霜霉病效应物 HaRxL106 与转录因子 BIM1 相互作用,改变植物生长、BR 信号转导和对病原体的敏感性

Maria Florencia Bogino, Juan Marcos Lapegna Senz, Lucille Tihomirova Kourdova, Nicolas Tamagnone, Andres Romanowski, Lennart Wirthmueller, Georgina Fabro
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引用次数: 0

摘要

Hyaloperonospora arabidopsidis(Hpa)是一种卵菌病原体,可引起拟南芥霜霉病。这种必须的生物营养体通过分泌大量效应蛋白(其中包括 RxLR 效应蛋白)来操纵寄主植物的平衡。确定效应蛋白的宿主靶标并了解如何操纵效应蛋白促进植物定殖是提高植物抗病原体能力的关键。在这里,我们描述了 RxLR 效应子 HaRxL106 与 BIM1(一种参与芸苔素类固醇(BR)信号转导的拟南芥转录因子(TF))之间的相互作用。我们报告了 HaRxL106 与 BIM1 在体外和植物体内的相互作用。效应因子需要 BIM1 来提高宿主植物对(半)生物营养型病原体的易感性,因此 BIM1 可被视为易感因子。从机理上讲,HaRxL106 需要 BIM1 来诱导 BR 响应基因的转录活化,并导致植物生长模式的改变,从而表现出避荫综合征。我们的研究结果支持了之前关于BR信号激活与植物免疫反应抑制之间拮抗相互作用的观察,并揭示了BIM1作为这种串扰中的一个新角色,是由病原效应因子HaRxL106操纵的。
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Downy mildew effector HaRxL106 interacts with the transcription factor BIM1 altering plant growth, BR signaling and susceptibility to pathogens
Hyaloperonospora arabidopsidis (Hpa) is an oomycete pathogen that causes downy mildew disease on Arabidopsis. This obligate biotroph manipulates the homeostasis of its host plant by secreting numerous effector proteins, among which are the RxLR-effectors. Identifying the host targets of effectors and understanding how their manipulation facilitates colonization of plants is key to improve plant resistance to pathogens. Here we characterize the interaction between the RxLR effector HaRxL106 and BIM1, an Arabidopsis transcription factor (TF) involved in Brassinosteroid (BR) signaling. We report that HaRxL106 interacts with BIM1 in vitro and in planta. BIM1 is required by the effector to increase the host plant susceptibility to (hemi)biotrophic pathogens, and thus can be regarded as a susceptibility factor. Mechanistically, HaRxL106 requires BIM1 to induce the transcriptional activation of BR-responsive genes and cause alterations in plant growth patterns that phenocopy the shade avoidance syndrome. Our results support previous observations of antagonistic interactions between activation of BR signaling and suppression of plant immune responses and reveal that BIM1, a new player in this crosstalk, is manipulated by the pathogenic effector HaRxL106.
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