“****”学者Plant Cell破解新机理

　　

     2014年10月17日，中科院上海生命科学研究院植物生理生态研究所龚继明研究组在《Plant Cell》上在线发表题为“The Arabidopsis ethylene/jasmonic acid-NRT signaling module coordinates nitrate reallocation and the trade-off between growth and environmental adaptation”的研究论文。该研究揭示乙烯和茉莉酸途径及其调控的硝酸盐转运蛋白共同组成一个功能模块，从而调控逆境下硝酸盐在体内的再分配过程，回答了硝酸根再分配与不同环境信号整合的问题，并加深了人们对于植物如何在逆境耐受性和生长发育间平衡的机理的认识。

     光合硝酸根同化（Nitrate photoassimilation）的偶联和解偶联对于植物的能量效率具有重要的调节作用。龚继明研究组之前克隆了该过程中两个关键的调节基因NRT1.8和NRT1.5，阐明了其作用机理（Plant Cell， 2010； Plant Physiology， 2012），并预示NRT1.8/NRT1.5调节的硝酸根再分配是植物面对一系列逆境的通用机制，但植物如何整合不同的环境信号来调控这种逆境诱导的硝酸根再分配过程（Stress-induced nitrate allocation to roots, SINAR）尚未得到解答。

    通过生物信息学分析，作者发现同时受到乙烯和茉莉酸途径调控的ERFs转录因子有可能是NRT1.8的直接上游因子。进一步的遗传分析和生化实验证实了这一点，并且证实NRT1.8受到逆境诱导的乙烯和茉莉酸通路的协同调控进而上调表达，而NRT1.5也受到同样的调控从而下调表达。EIN3/EIL1在此过程中位于ERFs的上游起着整合乙烯和茉莉酸信号的作用，而且还作为NRT1.5的直接上游调控乙烯介导的NRT1.5表达。NRT1.5受茉莉酸的下调则受未知因子调控。

     进一步研究表明，SINAR在植物的逆境耐受和生长发育之间起着一个平衡器的作用，而且该调节作用依赖于硝酸还原酶。该研究对于提高各类环境下植物的氮素利用效率有着重要的指导意义，同时也为科研工作者培育具多种优良性状的农作物提供了思想借鉴。

    该项工作得到国家杰出青年科学基金和创新群体基金的经费支持。

简易模式图：ET/JA 途径启动SINAR调节硝酸盐再分配和环境适应的信号转导机制

原文摘要：
The Arabidopsis ethylene/jasmonic acid-NRT signaling module coordinates nitrate reallocation and the trade-off between growth and environmental adaptation

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.