Sheath blight disease (ShB) has a severe impact on the production of rice. ABI3/VP1-like 1 (RAVL1) negatively regulated the rice defense mechanism against ShB, however, this regulatory mechanism is not clearly understood. In this study, we identified that indeterminate domain 3 (IDD3) was positively regulated by RAVL1. Further, chromatin immunoprecipitation (ChIP) assay, yeast one-hybrid assay and transient expression assay indicated a direct binding between RAVL1 and the IDD3 promoter region. IDD3 was ubiquitously expressed in different tissues and at different stages, and its expression was significantly enhanced by Rhizoctonia solani infection. IDD3 exhibited transcription activation activity in yeast and IDD3-GFP was found to be localized in the nucleus. IDD3 mutants exhibited no significant differences in response to ShB, while IDD3 overexpressors were more susceptible to ShB compared with wild type (WT) plants. Furthermore, IDD3 repressors were less susceptible to R. solani than WT plants. Interestingly, the expression of brassinosteroid-related genes (D2, D11 and BRI1) was lower in IDD3 repressors and higher in IDD3 overexpressors compared with WT. However, the ChIP assay revealed that IDD3 did not directly bind to the D2 and D11 promoters. Overexpression of IDD3 in BRI1 mutant d61-1 inhibited the activity of IDD3, reducing its susceptibility to ShB compared with IDD3 overexpressor and WT plants, indicating that IDD3 negatively regulated the rice defense mechanism against ShB by activating the BR signaling pathway. Thus, our analyses provided information to enhance the understanding of the rice defense mechanism against ShB.

鞘枯萎病（ShB）对水稻生产有严重影响。ABI3 / VP1样1（RAVL1）负调节水稻防御ShB的机制，但是，这种调节机制尚不清楚。在这项研究中，我们确定了RAVL1正调控不确定域3（IDD3）。此外，染色质免疫沉淀（ChIP）测定，酵母一杂交测定和瞬时表达测定表明RAVL1与IDD3启动子区域之间存在直接结合。IDD3在不同组织和不同阶段无处不在表达，其表达被solani Rhizoctonia solani显着增强。感染。IDD3在酵母中表现出转录激活活性，并且发现IDD3-GFP位于细胞核中。与野生型（WT）植物相比，IDD3突变体对ShB的反应无显着差异，而IDD3过表达者对ShB的敏感性更高。此外，IDD3阻遏都以不易纹枯病菌比野生型植物。有趣的是，与WT相比，IDD3阻遏物中油菜素甾体相关基因（D2，D11和BRI1）的表达较低，而IDD3过表达物中的表达较高。但是，ChIP分析显示IDD3没有直接结合到D2和D11启动子。的过表达IDD3在BRI1突变d61-1抑制IDD3的活性，相比降低其易感性纹枯病IDD3过表达和WT植物，表明IDD3负面通过激活BR信号传导途径对纹枯病水稻防卫机制调节。因此，我们的分析提供了信息，以增强对水稻针对ShB的防御机制的理解。