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一种分泌型真菌效应物通过宿主组蛋白低乙酰化抑制水稻免疫。

A secreted fungal effector suppresses rice immunity through host histone hypoacetylation.

机构信息

State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, 430070, China.

Hubei Key Laboratory of Plant Pathology, Huazhong Agricultural University, Wuhan, 430070, China.

出版信息

New Phytol. 2022 Sep;235(5):1977-1994. doi: 10.1111/nph.18265. Epub 2022 Jun 8.

Abstract

Histone acetylation is a critical epigenetic modification that regulates plant immunity. Fungal pathogens secrete effectors that modulate host immunity and facilitate infection, but whether fungal pathogens have evolved effectors that directly target plant histone acetylation remains unknown. Here, we identified a secreted protein, UvSec117, from the rice false smut fungus, Ustilaginoidea virens, as a key effector that can target the rice histone deacetylase OsHDA701 and negatively regulates rice broad-spectrum resistance against rice pathogens. UvSec117 disrupts host immunity by recruiting OsHDA701 to the nucleus and enhancing OsHDA701-modulated deacetylation, thereby reducing histone H3K9 acetylation levels in rice plants and interfering with defense gene activation. Host-induced gene silencing of UvSec117 promotes rice resistance to U. virens, thus providing an alternative way for developing rice false smut-resistant plants. This is the first direct evidence demonstrating that a fungal effector targets a histone deacetylase to suppress plant immunity. Our data provided insight into a counter-defense mechanism in a plant pathogen that inactivates host defense responses at the epigenetic level.

摘要

组蛋白乙酰化是一种关键的表观遗传修饰,它调节植物的免疫。真菌病原体分泌的效应物可以调节宿主的免疫并促进感染,但真菌病原体是否进化出了直接针对植物组蛋白乙酰化的效应物仍不清楚。在这里,我们从水稻纹枯病菌稻曲病菌中鉴定出一种分泌蛋白 UvSec117,它是一种关键的效应物,可以靶向水稻去乙酰化酶 OsHDA701,并负调控水稻对水稻病原体的广谱抗性。UvSec117 通过将 OsHDA701 招募到细胞核并增强 OsHDA701 调节的去乙酰化作用来破坏宿主免疫,从而降低水稻植株中组蛋白 H3K9 的乙酰化水平,并干扰防御基因的激活。UvSec117 的寄主诱导基因沉默促进了水稻对稻曲病菌的抗性,从而为培育水稻纹枯病抗性植物提供了一种替代方法。这是第一个直接证据,证明真菌效应物可以靶向组蛋白去乙酰化酶来抑制植物的免疫。我们的数据提供了一个关于植物病原体的反防御机制的见解,该机制可以在表观遗传水平上使宿主的防御反应失活。

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