Zhang Xing, Zhu Ziqiang, An Fengying, Hao Dongdong, Li Pengpeng, Song Jinghui, Yi Chengqi, Guo Hongwei
State Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing 100871, China.
Plant Cell. 2014 Mar;26(3):1105-17. doi: 10.1105/tpc.113.122002. Epub 2014 Mar 25.
The apical hook is an essential structure that enables epigeal plants to protrude through the soil. Arabidopsis thaliana HOOKLESS1 (HLS1) is reported to be a key regulator of hook development and a direct target gene of the ethylene (ET)-activated transcription factors ETHYLENE INSENSITIVE3 (EIN3) and its close homolog EIN3-Like1. Previous research has shown that the phytohormones jasmonate (JA) and ET antagonistically regulate apical hook development, although the underlying molecular mechanism is largely unknown. Here, we report that JA represses hook formation by reducing HLS1 expression. Our results further reveal that the JA-activated transcription factor MYC2 represses EIN3 function to reduce HLS1 expression through at least the following two layers of regulation: (1) MYC2 binds to the promoter of an F-box gene, EIN3 BINDING F-BOX PROTEIN1, to induce its expression and thus promote EIN3 degradation; and (2) MYC2 physically interacts with EIN3 and inhibits its DNA binding activity. Collectively, our findings shed light on the molecular mechanism underlying the antagonism between JA and ET during apical hook development and provide insight into the coaction of multiple phytohormones in the regulation of plant growth and development.
顶端弯钩是一种重要结构,能使出土植物穿透土壤。据报道,拟南芥无钩1(HLS1)是弯钩发育的关键调节因子,也是乙烯(ET)激活的转录因子乙烯不敏感3(EIN3)及其紧密同源物EIN3样1的直接靶基因。先前的研究表明,植物激素茉莉酸(JA)和ET对顶端弯钩发育起拮抗调节作用,但其潜在分子机制仍大多未知。在此,我们报道JA通过降低HLS1表达来抑制弯钩形成。我们的结果进一步揭示,JA激活的转录因子MYC2通过至少以下两层调节抑制EIN3功能以降低HLS1表达:(1)MYC2与一个F-box基因EIN3结合F-box蛋白1的启动子结合,诱导其表达,从而促进EIN3降解;(2)MYC2与EIN3发生物理相互作用并抑制其DNA结合活性。总的来说,我们的研究结果揭示了顶端弯钩发育过程中JA和ET之间拮抗作用的分子机制,并为多种植物激素在植物生长发育调控中的协同作用提供了见解。