Key Laboratory of Hebei Province for Plant Physiology and Molecular Pathology, College of Life Sciences, Hebei Agricultural University, Baoding 071000, China.
Mycotoxin and Molecular Plant Pathology Laboratory, Hebei Agricultural University, Baoding 071000, China.
Plant Physiol. 2019 Jun;180(2):1132-1151. doi: 10.1104/pp.18.01209. Epub 2019 Mar 29.
, a major hemibiotrophic bacterial pathogen, causes many devastating plant diseases. However, the transcriptional regulation of plant defense responses to remains largely unknown. Here, we found that gain-of-function of () enhanced the resistance of Arabidopsis () to DC3000 ( pv. DC3000). Disruption of also weakened the salicylic acid (SA)-induced defense response to DC3000 in mutants. Further investigation indicated that, under infection, transcription of is modulated by components of both the SA and ethylene (ET) signaling pathways. Intriguingly, the specific binding elements of ETHYLENE RESPONSE FACTOR (ERF) proteins, including dehydration responsive/C-repeat elements and the GCC box, were found in the putative promoter of Based on publicly available microarray data and transcriptional confirmation, we determined that is inducible by salicylic acid and DC3000 and is modulated by the SA and ET signaling pathways. Consistent with the function of , loss-of-function of weakened Arabidopsis resistance to DC3000 and the SA-induced defense response. Biochemical and molecular assays revealed that ERF11 binds specifically to the GCC box of the promoter to activate its transcription. Genetic studies further revealed that the -regulated Arabidopsis defense response to DC3000 functions directly downstream of ERF11. Our findings indicate that transcriptional activation of by ERF11 is a key step in SA/ET-regulated plant resistance against DC3000, enhancing our understanding of plant defense responses to hemibiotrophic bacterial pathogens.
丁香假单胞菌，一种重要的半活体营养型细菌病原体，会引起许多严重的植物疾病。然而，植物防御反应对丁香假单胞菌的转录调控在很大程度上仍是未知的。在这里，我们发现功能获得的（）增强了拟南芥（）对 DC3000（ pv. DC3000）的抗性。的破坏也削弱了突变体中水杨酸（SA）诱导的对 DC3000 的防御反应。进一步的研究表明，在感染下，的转录受 SA 和乙烯（ET）信号通路的组成部分调节。有趣的是，ETHYLENE RESPONSE FACTOR（ERF）蛋白的特定结合元件，包括脱水响应/C-重复元件和 GCC 框，在的假定启动子中被发现。基于公开的微阵列数据和转录确认，我们确定了由水杨酸和 DC3000 诱导，并由 SA 和 ET 信号通路调节。与的功能一致，的缺失削弱了拟南芥对 DC3000 的抗性和 SA 诱导的防御反应。生化和分子测定表明，ERF11 特异性结合的 GCC 框来激活其转录。遗传研究进一步表明，受调控的拟南芥对 DC3000 的防御反应直接位于 ERF11 下游。我们的研究结果表明，ERF11 对的转录激活是 SA/ET 调节植物对 DC3000 抗性的关键步骤，增强了我们对植物对半活体营养型细菌病原体防御反应的理解。
