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A BTP 1 prophage gene present in invasive non‐typhoidal S almonella determines composition and length of the O ‐antigen of the lipopolysaccharide
Author(s) -
Kintz Erica,
Davies Mark R.,
Hammarlöf Disa L.,
Canals Rocío,
Hinton Jay C. D.,
Woude Marjan W.
Publication year - 2015
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.12933
Subject(s) - prophage , biology , composition (language) , gene , antigen , microbiology and biotechnology , genetics , escherichia coli , bacteriophage , linguistics , philosophy
Summary S almonella   T yphimurium isolate D 23580 represents a recently identified ST 313 lineage of invasive non‐typhoidal Salmonellae (i NTS ). One of the differences between this lineage and other non‐i NTS S . Typhimurium isolates is the presence of prophage BTP 1. This prophage encodes a gtr C gene, implicated in O ‐antigen modification. GtrC BTP 1 is essential for maintaining O ‐antigen length in isolate D 23580, since a gtr BTP 1 mutant yields a short O ‐antigen. This phenotype can be complemented by gtrC BTP 1 or very closely related gtrC genes. The short O ‐antigen of the gtr BTP 1 mutant was also compensated by deletion of the BTP 1 phage tailspike gene in the D 23580 chromosome. This tailspike protein has a putative endorhamnosidase domain and thus may mediate O ‐antigen cleavage. Expression of the gtrC BTP 1 gene is, in contrast to expression of many other gtr operons, not subject to phase variation and transcriptional analysis suggests that gtrC is produced under a variety of conditions. Additionally, GtrC BTP 1 expression is necessary and sufficient to provide protection against BTP 1 phage infection of an otherwise susceptible strain. These data are consistent with a model in which GtrC BTP 1 mediates modification of the BTP 1 phage O ‐antigen receptor in lysogenic D 23580, and thereby preve nts superinfection by itself and other phage that uses the same O ‐antigen co‐receptor.

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