Buhrdorf Renate, Förster Cornelia, Haas Rainer, Fischer Wolfgang
Max von Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie, Ludwig-Maximilians-Universität, München, Germany.
Int J Med Microbiol. 2003 Jun;293(2-3):213-7. doi: 10.1078/1438-4221-00260.
The type IV secretion system encoded by the cag pathogenicity island of Helicobacter pylori is recognized as a major virulence determinant, governing the translocation of the CagA protein to eukaryotic cells. Despite the presence of 18 genes within the cag pathogenicity island which are essential for this process, several homologues encoding basic functions of a type IV secretion apparatus, such as a virB8 homologue, are still missing. We show here the presence of conserved VirB8 motifs in the cag-encoded apparatus protein HP530 and demonstrate that this protein adopts in E. coli a transmembrane topology similar to VirB8 and its homologues. Thus, we propose that HP530 is a type IV secretion component homologous to VirB8.
幽门螺杆菌cag致病岛编码的IV型分泌系统被认为是一种主要的毒力决定因素，它控制着CagA蛋白向真核细胞的转运。尽管cag致病岛内存在18个对该过程至关重要的基因，但仍缺少几个编码IV型分泌装置基本功能的同源物，如virB8同源物。我们在此展示了cag编码的装置蛋白HP530中存在保守的VirB8基序，并证明该蛋白在大肠杆菌中采用了与VirB8及其同源物相似的跨膜拓扑结构。因此，我们提出HP530是与VirB8同源的IV型分泌成分。
