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Suppression of LjBAK1-mediated immunity by SymRK promotes rhizobial infection in Lotus japonicus
Molecular Plant ( IF 17.1 ) Pub Date : 2021-07-24 , DOI: 10.1016/j.molp.2021.07.016
Yong Feng 1 , Ping Wu 1 , Chao Liu 1 , Liwei Peng 1 , Tao Wang 1 , Chao Wang 1 , Qian Tan 1 , Bixuan Li 1 , Yajuan Ou 1 , Hui Zhu 1 , Songli Yuan 1 , Renliang Huang 1 , Gary Stacey 2 , Zhongming Zhang 1 , Yangrong Cao 1
Affiliation  

An important question in biology is how organisms can associate with different microbes that pose no threat (commensals), pose a severe threat (pathogens), and those that are beneficial (symbionts). The root nodule symbiosis serves as an important model system for addressing such questions in the context of plant-microbe interactions. It is now generally accepted that rhizobia can actively suppress host immune responses during the infection process, analogous to the way in which plant pathogens can evade immune recognition. However, much remains to be learned about the mechanisms by which the host recognizes the rhizobia as pathogens and how, subsequently, these pathways are suppressed to allow establishment of the nitrogen-fixing symbiosis. In this study, we found that SymRK (Symbiosis Receptor-like Kinase) is required for rhizobial suppression of plant innate immunity in Lotus japonicus. SymRK associates with LjBAK1 (BRASSINOSTEROID INSENSITIVE 1-Associated receptor Kinase 1), a well-characterized positive regulator of plant innate immunity, and directly inhibits LjBAK1 kinase activity. Rhizobial inoculation enhances the association between SymRK and LjBAK1 in planta. LjBAK1 is required for the regulation of plant innate immunity and plays a negative role in rhizobial infection in L. japonicus. The data indicate that the SymRK-LjBAK1 protein complex serves as an intersection point between rhizobial symbiotic signaling pathways and innate immunity pathways, and support that rhizobia may actively suppress the host's ability to mount a defense response during the legume-rhizobium symbiosis.



中文翻译:

SymRK抑制LjBAK1介导的免疫促进莲花根瘤菌感染

生物学中的一个重要问题是有机体如何与不构成威胁(共生体)、构成严重威胁(病原体)和有益(共生体)的不同微生物相关联。根瘤共生是在植物-微生物相互作用的背景下解决此类问题的重要模型系统。现在普遍认为,根瘤菌可以在感染过程中主动抑制宿主的免疫反应,类似于植物病原体逃避免疫识别的方式。然而,关于宿主将根瘤菌识别为病原体的机制以及随后如何抑制这些途径以建立固氮共生关系,仍有许多需要了解。在这项研究中,莲藕。SymRK 与 LjBAK1(芸苔素不敏感 1 相关受体激酶 1)结合,这是一种充分表征的植物先天免疫正调节剂,并直接抑制 LjBAK1 激酶活性。根瘤菌接种增强了植物中 SymRK 和 LjBAK1 之间的关联。LjBAK1是植物先天免疫调节所必需的,在日本血吸虫的根瘤菌感染中起负面作用。数据表明,SymRK-LjBAK1蛋白复合物作为根瘤菌共生信号通路和先天免疫通路之间的交汇点,支持根瘤菌在豆科植物-根瘤菌共生过程中可能主动抑制宿主的防御反应能力。

更新日期:2021-07-24
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