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首页> 外文期刊>Journal of bacteriology >Characterization of the Distal Tail Fiber Locus and Determination of the Receptor for Phage AR1, Which Specifically InfectsEscherichia coli O157:H7
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Characterization of the Distal Tail Fiber Locus and Determination of the Receptor for Phage AR1, Which Specifically InfectsEscherichia coli O157:H7

机译：尾部尾巴纤维基因座的鉴定和噬菌体AR1受体的确定，该噬菌体专门感染大肠杆菌O157：H7

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Phage AR1 is similar to phage T4 in several essential genes but differs in host range. AR1 infects various isolates ofEscherichia coli O157:H7 but does not infect K-12 strains that are commonly infected by T4. We report here the determinants that confer this infection specificity. In T-even phages, gp37 and gp38 are components of the tail fiber that are critical for phage-host interaction. The counterparts in AR1 may be similarly important and, therefore, were characterized. The AR1 gp37 has a sequence that differs totally from those of T2 and T4, except for a short stretch at the N terminus. The gp38 sequence, however, has some conservation between AR1 and T2 but not between AR1 and T4. The sequences that are most closely related to the AR1 gp37 and gp38 are those of phage Ac3 in the T2 family. To identify the AR1-specific receptor, E. coliO157:H7 was mutated by Tn10 insertion and selected for an AR1-resistant phenotype. A mutant so obtained has an insertion occurring at ompC that encodes an outer membrane porin. To confirm the role of OmpC in the AR1 infection, homologous replacement was used to create an ompC disruption mutant (RM). When RM was complemented with OmpC originated from an O157:H7 strain, but not from K-12, its AR1 susceptibility was fully restored. Our results suggest that the host specificity of AR1 is mediated at least in part through the OmpC molecule.
机译：噬菌体AR1在几个必需基因中与噬菌体T4相似，但是宿主范围不同。 AR1会感染各种大肠杆菌O157：H7分离株，但不会感染通常被T4感染的K-12菌株。我们在这里报告了赋予这种感染特异性的决定因素。在T-even噬菌体中，gp37和gp38是尾纤维的组成部分，对噬菌体与宿主的相互作用至关重要。 AR1中的对应项可能同样重要，因此已进行了表征。 AR1 gp37的序列与T2和T4的序列完全不同，除了在N端的延伸很短。但是，gp38序列在AR1和T2之间有一定的保守性，但在AR1和T4之间没有。与AR1 gp37和gp38最相关的序列是T2家族中噬菌体Ac3的序列。为了鉴定AR1特异性受体， E。通过插入Tn 10 使大肠杆菌 O157：H7突变，并选择了抗AR1的表型。如此获得的突变体在 ompC 处发生插入，该插入编码外膜孔蛋白。为了确认OmpC在AR1感染中的作用，使用了同源置换产生了一个 ompC 破坏突变体（RM）。当RM补充来自O157：H7菌株而不是K-12的OmpC时，其AR1敏感性被完全恢复。我们的结果表明，AR1的宿主特异性至少部分通过OmpC分子介导。

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