Langenscheid Johannes, Killmann Helmut, Braun Volkmar
Mikrobiologie/Membranphysiologie, Universität Tübingen, Auf der Morgenstelle 28, D-72076 Tuebingen, Germany.
FEMS Microbiol Lett. 2004 May 1;234(1):133-7. doi: 10.1016/j.femsle.2004.03.019.
Infection of Escherichia coli K-12 by phages T1 and phi 80 requires the FhuA outer membrane protein and the TonB protein. Mutations in the N-terminal globular domain close to the predicted channel in the beta-barrel of FhuA were created. The FhuA Delta 107-111 N104K K110D L111P mutant and the FhuA(L(109)DPNGLK(110)) insertion mutant were sensitive to phage T1, but nearly resistant to phage phi 80. FhuA Delta 107-111 N104K K110D L111P mediated phage T1 infection in a tonB mutant without formation of TonB-independent phage T1 host-range mutants. The FhuA mutants showed no altered sensitivity to phage T5. Although the phages share overlapping binding sites in FhuA, the structural alterations elicited by the mutations resulted in very different phage sensitivities. In the FhuA deletion mutant, the TonB requirement for phage T1 infection was partially bypassed.
噬菌体T1和φ80感染大肠杆菌K-12需要FhuA外膜蛋白和TonB蛋白。在FhuAβ桶中靠近预测通道的N端球状结构域产生了突变。FhuA Δ107-111 N104K K110D L111P突变体和FhuA(L(109)DPNGLK(110))插入突变体对噬菌体T1敏感,但对噬菌体φ80几乎具有抗性。FhuA Δ107-111 N104K K110D L111P在tonB突变体中介导噬菌体T1感染,且未形成不依赖TonB的噬菌体T1宿主范围突变体。FhuA突变体对噬菌体T5的敏感性未改变。尽管这些噬菌体在FhuA中共享重叠的结合位点,但突变引起的结构改变导致了非常不同的噬菌体敏感性。在FhuA缺失突变体中,噬菌体T1感染对TonB的需求被部分绕过。