PDF(Pubmed)
Abstract：
CONCLUSIONS: Ambient concentrations of atmospheric nitrogen dioxide (NO2) inhibit the binding of PIF4 to promoter regions of auxin pathway genes to suppress hypocotyl elongation in Arabidopsis. Ambient concentrations (10-50 ppb) of atmospheric nitrogen dioxide (NO2) positively regulate plant growth to the extent that organ size and shoot biomass can nearly double in various species, including Arabidopsis thaliana (Arabidopsis). However, the precise molecular mechanism underlying NO2-mediated processes in plants, and the involvement of specific molecules in these processes, remain unknown. We measured hypocotyl elongation and the transcript levels of PIF4, encoding a bHLH transcription factor, and its target genes in wild-type (WT) and various pif mutants grown in the presence or absence of 50 ppb NO2. Chromatin immunoprecipitation assays were performed to quantify binding of PIF4 to the promoter regions of its target genes. NO2 suppressed hypocotyl elongation in WT plants, but not in the pifq or pif4 mutants. NO2 suppressed the expression of target genes of PIF4, but did not affect the transcript level of the PIF4 gene itself or the level of PIF4 protein. NO2 inhibited the binding of PIF4 to the promoter regions of two of its target genes, SAUR46 and SAUR67. In conclusion, NO2 inhibits the binding of PIF4 to the promoter regions of genes involved in the auxin pathway to suppress hypocotyl elongation in Arabidopsis. Consequently, PIF4 emerges as a pivotal participant in this regulatory process. This study has further clarified the intricate regulatory mechanisms governing plant responses to environmental pollutants, thereby advancing our understanding of how plants adapt to changing atmospheric conditions.
摘要：
结论：环境浓度的大气二氧化氮（NO2）抑制PIF4与生长素途径基因启动子区域的结合，从而抑制拟南芥下胚轴的伸长。大气二氧化氮（NO2）的环境浓度（10-50ppb）积极调节植物生长，使器官大小和芽生物量在各种物种中几乎可以增加一倍。包括拟南芥(拟南芥)。然而,植物中NO2介导过程的精确分子机制，以及特定分子参与这些过程，仍然未知。我们测量了编码bHLH转录因子的下胚轴伸长和PIF4的转录水平，及其在存在或不存在50ppbNO2的情况下生长的野生型（WT）和各种pif突变体中的靶基因。进行染色质免疫沉淀测定以定量PIF4与其靶基因的启动子区域的结合。NO2抑制WT植物的下胚轴伸长，但不是在pifq或pif4突变体中。NO2抑制了PIF4靶基因的表达，但不影响PIF4基因本身的转录水平或PIF4蛋白的水平。NO2抑制PIF4与其两个靶基因启动子区的结合,SAUR46和SAUR67。总之,NO2抑制PIF4与生长素途径相关基因的启动子区域的结合，从而抑制拟南芥的下胚轴伸长。因此,PIF4成为这一监管过程的关键参与者。这项研究进一步阐明了控制植物对环境污染物反应的复杂调控机制，从而提高我们对植物如何适应不断变化的大气条件的理解。
