Zhang Guo-Bin, Yi Hong-Ying, Gong Ji-Ming
National Key Laboratory of Plant Molecular Genetics and National Center for Plant Gene Research (Shanghai), Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200032, People's Republic of China.
National Key Laboratory of Plant Molecular Genetics and National Center for Plant Gene Research (Shanghai), Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200032, People's Republic of China
Plant Cell. 2014 Oct;26(10):3984-98. doi: 10.1105/tpc.114.129296. Epub 2014 Oct 17.
Stresses decouple nitrate assimilation and photosynthesis through stress-initiated nitrate allocation to roots (SINAR), which is mediated by the nitrate transporters NRT1.8 and NRT1.5 and functions to promote stress tolerance. However, how SINAR communicates with the environment remains unknown. Here, we present biochemical and genetic evidence demonstrating that in Arabidopsis thaliana, ethylene (ET) and jasmonic acid (JA) affect the crosstalk between SINAR and the environment. Electrophoretic mobility shift assays and chromatin immunoprecipitation assays showed that ethylene response factors (ERFs), including OCTADECANOID-RESPONSIVE ARABIDOPSIS AP2/ERF59, bind to the GCC boxes in the NRT1.8 promoter region, while ETHYLENE INSENSITIVE3 (EIN3) binds to the EIN3 binding site motifs in the NRT1.5 promoter. Genetic assays showed that cadmium and sodium stresses initiated ET/JA signaling, which converged at EIN3/EIN3-Like1 (EIL1) to modulate ERF expression and hence to upregulate NRT1.8. By contrast, ET and JA signaling mediated the downregulation of NRT1.5 via EIN3/EIL1 and other, unknown component(s). SINAR enhanced stress tolerance and decreased plant growth under nonstressed conditions through the ET/JA-NRT1.5/NRT1.8 signaling module. Interestingly, when nitrate reductase was impaired, SINAR failed to affect either stress tolerance or plant growth. These data suggest that SINAR responds to environmental conditions through the ET/JA-NRT signaling module, which further modulates stress tolerance and plant growth in a nitrate reductase-dependent manner.
胁迫通过胁迫引发的硝酸盐向根部分配（SINAR）使硝酸盐同化与光合作用解偶联，这一过程由硝酸盐转运蛋白NRT1.8和NRT1.5介导，并起到促进胁迫耐受性的作用。然而，SINAR如何与环境相互作用仍不清楚。在此，我们提供了生化和遗传学证据，证明在拟南芥中，乙烯（ET）和茉莉酸（JA）影响SINAR与环境之间的相互作用。电泳迁移率变动分析和染色质免疫沉淀分析表明，包括十八烷酸应答型拟南芥AP2/ERF59在内的乙烯反应因子（ERF）与NRT1.8启动子区域的GCC框结合，而乙烯不敏感3（EIN3）与NRT1.5启动子中的EIN3结合位点基序结合。遗传学分析表明，镉和钠胁迫引发ET/JA信号传导，该信号传导在EIN3/类EIN3 1（EIL1）处汇聚，以调节ERF表达，从而上调NRT1.8。相比之下，ET和JA信号传导通过EIN3/EIL1和其他未知成分介导NRT1.5的下调。SINAR通过ET/JA-NRT1.5/NRT1.8信号模块在非胁迫条件下增强胁迫耐受性并降低植物生长。有趣的是，当硝酸还原酶受损时，SINAR既不能影响胁迫耐受性也不能影响植物生长。这些数据表明，SINAR通过ET/JA-NRT信号模块对环境条件作出反应，该信号模块进一步以硝酸还原酶依赖性方式调节胁迫耐受性和植物生长。
