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镰刀菌禾谷专化型效应因子 FgEC1 靶向小麦 TaGF14b 蛋白以抑制 TaRBOHD 介导的 ROS 产生并促进侵染。

Fusarium graminearum effector FgEC1 targets wheat TaGF14b protein to suppress TaRBOHD-mediated ROS production and promote infection.

机构信息

Shenzhen Branch, Guangdong Laboratory of Lingnan Modern Agriculture, Key Laboratory of Synthetic Biology, Ministry of Agriculture and Rural Affairs, Agricultural Genomics Institute at Shenzhen, Chinese Academy of Agricultural Sciences, Shenzhen, 518120, China.

College of Life Science and Technology, Huazhong Agricultural University, Wuhan, 430070, China.

出版信息

J Integr Plant Biol. 2024 Oct;66(10):2288-2303. doi: 10.1111/jipb.13752. Epub 2024 Aug 7.

DOI:10.1111/jipb.13752
PMID:39109951
Abstract

Fusarium head blight (FHB), caused by Fusarium graminearum, is a devastating disease of wheat globally. However, the molecular mechanisms underlying the interactions between F. graminearum and wheat remain unclear. Here, we identified a secreted effector protein, FgEC1, that is induced during wheat infection and is required for F. graminearum virulence. FgEC1 suppressed flg22- and chitin-induced callose deposition and reactive oxygen species (ROS) burst in Nicotiana benthamiana. FgEC1 directly interacts with TaGF14b, which is upregulated in wheat heads during F. graminearum infection. Overexpression of TaGF14b increases FHB resistance in wheat without compromising yield. TaGF14b interacts with NADPH oxidase respiratory burst oxidase homolog D (TaRBOHD) and protects it against degradation by the 26S proteasome. FgEC1 inhibited the interaction of TaGF14b with TaRBOHD and promoted TaRBOHD degradation, thereby reducing TaRBOHD-mediated ROS production. Our findings reveal a novel pathogenic mechanism in which a fungal pathogen acts via an effector to reduce TaRBOHD-mediated ROS production.

摘要

镰刀菌穗腐病(FHB)是由禾谷镰刀菌引起的一种毁灭性小麦疾病,在全球范围内发生。然而,禾谷镰刀菌与小麦相互作用的分子机制尚不清楚。在这里,我们鉴定了一个分泌效应蛋白 FgEC1,它在小麦感染过程中被诱导,并且是禾谷镰刀菌毒力所必需的。FgEC1 抑制 flg22 和几丁质诱导的胼胝质沉积和活性氧(ROS)爆发在本氏烟中。FgEC1 直接与 TaGF14b 相互作用,后者在禾谷镰刀菌感染小麦头部时上调。TaGF14b 的过表达增加了小麦对 FHB 的抗性,而不影响产量。TaGF14b 与 NADPH 氧化酶呼吸爆发氧化还原酶同源物 D(TaRBOHD)相互作用,并保护其免受 26S 蛋白酶体的降解。FgEC1 抑制 TaGF14b 与 TaRBOHD 的相互作用并促进 TaRBOHD 降解,从而减少 TaRBOHD 介导的 ROS 产生。我们的研究结果揭示了一种新的致病机制,即真菌病原体通过效应蛋白起作用,降低 TaRBOHD 介导的 ROS 产生。

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