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The FERONIA–RESPONSIVE TO DESSICATION 26 module regulates vascular immunity to Ralstonia solanacearum
The Plant Cell ( IF 10.0 ) Pub Date : 2024-11-13 , DOI: 10.1093/plcell/koae302 Bingqian Wang, Cailin Luo, Xiaoxu Li, Alvaro Jimenez, Jun Cai, Jia Chen, Changsheng Li, Chunhui Zhang, Lijun Ou, Wenxuan Pu, Yu Peng, Zhenchen Zhang, Yong Cai, Marc Valls, Dousheng Wu, Feng Yu
The Plant Cell ( IF 10.0 ) Pub Date : 2024-11-13 , DOI: 10.1093/plcell/koae302 Bingqian Wang, Cailin Luo, Xiaoxu Li, Alvaro Jimenez, Jun Cai, Jia Chen, Changsheng Li, Chunhui Zhang, Lijun Ou, Wenxuan Pu, Yu Peng, Zhenchen Zhang, Yong Cai, Marc Valls, Dousheng Wu, Feng Yu
Some pathogens colonize plant leaves, but others invade the roots, including the vasculature, causing severe disease symptoms. Plant innate immunity has been extensively studied in leaf pathosystems; however, the precise regulation of immunity against vascular pathogens remains largely unexplored. We previously demonstrated that loss of function of the receptor kinase FERONIA (FER) increases plant resistance to the typical vascular bacterial pathogen Ralstonia solanacearum. Here, we show that upon infection with R. solanacearum, root xylem cell walls in Arabidopsis thaliana become highly lignified. FER is specifically upregulated in the root xylem in response to R. solanacearum infection, and inhibits lignin biosynthesis and resistance to this pathogen. We determined that FER interacts with and phosphorylates the transcription factor RESPONSIVE TO DESICCATION 26 (RD26), leading to its degradation. Overexpression and knockout of RD26 demonstrated that it positively regulates plant resistance to R. solanacearum by directly activating the expression of lignin-related genes. Tissue-specific expression of RD26 in the root xylem confirmed its role in vascular immunity. We confirmed that the FER–RD26 module regulates lignin biosynthesis and resistance against R. solanacearum in tomato (Solanum lycopersicum). Taken together, our findings unveil that the FER–RD26 cascade governs plant immunity against R. solanacearum in vascular tissues by regulating lignin deposition. This cascade may represent a key defense mechanism against vascular pathogens in plants.
中文翻译:
对干燥敏感的 FERONIA 26 模块调节对 Ralstonia solanacearum 的血管免疫
一些病原体定植于植物叶片,但其他病原体侵入根部,包括脉管系统,导致严重的疾病症状。植物先天免疫已在叶片病理系统中得到广泛研究;然而,对血管病原体免疫力的精确调节在很大程度上仍未得到探索。我们之前证明,受体激酶 FERONIA (FER) 的功能丧失会增加植物对典型维管细菌病原体 Ralstonia solanacearum 的抵抗力。在这里,我们表明,在感染青枯苔苣后,拟南芥中的根木质部细胞壁变得高度木质化。FER 在根木质部响应 R. solanacearum 感染而特异性上调,并抑制木质素的生物合成和对该病原体的抗性。我们确定 FER 与转录因子 RESPONSIVE TO DESICCATION 26 (RD26) 相互作用并磷酸化转录因子,导致其降解。RD26 的过表达和敲除表明它通过直接激活木质素相关基因的表达来正向调节植物对青枯的抗性。RD26 在根木质部的组织特异性表达证实了其在血管免疫中的作用。我们证实 FER-RD26 模块调节番茄 (Solanum lycopersicum) 中木质素的生物合成和对青枯 R. solanacearum 的抗性。综上所述,我们的研究结果揭示了 FER-RD26 级联反应通过调节木质素沉积来控制植物对维管组织中青枯菌的免疫力。这种级联反应可能代表了植物中针对维管病原体的关键防御机制。
更新日期:2024-11-13
中文翻译:
对干燥敏感的 FERONIA 26 模块调节对 Ralstonia solanacearum 的血管免疫
一些病原体定植于植物叶片,但其他病原体侵入根部,包括脉管系统,导致严重的疾病症状。植物先天免疫已在叶片病理系统中得到广泛研究;然而,对血管病原体免疫力的精确调节在很大程度上仍未得到探索。我们之前证明,受体激酶 FERONIA (FER) 的功能丧失会增加植物对典型维管细菌病原体 Ralstonia solanacearum 的抵抗力。在这里,我们表明,在感染青枯苔苣后,拟南芥中的根木质部细胞壁变得高度木质化。FER 在根木质部响应 R. solanacearum 感染而特异性上调,并抑制木质素的生物合成和对该病原体的抗性。我们确定 FER 与转录因子 RESPONSIVE TO DESICCATION 26 (RD26) 相互作用并磷酸化转录因子,导致其降解。RD26 的过表达和敲除表明它通过直接激活木质素相关基因的表达来正向调节植物对青枯的抗性。RD26 在根木质部的组织特异性表达证实了其在血管免疫中的作用。我们证实 FER-RD26 模块调节番茄 (Solanum lycopersicum) 中木质素的生物合成和对青枯 R. solanacearum 的抗性。综上所述,我们的研究结果揭示了 FER-RD26 级联反应通过调节木质素沉积来控制植物对维管组织中青枯菌的免疫力。这种级联反应可能代表了植物中针对维管病原体的关键防御机制。