Peng Jinying, Li Zhonghai, Wen Xing, Li Wenyang, Shi Hui, Yang Longshu, Zhu Huaiqiu, Guo Hongwei
The State Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Peking-Tsinghua Center of Life Sciences, Beijing, China.
Department of Biomedical Engineering, College of Engineering, and Center for Theoretical Biology, Peking University, Beijing, China.
PLoS Genet. 2014 Oct 16;10(10):e1004664. doi: 10.1371/journal.pgen.1004664. eCollection 2014 Oct.
Ethylene has been regarded as a stress hormone to regulate myriad stress responses. Salinity stress is one of the most serious abiotic stresses limiting plant growth and development. But how ethylene signaling is involved in plant response to salt stress is poorly understood. Here we showed that Arabidopsis plants pretreated with ethylene exhibited enhanced tolerance to salt stress. Gain- and loss-of-function studies demonstrated that EIN3 (ETHYLENE INSENSITIVE 3) and EIL1 (EIN3-LIKE 1), two ethylene-activated transcription factors, are necessary and sufficient for the enhanced salt tolerance. High salinity induced the accumulation of EIN3/EIL1 proteins by promoting the proteasomal degradation of two EIN3/EIL1-targeting F-box proteins, EBF1 and EBF2, in an EIN2-independent manner. Whole-genome transcriptome analysis identified a list of SIED (Salt-Induced and EIN3/EIL1-Dependent) genes that participate in salt stress responses, including several genes encoding reactive oxygen species (ROS) scavengers. We performed a genetic screen for ein3 eil1-like salt-hypersensitive mutants and identified 5 EIN3 direct target genes including a previously unknown gene, SIED1 (At5g22270), which encodes a 93-amino acid polypeptide involved in ROS dismissal. We also found that activation of EIN3 increased peroxidase (POD) activity through the direct transcriptional regulation of PODs expression. Accordingly, ethylene pretreatment or EIN3 activation was able to preclude excess ROS accumulation and increased tolerance to salt stress. Taken together, our study provides new insights into the molecular action of ethylene signaling to enhance plant salt tolerance, and elucidates the transcriptional network of EIN3 in salt stress response.
乙烯被视为一种调节多种胁迫反应的胁迫激素。盐胁迫是限制植物生长发育的最严重非生物胁迫之一。但乙烯信号如何参与植物对盐胁迫的反应仍知之甚少。在这里,我们表明用乙烯预处理的拟南芥植株对盐胁迫的耐受性增强。功能获得和功能缺失研究表明,两个乙烯激活的转录因子EIN3(乙烯不敏感3)和EIL1(EIN3样1)对于增强的耐盐性是必要且充分的。高盐度通过以EIN2非依赖的方式促进两种靶向EIN3/EIL1的F-box蛋白EBF1和EBF2的蛋白酶体降解,诱导EIN3/EIL1蛋白的积累。全基因组转录组分析确定了一系列参与盐胁迫反应的盐诱导和EIN3/EIL1依赖(SIED)基因,包括几个编码活性氧(ROS)清除剂的基因。我们对ein3 eil1样盐超敏突变体进行了遗传筛选,鉴定出5个EIN3直接靶基因,包括一个以前未知的基因SIED1(At5g22270),它编码一种参与ROS清除的93个氨基酸的多肽。我们还发现EIN3的激活通过直接转录调控过氧化物酶(POD)的表达增加了POD活性。因此,乙烯预处理或EIN3激活能够防止过量ROS积累并提高对盐胁迫的耐受性。综上所述,我们的研究为乙烯信号增强植物耐盐性的分子作用提供了新见解,并阐明了EIN3在盐胁迫反应中的转录网络。