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首页> 外文期刊>Journal of Experimental Botany >Transcription factors WRKY70 and WRKY11 served as regulators in rhizobacterium Bacillus cereus AR156-induced systemic resistance to Pseudomonas syringae pv. tomato DC3000 in Arabidopsis
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Transcription factors WRKY70 and WRKY11 served as regulators in rhizobacterium Bacillus cereus AR156-induced systemic resistance to Pseudomonas syringae pv. tomato DC3000 in Arabidopsis

机译:转录因子WRKY70和WRKY11在蜡状芽孢杆菌AR156诱导的对丁香假单胞菌pv的系统抗性中起调节作用。拟南芥番茄DC3000

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摘要

The activation of both the SA and JA/ETsignalling pathways may lead to more efficient general and broad resistance to Pst DC3000 by non-pathogenic rhizobacteria. However, the mechanisms that govern this simultaneous activation are unclear. Using Arabidopsis as a model system, two transcription factors, WRKY11 and WRKY70, were identified as important regulators involved in Induced Systemic Resistance (ISR) triggered by Bacillus cereus AR156. The results revealed that AR156 treatment significantly stimulated the transcription of WRKY70, but suppressed that of WRKY11 in Arabidopsis leaves. Furthermore, they were shown to be required for AR156 enhancing the activation of cellular defence responses and the transcription level of the plant defence response gene. Overexpression of the two transcription factors in Arabidopsis also showed that they were essential for AR156 to elicit ISR. AR156-triggered ISR was completely abolished in the double mutant of the two transcription factors, but still partially retained in the single mutants, indicating that the regulation of the two transcription factors depend on two different pathways. The target genes of the two transcription factors and epistasis analysis suggested that WRKY11 regulated AR156-triggered ISR through activating the JA signalling pathway, and WRKY70 regulated the ISR through activating the SA signalling pathway. In addition, both WRKY11 and WRKY70 modulated AR156-triggered ISR in a NPR1-dependent manner. In conclusion, WRKY11 and WRKY70 played an important role in regulating the signalling transduction pathways involved in AR156-triggered ISR. This study is the first to illustrate the mechanism by which a single rhizobacterium elicits ISR by simultaneously activating both the SA and JA/ET signalling pathways.
机译:SA和JA / ET信号通路的激活均可能导致非致病性根瘤菌对Pst DC3000产生更有效的一般性和广泛耐药性。但是,尚不清楚控制该同时激活的机制。使用拟南芥作为模型系统,两个转录因子WRKY11和WRKY70被确定为由蜡样芽孢杆菌AR156触发的诱导的系统抗性(ISR)的重要调控因子。结果表明,AR156处理显着刺激了拟南芥叶片中WRKY70的转录,但抑制了WRKY11的转录。此外,它们被证明是AR156增强细胞防御反应激活和植物防御反应基因转录水平所必需的。拟南芥中两个转录因子的过表达也表明它们对于AR156引发ISR至关重要。 AR156触发的ISR在两个转录因子的双突变体中被完全废除,但仍部分保留在单个突变体中,这表明两个转录因子的调控取决于两个不同的途径。两种转录因子的靶基因及上位性分析表明,WRKY11通过激活JA信号通路调控AR156触发的ISR,WRKY70通过激活SA信号通路调控ISR。此外,WRKY11和WRKY70均以NPR1依赖的方式调制AR156触发的ISR。总之,WRKY11和WRKY70在调节AR156触发的ISR涉及的信号转导途径中起着重要作用。这项研究首次阐明了单个根瘤菌通过同时激活SA和JA / ET信号通路来引发ISR的机制。

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