Endriss Franziska, Braun Volkmar
Mikrobiologie/Membranphysiologie, Universität Tübingen, Tübingen, Germany.
J Bacteriol. 2004 Jul;186(14):4818-23. doi: 10.1128/JB.186.14.4818-4823.2004.
Precise deletions of cell surface-exposed loops of FhuA resulted in mutants of Escherichia coli with distinct phenotypes. Deletion of loop 3 or 11 inactivated ferrichrome transport activity. Deletion of loop 8 inactivated receptor activity for colicin M and the phages T1, T5, and phi80. The loop 7 deletion mutant was colicin M resistant but fully phage sensitive. The loop 4 deletion mutant was resistant to the TonB-dependent phages T1 and phi80 but fully sensitive to the TonB-independent phage T5. The phenotypes of the deletion mutants revealed important sites for the multiple FhuA transport and receptor activities. The ligand binding sites are nonidentical and are distributed among the entire exposed surface. Presumably, FhuA evolved as a ferrichrome transporter and was subsequently used as a receptor by the phages and colicin M, which selected the same as well as distinct loops as receptor sites.
FhuA细胞表面暴露环的精确缺失产生了具有不同表型的大肠杆菌突变体。缺失环3或11会使高铁色素转运活性失活。缺失环8会使对大肠杆菌素M以及噬菌体T1、T5和φ80的受体活性失活。环7缺失突变体对大肠杆菌素M具有抗性,但对噬菌体完全敏感。环4缺失突变体对依赖TonB的噬菌体T1和φ80具有抗性,但对不依赖TonB的噬菌体T5完全敏感。缺失突变体的表型揭示了FhuA多种转运和受体活性的重要位点。配体结合位点不相同,分布在整个暴露表面。据推测,FhuA最初是作为高铁色素转运蛋白进化而来的,随后被噬菌体和大肠杆菌素M用作受体,它们选择了相同以及不同的环作为受体位点。