Agrobacterium induces expression of a host F-box protein required for tumorigenicity.

Agrobacterium induces expression of a host F-box protein required for tumorigenicity.
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DOI:
10.1016/j.chom.2010.02.009
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发表时间:
2010-03-18
影响因子:
30.3
通讯作者:
Citovsky V
Citovsky V
中科院分区:
医学1区
文献类型:
--
作者:
Zaltsman A;Krichevsky A;Loyter A;Citovsky V

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在植物-病原体相互作用中,宿主防御入侵的病原体,而病原体旨在抑制或破坏这种防御。虽然防御抑制策略对于许多病原体来说是相对较好理解的,但病原体可以积极利用宿主防御机制的机制仍然不清楚。我们报告说,农杆菌,一种微生物,elastenous肿瘤生长在许多植物物种,诱导表达的植物防御相关的F-盒蛋白,VBF,它纳入自己的遗传转化途径。我们的数据表明,VBF的功能可能是通过SCFVBF途径从其相关的毒力VirE 2和宿主VIP 1蛋白的细菌转移的DNA脱壳。VBF的抑制提高了VIP 1的细胞内含量,但使植物在很大程度上对农杆菌具有抗性,这表明在感染途径中,VBF在功能上对VIP 1具有上位性。当在农杆菌中表达并输出到植物细胞中时,VBF促进肿瘤形成。
In plant-pathogen interactions, the host defends against the invading pathogen and the pathogen aims to suppress or subvert this defense. Whereas the defense suppression strategy is relatively well understood for many pathogens, the mechanisms by which pathogens can actively utilize the defense machinery of the host remain obscure. We report that Agrobacterium, a microorganism that elicits neoplastic growths on many plant species, induces expression of a plant defense-related F-box protein, VBF, which it incorporates into its own pathway for genetic transformation. Our data suggest that VBF may function to uncoat the bacterial transferred DNA from its associated virulence VirE2 and host VIP1 proteins via the SCFVBF pathway. Suppression of VBF elevates the intracellular content of VIP1, but renders the plant largely resistant to Agrobacterium, indicating that, in the infection pathway, VBF is functionally epistatic to VIP1. When expressed in Agrobacterium and exported into the plant cell, VBF facilitates tumor formation.
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