Université de Montréal, Faculté de Médecine Vétérinaire, 3200 Sicotte, Saint-Hyacinthe, Québec J2S 7C6, Canada.
Infect Immun. 2011 May;79(5):1826-32. doi: 10.1128/IAI.01129-10. Epub 2011 Feb 22.
Some enterotoxigenic Escherichia coli strains express the TibA adhesin/invasin, a multifunctional autotransporter that mediates the autoaggregation of bacteria, biofilm formation, adhesion to cultured epithelial cells, and invasion of these cells. To elucidate the structure-function relationship in TibA, we generated mutants by transposon-based linker scanning mutagenesis and by site-directed mutagenesis. Several insertion mutants had a defect in either adhesion or autoaggregation. Mutants with a defect in autoaggregation were found in the N-terminal half of the extracellular domain, while mutants with a defect in adhesion were found in the C-terminal half. The deletion of the putative N-terminal autoaggregation domain abolished the autoaggregation of the bacteria but did not affect adhesion. The deletion of a proline-rich region located at the C terminus of the extracellular domain abolished the adhesion properties of TibA but did not affect invasion. This finding suggests that adhesion and invasion may rely on distinct mechanisms. Thus, our results reveal that TibA possesses a modular organization, with the extracellular domain being separated into an autoaggregation module and an adhesion module.
一些产肠毒素性大肠杆菌菌株表达 TibA 粘附素/侵袭素，这是一种多功能的自转运体，介导细菌的自动聚集、生物膜形成、黏附培养的上皮细胞和侵袭这些细胞。为了阐明 TibA 的结构-功能关系，我们通过转座子连接扫描诱变和定点诱变生成了突变体。一些插入突变体在粘附或自动聚集方面存在缺陷。在细胞外域的 N 端发现了自动聚集缺陷的突变体，而在 C 端发现了粘附缺陷的突变体。推定的 N 端自动聚集结构域的缺失消除了细菌的自动聚集，但不影响粘附。位于细胞外域 C 端的富含脯氨酸区域的缺失消除了 TibA 的粘附特性，但不影响侵袭。这一发现表明，粘附和侵袭可能依赖于不同的机制。因此，我们的结果表明，TibA 具有模块化的组织，细胞外域分为自动聚集模块和粘附模块。
