Graduate School of Integrated Sciences for Life, Hiroshima University, Higashi, Hiroshima, 739-8526, Japan.
School of Science, Hiroshima University, Higashi, Hiroshima, 739-8526, Japan.
Planta. 2024 Jul 3;260(2):42. doi: 10.1007/s00425-024-04468-1.
Ambient concentrations of atmospheric nitrogen dioxide (NO) 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 (NO) 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 NO-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 NO. Chromatin immunoprecipitation assays were performed to quantify binding of PIF4 to the promoter regions of its target genes. NO suppressed hypocotyl elongation in WT plants, but not in the pifq or pif4 mutants. NO 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. NO inhibited the binding of PIF4 to the promoter regions of two of its target genes, SAUR46 and SAUR67. In conclusion, NO 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.
大气中的二氧化氮 (NO) 浓度会抑制 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。大气中的二氧化氮 (NO) 浓度（10-50 ppb）正向调节植物生长，以至于包括拟南芥在内的各种物种的器官大小和地上生物量几乎增加一倍。然而，NO 在植物中介导的过程的确切分子机制，以及特定分子在这些过程中的参与，仍然未知。我们在存在或不存在 50 ppb NO 的情况下，测量了野生型（WT）和各种 pif 突变体中 PIF4 及其靶基因的下胚轴伸长和转录水平，PIF4 编码一个 bHLH 转录因子。进行染色质免疫沉淀测定以定量 PIF4 与其靶基因启动子区域的结合。NO 抑制了 WT 植物的下胚轴伸长，但 pifq 或 pif4 突变体不受影响。NO 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。NO 抑制了 PIF4 与其两个靶基因 SAUR46 和 SAUR67 启动子区域的结合。总之，NO 抑制了 PIF4 与生长素途径基因启动子区域的结合，从而抑制了拟南芥下胚轴的伸长。因此，PIF4 成为该调节过程中的关键参与者。本研究进一步阐明了调控植物对环境污染物反应的复杂调节机制，从而加深了我们对植物如何适应不断变化的大气条件的理解。
