Endophytic commensal bacteria capitalize on the AvrPto-FER pathway to enhance proliferation during early stages of pathogen invasion.

Yi Zhang,Dan Hu,Hong-Xia Sun,Jia Chen,Jia-Hao Yang,Xin-Mei Li,Xiu-Shan Li,Yan Chen,Feng Yu
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Abstract

Leaves typically harbor a community of pre-existing beneficial and commensal bacteria that contribute to plant health. When pathogens invade, plants employ a series of strategies to response to the invasion, including the modulation of the microbial community structure. However, it remains unclear how commensal bacteria respond to pathogen at the early stage, and whether this response is specifically regulated. Here, we show that infection of Arabidopsis thaliana leaves by the pathogen Pseudomonas syringae pv. tomato DC3000 leads to a significant increase in the population of commensal bacteria, characterized by enrichment of Gammaproteobacteria and Alphaproteobacteria, alongside a reduction in Firmicutes and Betaproteobacteria. This cascade of events specifically occurs because AvrPto, an effector secreted by Pst DC3000, targets and inhibits the host receptor kinase FER, resulting in suppression of FER-mediated pattern-triggered immunity via the previously identified RIPK-RBOHD module. This specific suppression via FER pathway creates a condition that facilitates rapid proliferation of pre-existing commensal bacteria during early pathogen invasion. Our work provides a paradigm for the study of the interaction and ecological generality between commensal bacteria and pathogens with spatiotemporal patterns.
内生共生细菌利用avrtp - fer途径在病原体入侵的早期阶段增强增殖。
叶子通常含有一个预先存在的有益和共生细菌群落,这些细菌有助于植物健康。当病原体入侵时,植物采用一系列的策略来应对入侵,包括微生物群落结构的调节。然而,目前尚不清楚共生菌在早期如何对病原体产生反应,以及这种反应是否受到特异性调节。本研究表明,拟南芥叶片受到丁香假单胞菌pv的侵染。番茄DC3000导致共生菌数量显著增加,其特征是γ变形菌门和α变形菌门的富集,同时厚壁菌门和β变形菌门的减少。这种级联事件的发生是因为AvrPto(一种由Pst DC3000分泌的效应物)靶向并抑制宿主受体激酶FER,从而通过先前确定的RIPK-RBOHD模块抑制FER介导的模式触发免疫。这种通过FER途径的特异性抑制创造了一种条件,促进了在早期病原体入侵期间预先存在的共生细菌的快速增殖。我们的工作为研究共生菌与病原菌之间的时空相互作用和生态共性提供了一个范例。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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