Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Enzyme
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Query: UNIPROT:P43026 (
lipopolysaccharide
)
62,215
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The
lipopolysaccharide
(
LPS
) of Helicobacter pylori expresses the Lewis x (Lex) and/or Ley antigen. We have shown previously that H. pylori
LPS
displays phase variation whereby an Lex-positive strain yields variants with different
LPS
serotypes, for example, Lex plus Ley or nonfucosylated polylactosamine. H. pylori has two
alpha3-fucosyltransferase
genes that both contain poly(C) tracts. We now demonstrate that these tracts can shorten or lengthen randomly, which results in reversible frameshifting and inactivation of the gene products. We provide genetic and serological evidence that this mechanism causes H. pylori
LPS
phase variation and demonstrate that the on or off status of
alpha3-fucosyltransferase
genes determines the
LPS
serotypes of phase variants and clinical isolates. The role of the
alpha3-fucosyltransferase
gene products in determining the
LPS
serotype was confirmed by structural-chemical analysis of
alpha3-fucosyltransferase
knockout mutants. The data also show that the two
alpha3-fucosyltransferase
genes code for enzymes with different fine specificities, and we propose the names futA and futB to designate the orthologs of the H. pylori 26695
alpha3-fucosyltransferase
genes HP0379 and HP0651, respectively. The data also show that the alpha3-fucosylation precedes alpha2-fucosylation [corrected], an order of events opposite to that which prevails in mammals. Finally, the data provide an understanding at the molecular level of the mechanisms underlying
LPS
diversity in H. pylori, which may play an important role in adaptation to the host.
...
PMID:Phase variation in Helicobacter pylori lipopolysaccharide due to changes in the lengths of poly(C) tracts in alpha3-fucosyltransferase genes. 1049 17