Diapause is a long-lived stage which has evolved into an important strategy for insects to circumvent extreme environments.In the pupal stage,Helicoverpa armigera can enter diapause,a state characterized by significan...Diapause is a long-lived stage which has evolved into an important strategy for insects to circumvent extreme environments.In the pupal stage,Helicoverpa armigera can enter diapause,a state characterized by significantly decreased metabolic activity and enhanced stress resistance,to survive cold winters.Previous studies have shown that reactive oxygen species(ROS)can promote the diapause process by regulating a distinct insulin signaling pathway.However,the source of ROS in the diapause-destined pupal brains and mechanisms by which ROS regulate diapause are still unknown.In this study,we showed that diapause-destined pupal brains accumulated high levels of mitochondrial ROS(mtROS)and total ROS during the diapause process,suggesting that mitochondria are the main source of ROS in diapause-destined pupal brains.In addition,injection of 2-deoxy-D-glucose(DOG),a glucose metabolism inhibitor,could delay pupal development by elevating mtROS levels in the nondiapause-destined pupal brains.Furthermore,the injection of a metabolite mixture to increase metabolic activity could avert the diapause process in diapause-destined pupae by decreasing mtROS levels.We also found that ROS could activate HSP60 expression and promote the stability of the HSP60-Lon complex,increasing its ability to degrade mitochondrial transcription factor A(TFAM)and decreasing mitochondrial activity or biogenesis under oxidative stress.Thus,this study illustrated the beneficial function of ROS in diapause or lifespan extension by decreasing mitochondrial activity.展开更多
Reactive oxygen species(ROS) play a crucial role in numerous biological processes in plants, including development, responses to environmental stimuli, and programmed cell death(PCD). Deficiency in MOSAIC DEATH 1(MOD1...Reactive oxygen species(ROS) play a crucial role in numerous biological processes in plants, including development, responses to environmental stimuli, and programmed cell death(PCD). Deficiency in MOSAIC DEATH 1(MOD1), a plastid-localized enoyl-ACP reductase essential for de novo fatty acid biosynthesis in Arabidopsis thaliana, leads to the increased malate export from chloroplasts to mitochondria, and the subsequent accumulation of mitochondria-generated ROS and PCD. In this study, we report the identification and characterization of a mod1 suppressor, som592. SOM592 encodes mitochondrion-localized NAD^+ transporter 2(NDT2). We show that the mitochondrial NAD pool is elevated in the mod1 mutant. The som592 mutation fully suppressed mitochondrial NADH hyper-accumulation, ROS production, and PCD in the mod1 mutant, indicating a causal relationship between mitochondrial NAD accumulation and ROS/PCD phenotypes. We also show that in wild-type plants, the mitochondrial NAD+uptake is involved in the regulation of ROS production in response to continuous photoperiod. Elevation of the alternative respiration pathway can suppress ROS accumulation and PCD in mod1, but leads to growth restriction. These findings uncover a regulatory mechanism for mitochondrial ROS production via NADH homeostasis in Arabidopsis thaliana that is likely important for growth regulation in response to altered photoperiod.展开更多
目的探讨PYHIN1(pyrin and HIN domain-containing protein 1)/Caspase 1炎症复合体信号通路在主动脉内皮细胞(HAEC)中的表达水平及作用机制。方法体外培养人主动脉内皮细胞,分为对照组和实验组,对照组用天然低密度脂蛋白(nLDL)处理,实...目的探讨PYHIN1(pyrin and HIN domain-containing protein 1)/Caspase 1炎症复合体信号通路在主动脉内皮细胞(HAEC)中的表达水平及作用机制。方法体外培养人主动脉内皮细胞,分为对照组和实验组,对照组用天然低密度脂蛋白(nLDL)处理,实验组用不同浓度的氧化低密度脂蛋白(oxLDL)处理诱导内皮细胞损伤,模拟动脉粥样硬化细胞模型。观察PYHIN1/Caspase 1炎症复合体的表达以及线粒体活性氧(mtROS)在内皮细胞黏附中的作用。结果与对照组相比,实验组以浓度依赖的方式促进PYHIN1、Caspase 1、IL-18和ICAM1的表达(P<0.05)。同时,实验组细胞黏附增强,mtROS显著增加,SOD活性降低;加入mtROS的抑制剂后,细胞的黏附能力降低(P<0.05)。结论oxLDL通过促进mtROS产生增强内皮细胞的黏附作用。展开更多
