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pv. III 型效应物 XopL 靶向质子泵相互作用蛋白 1 并抑制 中的先天免疫。

The Type III Effector XopL in pv. Targets the Proton Pump Interactor 1 and Suppresses Innate Immunity in .

机构信息

State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources, Guangxi University, Nanning 530005, China.

Guangxi Key Laboratory for Polysaccharide Materials and Modifications, Guangxi Minzu University, Nanning 530006, China.

出版信息

Int J Mol Sci. 2024 Aug 23;25(17):9175. doi: 10.3390/ijms25179175.

Abstract

pathovar () is a significant phytopathogen causing black rot disease in crucifers. injects a variety of type III effectors (T3Es) into the host cell to assist infection or propagation. A number of T3Es inhibit plant immunity, but the biochemical basis for a vast majority of them remains unknown. Previous research has revealed that the evolutionarily conserved XopL-family effector XopL inhibits plant immunity, although the underlying mechanisms remain incompletely elucidated. In this study, we identified proton pump interactor (PPI1) as a specific virulence target of XopL in . Notably, the C-terminus of PPI1 and the Leucine-rich repeat (LRR) domains of XopL are pivotal for facilitating this interaction. Our findings indicate that PPI1 plays a role in the immune response of to . These results propose a model in which XopL binds to PPI1, disrupting the early defense responses activated in during infection and providing valuable insights into potential strategies for regulating plasma membrane (PM) H-ATPase activity during infection. These novel insights enhance our understanding of the pathogenic mechanisms of T3Es and contribute to the development of effective strategies for controlling bacterial diseases.

摘要

()是一种重要的植物病原菌,可引起十字花科植物的黑腐病。它会向宿主细胞中注射多种 III 型效应物(T3E),以协助感染或繁殖。许多 T3E 抑制植物免疫,但它们的绝大多数生化基础仍然未知。先前的研究表明,进化保守的 XopL 家族效应物 XopL 抑制植物免疫,尽管其潜在机制仍不完全清楚。在本研究中,我们鉴定出质子泵相互作用蛋白 (PPI1)是 XopL 在 中的一个特定毒力靶标。值得注意的是,PPI1 的 C 端和 XopL 的富含亮氨酸重复 (LRR)结构域对于促进这种相互作用至关重要。我们的研究结果表明,PPI1 在 对 的免疫反应中发挥作用。这些结果提出了一个模型,即 XopL 结合到 PPI1 上,破坏了 在 感染过程中被激活的早期防御反应,并为在感染过程中调节质膜 (PM) H+-ATP 酶活性提供了有价值的见解。这些新的见解增强了我们对 T3E 致病机制的理解,并有助于开发控制细菌病害的有效策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d7b/11394911/48fb6dd0d8ac/ijms-25-09175-g001.jpg

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