Regulation of mitochondrial NAD pool via NAD+ transporter 2 is essential for matrix NADH homeostasis and ROS production in Arabidopsis
Regulation of mitochondrial NAD pool via NAD+ transporter 2 is essential for matrix NADH homeostasis and ROS production in Arabidopsis
复制标题
通过 NAD( ) 转运蛋白 2 调节线粒体 NAD 池对于拟南芥中基质 NADH 稳态和 ROS 产生至关重要
DOI:
10.1007/s11427-019-9563-y
复制
发表时间:
2019-08-01
影响因子:
9.1
通讯作者:
Li, Jiayang
中科院分区:
文献类型:
--
作者:
Luo, Lilan;He, Yajun;Li, Jiayang
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.