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A deletion in the wapB promoter in many serotypes of Pseudomonas aeruginosa accounts for the lack of a terminal glucose residue in the core oligosaccharide and resistance to killing by R 3‐pyocin
Author(s) -
Kocíncová Dana,
Lam Joseph S.
Publication year - 2013
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.12289
Subject(s) - biology , pseudomonas aeruginosa , random hexamer , virulence , operon , bacteriocin , oligosaccharide , microbiology and biotechnology , virulence factor , lipid a , plasmid , sigma factor , bacteria , biochemistry , genetics , rna , escherichia coli , gene , rna polymerase
Summary P seudomonas aeruginosa is an opportunistic human pathogen producing a variety of virulence factors. One of them is lipopolysaccharide, consisting of endotoxic lipid A and long‐chain O ‐antigen polysaccharide, which are connected together through a short linker region, called core oligosaccharide. Chemical structures of the core oligosaccharide are well conserved, with one exception, in that certain strains of P . aeruginosa add a terminal glucose residue ( Glc IV ) to core by a transferase reaction, due to the activity of a glucosyltransferase, WapB . Here, we investigated the regulation of wapB expression. Our results showed that while the majority of analysed genomes of P . aeruginosa contain wapB , many of these have a conserved identical 5‐nucleotide deletion in the upstream region that inactivated the promoter. This deletion is within the −10 hexamer that is recognized by a principle sigma factor ( RpoD , or σ70) as proven by data from an electromobility shift assay. These results provide the molecular basis of why LPS core of many P . aeruginosa strains is lacking Glc IV . In addition, we show that absence of Glc IV due to an inactive wapB promoter confers resistance to killing by R 3‐pyocin, a phage tail‐like bacteriocin of P . aeruginosa .