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一种细菌毒力蛋白可抑制宿主先天免疫,从而引发植物病害。

A bacterial virulence protein suppresses host innate immunity to cause plant disease.

作者信息

Nomura Kinya, Debroy Sruti, Lee Yong Hoon, Pumplin Nathan, Jones Jonathan, He Sheng Yang

机构信息

Department of Energy Plant Research Laboratory, Michigan State University, East Lansing, MI 48824, USA.

出版信息

Science. 2006 Jul 14;313(5784):220-3. doi: 10.1126/science.1129523.

Abstract

Plants have evolved a powerful immune system to defend against infection by most microbial organisms. However, successful pathogens, such as Pseudomonas syringae, have developed countermeasures and inject virulence proteins into the host plant cell to suppress immunity and cause devastating diseases. Despite intensive research efforts, the molecular targets of bacterial virulence proteins that are important for plant disease development have remained obscure. Here, we show that a conserved P. syringae virulence protein, HopM1, targets an immunity-associated protein, AtMIN7, in Arabidopsis thaliana. HopM1 mediates the destruction of AtMIN7 via the host proteasome. Our results illustrate a strategy by which a bacterial pathogen exploits the host proteasome to subvert host immunity and causes infection in plants.

摘要

植物进化出了强大的免疫系统来抵御大多数微生物的感染。然而,像丁香假单胞菌这样成功的病原体已经开发出应对措施,并将毒力蛋白注入宿主植物细胞以抑制免疫并引发毁灭性疾病。尽管进行了深入的研究,但对植物病害发展至关重要的细菌毒力蛋白的分子靶点仍不清楚。在这里,我们表明一种保守的丁香假单胞菌毒力蛋白HopM1靶向拟南芥中一种与免疫相关的蛋白AtMIN7。HopM1通过宿主蛋白酶体介导AtMIN7的降解。我们的结果阐明了一种细菌病原体利用宿主蛋白酶体来颠覆宿主免疫并在植物中引发感染的策略。

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