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毒力蛋白 VirD5 与 Spt4 相互作用,通过与宿主细胞的动粒结合。

Virulence protein VirD5 of binds to kinetochores in host cells via an interaction with Spt4.

机构信息

Department of Molecular and Developmental Genetics, Institute of Biology, Leiden University, 2333BE Leiden, The Netherlands.

Department of Molecular and Developmental Genetics, Institute of Biology, Leiden University, 2333BE Leiden, The Netherlands

出版信息

Proc Natl Acad Sci U S A. 2017 Sep 19;114(38):10238-10243. doi: 10.1073/pnas.1706166114. Epub 2017 Sep 5.

Abstract

The bacterium causes crown gall tumor formation in plants. During infection the bacteria translocate an oncogenic piece of DNA (transferred DNA, T-DNA) into plant cells at the infection site. A number of virulence proteins are cotransported into host cells concomitantly with the T-DNA to effectuate transformation. Using yeast as a model host, we find that one of these proteins, VirD5, localizes to the centromeres/kinetochores in the nucleus of the host cells by its interaction with the conserved protein Spt4. VirD5 promotes chromosomal instability as seen by the high-frequency loss of a minichromosome in yeast. By using both yeast and plant cells with a chromosome that was specifically marked by a repeat, chromosome segregation errors and the appearance of aneuploid cells due to the presence of VirD5 could be visualized in vivo. Thus, VirD5 is a prokaryotic virulence protein that interferes with mitosis.

摘要

这种细菌会导致植物冠瘿瘤的形成。在感染过程中,细菌会将致癌的一小段 DNA(转移 DNA,T-DNA)转移到感染部位的植物细胞中。许多毒力蛋白与 T-DNA 一起被共转运到宿主细胞中,以实现转化。我们利用酵母作为模型宿主发现,这些蛋白中的一个,VirD5,通过与保守蛋白 Spt4 的相互作用,定位于宿主细胞的着丝粒/动粒。VirD5 促进了染色体的不稳定性,表现在酵母中高频丢失一个小染色体。通过使用在染色体上特异性标记一个 重复序列的酵母和植物细胞,我们可以在体内观察到由于 VirD5 的存在导致的染色体分离错误和非整倍体细胞的出现。因此,VirD5 是一种干扰有丝分裂的原核毒力蛋白。

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