Taxonomic group: bacteria / Proteobacteria
(Phylum: Proteobacteria)
Host organism: Homo sapiens
Associated disease: functional gastrointestinal disorders [ICD11:
DD9Y 
];
infection due to Yersinia enterocolitica [ICD11:
XN91V ]
The structure was elucidated in this paperNCBI PubMed ID: 20385763Journal NLM ID: 0246127Publisher: American Society for Microbiology
Correspondence: bengoechea
caubet-cimera.es
Institutions: Fundació Caubet- CIMERA Illes Balears, Recinto Hospital Joan March, Carretera Soller km 12, 07110 Bunyola, Spain, Área de Microbiología, Facultad Biología, Universitat Illes Balears, Palma Mallorca, Consejo Superior de Investigaciones Científicas (CSIC), Madrid, Spain
Yersinia enterocolitica is an important human pathogen. Y. enterocolitica must adapt to the host environment, and temperature is an important cue regulating the expression of most Yersinia virulence factors. Here, we report that Y. enterocolitica 8081 serotype O:8 synthesized tetra-acylated lipid A at 37 degrees C but that hexa-acylated lipid A predominated at 21 degrees C. By mass spectrometry and genetic methods, we have shown that the Y. enterocolitica msbB, htrB, and lpxP homologues encode the acyltransferases responsible for the addition of C(12), C(14) and C(16:1), respectively, to lipid A. The expression levels of the acyltransferases were temperature regulated. Levels of expression of msbB and lpxP were higher at 21 degrees C than at 37 degrees C, whereas the level of expression of htrB was higher at 37 degrees C. At 21 degrees C, an lpxP mutant was the strain most susceptible to polymyxin B, whereas at 37 degrees C, an htrB mutant was the most susceptible. We present evidence that the lipid A acylation status affects the expression of Yersinia virulence factors. Thus, expression of flhDC, the flagellar master regulatory operon, was downregulated in msbB and lpxP mutants, with a concomitant decrease in motility. Expression of the phospholipase yplA was also downregulated in both mutants. inv expression was downregulated in msbB and htrB mutants, and consistent with this finding, invasion of HeLa cells was diminished. However, the expression of rovA, the positive regulator of inv, was not affected in the mutants. The levels of pYV-encoded virulence factors Yops and YadA in the acyltransferase mutants were not affected. Finally, we show that only the htrB mutant was attenuated in vivo.
lipid A, Yersinia enterocolitica, virulence factor, acylation
Structure type: oligomer ; 1824
Location inside paper: p.2772, fig.1A, YeO8 21°C
Compound class: lipid A
Contained glycoepitopes: IEDB_135394,IEDB_135515,IEDB_141807,IEDB_151531,IEDB_534864
Methods: virulence assays, PCR, SDS-PAGE, MALDI-TOF MS, biological assays, genetic methods, statistical analysis
Comments, role: major species lipid A isolated from Y. enterocolitica serotype O:8 strain 8081 grown at 21°C.
Related record ID(s): 25393, 32017, 32018
NCBI Taxonomy refs (TaxIDs): 34054
Show glycosyltransferases
There is only one chemically distinct structure:
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