Open AccessThe failure of different strains of Yersinia pestis to produce lipopolysaccharide O‐antigen under different growth conditions is due to mutations in the O‐antigen gene cluster
Author(s) -
Prior Joann L.,
Parkhill Julian,
Hitchen Paul G.,
Mungall Karen L.,
Stevens Kim,
Morris Howard R.,
Reason Andrew J.,
Oyston Petra C.F.,
Dell Anne,
Wren Brendan W.,
Titball Richard W.
Publication year - 2001
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2001.tb10608.x
Subject(s) - yersinia pestis , antigen , lipopolysaccharide , plasmid , microbiology and biotechnology , biology , gene cluster , strain (injury) , gene , lipid a , gel electrophoresis , molecular mass , antiserum , enterobacteriaceae , chemistry , escherichia coli , biochemistry , virulence , genetics , anatomy , enzyme , endocrinology
The lipopolysaccharide (LPS) from eight strains of Yersinia pestis which had been cultured at 28°C appeared to be devoid of an O‐antigen when analysed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis. LPS isolated from three of these strains which had been cultured at 37°C also appeared to be devoid of an O‐antigen. When the LPS from Y. pestis strain CO92 was purified and analysed by matrix‐assisted laser desorption‐ionisation time‐of‐flight mass spectrometry, the observed signals were in the mass range predicted for molecules containing lipid A plus the core oligosaccharide but lacking an O‐antigen. The nucleotide sequence of Y. pestis strain CO92 revealed the presence of a putative O‐antigen gene cluster. However, frame‐shift mutations in the ddhB , gmd , fcl and ushA genes are likely to prevent expression of the O‐antigen thus explaining the loss of phenotype.