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吲哚乙酸是转移DNA的产物,它能抑制根癌土壤杆菌C58的vir基因表达和生长。

Indoleacetic acid, a product of transferred DNA, inhibits vir gene expression and growth of Agrobacterium tumefaciens C58.

作者信息

Liu Pu, Nester Eugene W

机构信息

Departments of Microbiology and Biology, Box 357242, University of Washington, Seattle, WA 98195, USA.

出版信息

Proc Natl Acad Sci U S A. 2006 Mar 21;103(12):4658-62. doi: 10.1073/pnas.0600366103. Epub 2006 Mar 14.

DOI:10.1073/pnas.0600366103
PMID:16537403
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1450227/
Abstract

Agrobacterium tumefaciens induces crown gall tumors by transferring a piece of its tumor-inducing plasmid into plant cells. This transferred DNA encodes the synthesis of indole acetic acid (IAA) and cytokinin, and their overproduction results in tumor formation. The transfer is initiated by a two-component regulatory system, VirA/G recognizing plant signal molecules in the plant rhizosphere and activating a regulon on the tumor-inducing plasmid, which is required for the processing and transfer of DNA and protein. Although a great deal is known about vir gene activation, nothing is known about whether or how the vir gene regulon is inactivated after plant cell transformation. Presumably, just as a mechanism exists for activating the vir gene regulon only when a plant is in the immediate environment, a mechanism should exist for inactivating the same regulon once it has fulfilled its mission to transferred DNA into plant cells. We now show that IAA inactivates vir gene expression by competing with the inducing phenolic compound acetosyringone for interaction with VirA. IAA does not inhibit the vir genes in cells containing a constitutive sensor virA locus, which does not require any signal molecules to become phosphorylated. At higher concentrations, IAA inhibits the growth of Agrobacterium and many other plant-associated bacteria but not the growth of bacteria that occupy other ecological niches. These observations provide the missing link in the cycle of vir gene activation and inactivation.

摘要

根癌土壤杆菌通过将其致瘤质粒的一部分转移到植物细胞中来诱导冠瘿瘤的形成。这种转移的DNA编码吲哚乙酸(IAA)和细胞分裂素的合成,它们的过量产生导致肿瘤形成。转移由一个双组分调节系统启动,VirA/G识别植物根际中的植物信号分子并激活致瘤质粒上的一个调节子,这对于DNA和蛋白质的加工及转移是必需的。尽管对vir基因激活了解很多,但对于植物细胞转化后vir基因调节子是否以及如何失活却一无所知。据推测,正如存在一种仅在植物处于直接环境中时激活vir基因调节子的机制一样,一旦它完成了将DNA转移到植物细胞中的任务,应该也存在一种使同一调节子失活的机制。我们现在表明,IAA通过与诱导性酚类化合物乙酰丁香酮竞争与VirA相互作用来使vir基因表达失活。IAA不会抑制含有组成型传感器virA位点的细胞中的vir基因,该位点不需要任何信号分子即可被磷酸化。在较高浓度下,IAA会抑制根癌土壤杆菌和许多其他与植物相关的细菌的生长,但不会抑制占据其他生态位的细菌的生长。这些观察结果提供了vir基因激活和失活循环中缺失的环节。

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