CAJ | 학술논문

盐胁迫严重限制着植物的生长发育，造成农业产量下降。植物遭受盐胁迫时，细胞代谢受到抑制，体内会积累较多活性氧（ROS）进而对植物造成氧化胁迫，诱导自噬现象的产生。本文主要研究了植物对于盐胁迫诱导的自噬及其反应的调控机制。研究中发现，在高盐浓度处理的拟南芥幼苗中自噬现象迅速产生，伴随着NADPH氧化酶活性的明显上升。此外，通过用荧光探针LysoTracker Red （LTR）定位自噬小体，激光共聚焦观察发现AtTOR不仅可以在正常生理环境下抑制自噬小体的生成，而且可以在高盐浓度胁迫环境下抑制自噬。进而我们发现在高盐浓度处理的同时添加NADPH氧化酶抑制剂DPI后，处理过后的WT株系拟南芥根细胞自噬现象受到明显抑制，而AtTOR突变体中并未有明显的变化。因此NADPH氧化酶很有可能参与AtTOR对盐胁迫诱导自噬的信号通路的调控。该研究结果为进一步分析植物耐受性机理和自噬的信号通路提供理论依据。
염협박엄중한제착식물적생장발육，조성농업산량하강。식물조수염협박시，세포대사수도억제，체내회적루교다활성양（ROS）진이대식물조성양화협박，유도자서현상적산생。본문주요연구료식물대우염협박유도적자서급기반응적조공궤제。연구중발현，재고염농도처리적의남개유묘중자서현상신속산생，반수착NADPH양화매활성적명현상승。차외，통과용형광탐침LysoTracker Red （LTR）정위자서소체，격광공취초관찰발현AtTOR불부가이재정상생리배경하억제자서소체적생성，이차가이재고염농도협박배경하억제자서。진이아문발현재고염농도처리적동시첨가NADPH양화매억제제DPI후，처리과후적WT주계의남개근세포자서현상수도명현억제，이AtTOR돌변체중병미유명현적변화。인차NADPH양화매흔유가능삼여AtTOR대염협박유도자서적신호통로적조공。해연구결과위진일보분석식물내수성궤리화자서적신호통로제공이론의거。
Salinity seriously limits plant growth and development,reducing the crop productivity.Downregulation of cellular metabolism during salt stress causes reactive oxygen species (ROS)accumulation,contributing to oxidative stress and thus inducing autophagy.In this article we put emphasis on specific autophagic activity in plants during salt stress and its regulation mechanism.We found that autophagy was induced in the short term when treated with high salt concentrations,which was accompanied by a large increase in NADPH oxidase activity.In addition,we used LysoTrack-er Red (LTR)fluorescent probe as an indicator of autophagy to find that AtTOR inhibits the formation of autophagic body both in normal conditions and high salt stress conditions.After added with NADPH inhibitor DPI,autophagy was found significantly inhibited in WT during treatment with high concentrations of salt,while,no remarkable change was found in AtTOR mutant.Therefore NADPH oxidase is likely involved in the upstream regulation of AtTOR during salt stress-induced autophagy.The data may provide theoretic foundation for further studying the adaptive mechanisms and autophagic signaling pathway in plant.