作者: R. Schulein , P. Guye , T. A. Rhomberg , M. C. Schmid , G. Schroder
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摘要: Bacterial type IV secretion (T4S) systems mediate the transfer of macromolecular substrates into various target cells, e.g., conjugative DNA bacteria or virulence proteins eukaryotic host cells. The T4S apparatus VirB vascular tumor-inducing pathogen Bartonella henselae causes subversion human endothelial cell (HEC) function. Here we report identification multiple protein VirB, which, upon translocation HEC, all known VirB-dependent cellular changes. These Bartonella-translocated effector (Beps) A-G are encoded together with system and coupling VirD4 on a Bartonella-specific pathogenicity island. Beps display modular architecture, suggesting an evolution by extensive domain duplication reshuffling. C terminus each Bep harbors at least one copy Bep-intracellular delivery short positively charged tail sequence. This biparte constitutes signal that is sufficient to VirB/VirD4-dependent intracellular reporter fusions. also present in relaxases bacterial conjugation systems. We exemplarily show such relaxase mediates through VirB/VirD4 HEC. Conjugative may thus represent evolutionary origin here defined for