mitochondrial ultrastructure was altered in the mutant. Together, our findings indicate that DEK43, a dual-localized PPR protein,plays an important role in maintaining mitochondrial function and maize kernel development.
文摘SIRT1(Sirtuin type 1)是依赖NAD+的组蛋白去乙酰化酶,对作用底物组蛋白赖氨酸残基进行去乙酰化修饰而发挥多种生理功能.SIRT1通过增加脂肪分解,减少脂肪堆积;增加糖异生,维持正常血糖水平;增加胰岛素敏感性,改善胰岛素抵抗;抑制蛋白水解酶活性,减少骨骼肌质量丢失等多种途径调节机体物质代谢,改善代谢的失衡.因此,提高SIRT1活性已成为治疗多种疾病的方法之一.运动是刺激SIRT1表达的有效因素,小分子多酚类是SIRT1的激活剂,低强度激光照射可改善SIRT1活性,这些方法均已广泛用于多种疾病的防治.
