背景回顾：Plant submergence stress is a growing problem for global agriculture. During desubmergence, rising O₂ concentrations meet a highly reduced mitochondrial electron transport chain (mETC) in the cells. This combination favors the generation of reactive oxygen species (ROS) by the mitochondria, which at excess can cause damage. 

提出问题：The cellular mechanisms underpinning the management of reoxygenation stress are not fully understood. 

主要研究：We investigated the role of alternative NADH dehydrogenases (NDs), as components of the alternative mETC in Arabidopsis, in anoxia-reoxygenation stress management. 

结果1-NDA1/2功能：Simultaneous loss of the matrix-facing NDs, NDA1 and NDA2, decreased seedling survival after reoxygenation, while overexpression increased survival. 

结果2-mETC-光合：Absence of NDAs led to reduced maximum potential quantum efficiency of photosystem II linking the alternative mETC to photosynthetic function in the chloroplast. 

结果3-NAD1/2的转录调控机制：NDA1 and NDA2 were induced upon reoxygenation and transcriptional activation of NDA1 was controlled by the transcription factors ANAC016 and ANAC017 that bind to the mitochondrial dysfunction motif (MDM) in the NDA1 promoter. 

结果4-NAD1/2-ROS：Absence of NDA1 and NDA2 did not alter recovery of cytosolic ATP levels and NADH/NAD⁺ ratio at reoxygenation. Rather, absence of NDAs led to elevated ROS production while their overexpression limited ROS.

结论：Our observations indicate that the control of ROS formation by the alternative mETC is important for photosynthetic recovery and for seedling survival of anoxia-reoxygenation stress.

NBT染色（上）和DAB染色（下）显示NAD1/2抑制了缺氧-复氧胁迫所导致的ROS爆发

植物淹水胁迫对于全球农业来说是一个日益严重的问题。在经历淹水胁迫后植物细胞中的线粒体电子传递链（mETC）急剧减少，但水退之后增加的氧气浓度会导致线粒体活性氧物质（ROS）的爆发，从而对植物造成损伤。然而，植物中关于复氧胁迫管理的细胞机制还不清楚。作者研究了拟南芥中作为交替mETC组分的交替NADH脱氢酶（NDs）在缺氧-复氧胁迫管理中的作用。同时敲除两个面向线粒体基质的ND酶NDA1和NDA2会导致复氧后的成活率降低，而过表达这两个基因则会增加复氧后的成活率。NDAs的缺失会导致光系统Ⅱ潜在最大光化学量子效率的降低，这将交替mETC与叶绿体的光合功能联系起来。NDA1和NDA2基因的表达受到复氧的诱导，而NDA1的转录激活则是受到ANAC016/017两个转录因子的控制，这两个转录因子能够直接集合NDA1启动子上的线粒体功能障碍基序（MDM）。NDA1和NDA2的缺失并不会改变复氧时胞质ATP水平以及NADH/NAD+比率的恢复。相反，NDAs的缺失会导致ROS生成的增加，NDAs的过表达则会限制ROS。本文的研究结果揭示了交替mETC对于ROS形成的控制有助于植物在缺氧-复氧胁迫下的光合能力恢复和幼苗存活。