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植物防御途径被根癌农杆菌用于遗传转化而被颠覆。

Plant defense pathways subverted by Agrobacterium for genetic transformation.

机构信息

Department of Biochemistry and Cell Biology, State University of New York, Stony Brook, NY, USA.

出版信息

Plant Signal Behav. 2010 Oct;5(10):1245-8. doi: 10.4161/psb.5.10.12947. Epub 2010 Oct 1.

Abstract

The soil phytopathogen Agrobacterium has the unique ability to introduce single-stranded transferred DNA (T-DNA) from its tumor-inducing (Ti) plasmid into the host cell in a process known as horizontal gene transfer. Following its entry into the host cell cytoplasm, the T-DNA associates with the bacterial virulence (Vir) E2 protein, also exported from Agrobacterium, creating the T-DNA nucleoprotein complex (T-complex), which is then translocated into the nucleus where the DNA is integrated into the host chromatin. VirE2 protects the T-DNA from the host DNase activities, packages it into a helical filament, and interacts with the host proteins, one of which, VIP1, facilitates nuclear import of the T-complex and its subsequent targeting to the host chromatin. Although the VirE2 and VIP1 protein components of the T-complex are vital for its intracellular transport, they must be removed to expose the T-DNA for integration. Our recent work demonstrated that this task is aided by an host defense-related F-box protein VBF that is induced by Agrobacterium infection and that recognizes and binds VIP1. VBF destabilizes VirE2 and VIP1 in yeast and plant cells, presumably via SCF-mediated proteasomal degradation. VBF expression in and export from the Agrobacterium cell lead to increased tumorigenesis. Here, we discuss these findings in the context of the "arms race" between Agrobacterium infectivity and plant defense.

摘要

土壤植物病原体农杆菌具有将其诱导肿瘤(Ti)质粒中的单链转移 DNA(T-DNA)引入宿主细胞的独特能力,这个过程被称为水平基因转移。在进入宿主细胞质后,T-DNA与细菌毒力(Vir)E2 蛋白结合,该蛋白也从农杆菌中输出,形成 T-DNA 核蛋白复合物(T-复合物),然后被转运到细胞核中,T-DNA 整合到宿主染色质中。VirE2 保护 T-DNA 免受宿主 DNA 酶的作用,将其包装成螺旋丝,并与宿主蛋白相互作用,其中之一 VIP1 促进 T-复合物的核输入及其随后靶向宿主染色质。尽管 T-复合物的 VirE2 和 VIP1 蛋白成分对于其细胞内运输至关重要,但必须将其去除以暴露 T-DNA 进行整合。我们最近的工作表明,这项任务是由一种受宿主防御相关的 F-box 蛋白 VBF 辅助完成的,该蛋白被农杆菌感染诱导,并识别和结合 VIP1。VBF 在酵母和植物细胞中使 VirE2 和 VIP1 不稳定,推测是通过 SCF 介导的蛋白酶体降解。VBF 在农杆菌细胞中的表达和输出导致肿瘤形成增加。在这里,我们将这些发现置于农杆菌感染性和植物防御之间的“军备竞赛”背景下进行讨论。

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