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

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 .