E3泛素连接酶在植物生长发育中发挥重要作用，但其调控ABA抑制主根生长的机制不清楚。我们筛选到一株拟南芥主根生长对脱落酸（ABA）不敏感的突变体，突变基因编码RING E3泛素连接酶ATL17（Arabidopsis Tóxicos en Levadura17）。初步研究表明，ATL17具有E3泛素连接酶活性，其在ABA抑制主根生长中的作用与生长素相关。本项目拟进一步探明ATL17泛素化的底物蛋白及底物的降解机制，阐明ABA抑制主根发育过程中ATL17对生长素分布和运输、PLETHORAs表达及细胞分裂进程的调控作用。另外，通过分析相关突变体杂交材料明确ABA作用下ATL17与ABI1（ABA insensitive1）、ABI2、ABI4和ABI5的作用关系。最终阐明ATL17介导泛素化修饰调控ABA抑制主根生长的分子机制。本项目有望揭示拟南芥ABA信号中调节主根发育的新成分和新机制。

E3 ubiquitin ligases play pivotal roles in growth and development in plants. However, it is unclear the mechanisms for ABA inhibition of primary root growth modulated by E3 ubiquitin ligases. Here, we obtained an Arabidopsis mutant that was insensitive to ABA-inhibited primary root elongation by screening a mutant pool. The mutation gene encoded the RING E3 ubiquitin ligase ATL17 (Arabidopsis Tóxicos en Levadura17). Preliminary results indicated that ATL17 had E3 ligase activity. Its actions on ABA inhibition of root growth were closely related to auxin. In this project, we will further identify the substrate protein of ATL17, and investigate the degradation mechanism of the substrate by ATL17. Moreover, the functions and mechanisms for ATL17 regulating auxin distribution and transport, PLETHORAs expression and cell division progression will be uncovered. In addition, we will elucidate the regulatory relationships beween ATL17 and the ABA signaling key components ABI1 (ABA insensitive1), ABI2, ABI4 and ABI5 by analyzing the relevant mutants in ABA-inhibited primary root growth. Together, the molecular mechanisms that ATL17 regulated ABA inhibition of primary root growth through protein ubiquitination in Arabidopsis will be unravelled. A novel mechanism by which a new ABA signal component modulates primary root development may be unveiled in Arabidopsis based on this project.