Affiliation:
1. Institute of Microbiology and Immunology, National Yang Ming University, Pai-Tao, Taipei, 112, Taiwan
Abstract
ABSTRACT
Phage AR1 is similar to phage T4 in several essential genes but differs in host range. AR1 infects various isolates of
Escherichia 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. coli
O157:H7 was mutated by Tn
10
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.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
35 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献