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首页> 外文期刊>The New Phytologist >Terminating rice innate immunity induction requires a network of antagonistic and redox-responsive E3 ubiquitin ligases targeting a fungal sirtuin
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Terminating rice innate immunity induction requires a network of antagonistic and redox-responsive E3 ubiquitin ligases targeting a fungal sirtuin

机译：终止水稻先天免疫诱导需要靶向真菌SIRTUIN的拮抗和氧化还原响应E3抗逆转录和氧化还原的e3网络

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摘要

Fungal phytopathogens can suppress plant immune mechanisms in order to colonize living host cells. Identifying all the molecular components involved is critical for elaborating a detailed systems-level model of plant infection probing pathogen weaknesses; yet, the hierarchy of molecular events controlling fungal responses to the plant cell is not clear. Here we show how, in the blast fungus Magnaporthe oryzae, terminating rice innate immunity requires a dynamic network of redox-responsive E3 ubiquitin ligases targeting fungal sirtuin 2 (Sir2), an antioxidation regulator required for suppressing the host oxidative burst. Immunoblotting, immunopurification, mass spectrometry and gene functional analyses showed that Sir2 levels responded to oxidative stress via a mechanism involving ubiquitination and three antagonistic E3 ubiquitin ligases: Grr1 and Ptr1 maintained basal Sir2 levels in the absence of oxidative stress; Upl3 facilitated Sir2 accumulation in response to oxidative stress. Grr1 and Upl3 interacted directly with Sir2 in a manner that decreased and scaled with oxidative stress, respectively. Deleting UPL3 depleted Sir2 during growth in rice cells, triggering host immunity and preventing infection. Overexpressing SIR2 in the Delta upl3 mutant remediated pathogenicity. Our work reveals how redox-responsive E3 ubiquitin ligases in M. oryzae mediate Sir2 accumulation-dependent antioxidation to modulate plant innate immunity and host susceptibility.
机译：真菌植物病变可以抑制植物免疫机制以殖民化生物宿主细胞。鉴定所涉及的所有分子组分对于阐述植物感染探测病原体缺点的详细系统级模型至关重要;然而，控制对植物细胞的真菌反应的分子事件的层次尚不清楚。在这里，我们展示了如何在喷射真菌Magnaporthe oryzae中，终止水稻先天免疫需要靶向真菌Sirtuin 2（SiR 2）的氧化还原响应E3泛素敏捷酶的动态网络，抑制宿主氧化突发所需的抗氧化调节剂。免疫印迹，免疫纯化，质谱和基因官能分析表明，SiR2水平通过涉及泛素化的机制和三种拮抗型E3泛素连接酶的机理反应氧化胁迫：GRR1和PTR1在没有氧化应激的情况下保持基础SIR2水平;响应于氧化应激的UPL3促进SIR2积累。 GRR1和UPL3分别以分别用氧化应力降低和缩放的方式直接与SIR2相互作用。在水稻细胞生长期间删除UPL3耗尽的SIR2，触发宿主免疫并预防感染。过表达SIR2在DELTA UPL3突变体修复致病性中。我们的作品揭示了氧化氢氧化锰响应e3泛素的抗氧化酶在M. Oryzae中介导SiR2积累依赖性抗氧化，以调节植物先天免疫和宿主敏感性。

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