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一种病毒的 p3a 蛋白靶向并抑制 TaDOF 转录因子,以促进易感性基因的表达并促进病毒感染。

A viral p3a protein targets and inhibits TaDOF transcription factors to promote the expression of susceptibility genes and facilitate viral infection.

机构信息

State Key Laboratory for Crop Stress Resistance and High-Efficiency Production, Key Laboratory of Plant Protection Resources and Pest Management of Ministry of Education, Key Laboratory of Integrated Pest Management on Crops in Northwestern Loess Plateau of Ministry of Agriculture and Rural Affairs, College of Plant Protection, Northwest A&F University, Yangling Shaanxi, China.

Yangling Vocational & Technical College, Yangling Shaanxi, China.

出版信息

PLoS Pathog. 2024 Nov 7;20(11):e1012680. doi: 10.1371/journal.ppat.1012680. eCollection 2024 Nov.

Abstract

The interactions among viruses and host plants are complex and fascinating because these organisms interact with and adapt to each other continuously. Many plant transcription factors play important roles in plant growth and development and in the resistance to viral infection. To facilitate the infection of plants, some viral proteins typically target and inhibit the function of plant transcription factors. In this study, we found an interesting phenomenon wherein the p3a protein of barley yellow dwarf virus (BYDV) can interact with the zinc finger domain of the TaDOF transcription factor in wheat; the zinc finger domain of TaDOF can interact with the promoter of TaHSP70 and inhibit the transcription of the TaHSP70 gene; and p3a interacts with the TaDOF zinc finger domain through competitive binding, alleviating TaDOF zinc finger domain-mediated inhibition of the TaHSP70 promoter, thereby promoting TaHSP70 expression and promoting infection by BYDV. This study demonstrates that BYDV p3a is an immunosuppressive factor and enriches our understanding of the pathogenesis of BYDV.

摘要

病毒和宿主植物之间的相互作用是复杂而引人入胜的,因为这些生物体不断地相互作用和适应。许多植物转录因子在植物生长发育和抗病毒感染中发挥重要作用。为了促进植物的感染,一些病毒蛋白通常靶向并抑制植物转录因子的功能。在这项研究中,我们发现了一个有趣的现象,大麦黄花叶病毒(BYDV)的 p3a 蛋白可以与小麦 TaDOF 转录因子的锌指结构域相互作用;TaDOF 的锌指结构域可以与 TaHSP70 的启动子相互作用并抑制 TaHSP70 基因的转录;p3a 通过竞争性结合与 TaDOF 锌指结构域相互作用,减轻 TaDOF 锌指结构域介导的对 TaHSP70 启动子的抑制作用,从而促进 TaHSP70 的表达并促进 BYDV 的感染。本研究表明,BYDV p3a 是一种免疫抑制因子,丰富了我们对 BYDV 发病机制的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac07/11542804/7b8a9759071f/ppat.1012680.g001.jpg

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