基金supported by the China Postdoctoral Science Foundation (2017M622872)
文摘Diapause is a long-lived stage which has evolved into an important strategy for insects to circumvent extreme environments.In the pupal stage,Helicoverpa armigera can enter diapause,a state characterized by significantly decreased metabolic activity and enhanced stress resistance,to survive cold winters.Previous studies have shown that reactive oxygen species(ROS)can promote the diapause process by regulating a distinct insulin signaling pathway.However,the source of ROS in the diapause-destined pupal brains and mechanisms by which ROS regulate diapause are still unknown.In this study,we showed that diapause-destined pupal brains accumulated high levels of mitochondrial ROS(mtROS)and total ROS during the diapause process,suggesting that mitochondria are the main source of ROS in diapause-destined pupal brains.In addition,injection of 2-deoxy-D-glucose(DOG),a glucose metabolism inhibitor,could delay pupal development by elevating mtROS levels in the nondiapause-destined pupal brains.Furthermore,the injection of a metabolite mixture to increase metabolic activity could avert the diapause process in diapause-destined pupae by decreasing mtROS levels.We also found that ROS could activate HSP60 expression and promote the stability of the HSP60-Lon complex,increasing its ability to degrade mitochondrial transcription factor A(TFAM)and decreasing mitochondrial activity or biogenesis under oxidative stress.Thus,this study illustrated the beneficial function of ROS in diapause or lifespan extension by decreasing mitochondrial activity.
基金supported by the National Natural Science Foundation of China (31521001, 91854103, 31661143025)
文摘Reactive oxygen species(ROS) play a crucial role in numerous biological processes in plants, including development, responses to environmental stimuli, and programmed cell death(PCD). Deficiency in MOSAIC DEATH 1(MOD1), a plastid-localized enoyl-ACP reductase essential for de novo fatty acid biosynthesis in Arabidopsis thaliana, leads to the increased malate export from chloroplasts to mitochondria, and the subsequent accumulation of mitochondria-generated ROS and PCD. In this study, we report the identification and characterization of a mod1 suppressor, som592. SOM592 encodes mitochondrion-localized NAD^+ transporter 2(NDT2). We show that the mitochondrial NAD pool is elevated in the mod1 mutant. The som592 mutation fully suppressed mitochondrial NADH hyper-accumulation, ROS production, and PCD in the mod1 mutant, indicating a causal relationship between mitochondrial NAD accumulation and ROS/PCD phenotypes. We also show that in wild-type plants, the mitochondrial NAD+uptake is involved in the regulation of ROS production in response to continuous photoperiod. Elevation of the alternative respiration pathway can suppress ROS accumulation and PCD in mod1, but leads to growth restriction. These findings uncover a regulatory mechanism for mitochondrial ROS production via NADH homeostasis in Arabidopsis thaliana that is likely important for growth regulation in response to altered photoperiod.
文摘目的探讨PYHIN1(pyrin and HIN domain-containing protein 1)/Caspase 1炎症复合体信号通路在主动脉内皮细胞(HAEC)中的表达水平及作用机制。方法体外培养人主动脉内皮细胞,分为对照组和实验组,对照组用天然低密度脂蛋白(nLDL)处理,实验组用不同浓度的氧化低密度脂蛋白(oxLDL)处理诱导内皮细胞损伤,模拟动脉粥样硬化细胞模型。观察PYHIN1/Caspase 1炎症复合体的表达以及线粒体活性氧(mtROS)在内皮细胞黏附中的作用。结果与对照组相比,实验组以浓度依赖的方式促进PYHIN1、Caspase 1、IL-18和ICAM1的表达(P<0.05)。同时,实验组细胞黏附增强,mtROS显著增加,SOD活性降低;加入mtROS的抑制剂后,细胞的黏附能力降低(P<0.05)。结论oxLDL通过促进mtROS产生增强内皮细胞的黏附作用。
