Salicylic acid (SA) and ethylene (ET) are important phytohormones that regulate numerous plant growth, development, and stress response processes. Previous studies have suggested functional interplay of SA and ET in defense responses, but precisely how these two hormones coregulate plant growth and development processes remains unclear. Our present work reveals antagonism between SA and ET in apical hook formation, which ensures successful soil emergence of etiolated dicotyledonous seedlings. Exogenous SA inhibited ET-induced expression of HOOKLESS1 (HLS1) in Arabidopsis (Arabidopsis thaliana) in a manner dependent on ETHYLENE INSENSITIVE3 (EIN3) and EIN3-LIKE1 (EIL1), the core transcription factors in the ET signaling pathway. SA-activated NONEXPRESSER OF PR GENES1 (NPR1) physically interacted with EIN3 and interfered with the binding of EIN3 to target gene promoters, including the HLS1 promoter. Transcriptomic analysis revealed that NPR1 and EIN3/EIL1 coordinately regulated subsets of genes that mediate plant growth and stress responses, suggesting that the interaction between NPR1 and EIN3/EIL1 is an important mechanism for integrating the SA and ET signaling pathways in multiple physiological processes. Taken together, our findings illuminate the molecular mechanism underlying SA regulation of apical hook formation as well as the antagonism between SA and ET in early seedling establishment and possibly other physiological processes.Salicylic acid antagonizes ethylene in apical hook development through NPR1-mediated repression of HLS1 expression and transcriptional activity of EIN3/EIL1.
水杨酸(SA)和乙烯(ET)是重要的植物激素,它们调控着众多植物的生长、发育以及应激反应过程。先前的研究表明,SA和ET在防御反应中存在功能上的相互作用,但这两种激素究竟如何共同调控植物的生长和发育过程仍不清楚。我们目前的研究揭示了SA和ET在顶端弯钩形成过程中存在拮抗作用,这确保了黄化双子叶植物幼苗能够成功出土。外源SA以依赖于乙烯不敏感3(EIN3)和乙烯不敏感3类似物1(EIL1)(乙烯信号通路中的核心转录因子)的方式抑制拟南芥(Arabidopsis thaliana)中ET诱导的无钩基因1(HLS1)的表达。SA激活的病程相关基因非表达子1(NPR1)与EIN3发生物理相互作用,并干扰EIN3与靶基因启动子(包括HLS1启动子)的结合。转录组分析表明,NPR1和EIN3/EIL1协同调控介导植物生长和应激反应的基因子集,这表明NPR1和EIN3/EIL1之间的相互作用是在多种生理过程中整合SA和ET信号通路的重要机制。综上所述,我们的研究结果阐明了SA调控顶端弯钩形成的分子机制,以及SA和ET在幼苗早期建成以及可能在其他生理过程中的拮抗作用。水杨酸通过NPR1介导的对HLS1表达的抑制以及EIN3/EIL1转录活性的抑制,在顶端弯钩发育过程中拮抗乙烯。