PMID- 10096092
OWN - NLM
STAT- MEDLINE
DCOM- 19990715
LR  - 20171116
IS  - 0950-382X (Print)
IS  - 0950-382X (Linking)
VI  - 31
IP  - 4
DP  - 1999 Feb
TI  - Molecular genetic basis for the variable expression of Lewis Y antigen in
      Helicobacter pylori: analysis of the alpha (1,2) fucosyltransferase gene.
PG  - 1265-74
AB  - Helicobacter pylori lipopolysaccharides (LPS) express human oncofetal antigens
      Lewis X and Lewis Y. The synthesis of Lewis Y involves the actions of alpha (1,3)
      and alpha (1,2) fucosyltransferases (FucTs). Here, we report the molecular
      cloning and characterization of genes encoding H. pylori alpha (1,2) FucT (Hp
      fucT2) from various H. pylori strains. We constructed Hp fucT2 knock-out mutants 
      and demonstrated the loss of Lewis Y production in these mutants by enzyme-linked
      immunosorbent assay (ELISA) and immunoelectron microscopy. The Hp fucT2 gene
      contains a hypermutable sequence [poly (C) and TAA repeats], which provides a
      possibility of frequent shifting into and out of coding frame by a polymerase
      slippage mechanism. Thus, the Hp fucT2 gene displays two major genotypes,
      consisting of either a single full-length open reading frame (ORF; as in the
      strain UA802) or truncated ORFs (as in the strain 26695). In vitro expression of 
      Hp fucT2 genes demonstrated that both types of the gene have the potential to
      produce the full-length protein. The production of the full-length protein by the
      26695 fucT2 gene could be attributed to translational-1 frameshifting, as a
      perfect translation frameshift cassette resembling that of the Escherichia coli
      dnaX gene is present. Examination of the strain UA1174 revealed that its fucT2
      gene has a frameshifted ORF at the DNA level, which cannot be compensated by
      translation frameshifting, accounting for its Lewis Y off phenotype. In another
      strain, UA1218, the fucT2 gene is apparently turned off because of the loss of
      its promoter. Based on these data, we proposed a model for the variable
      expression of Lewis Y by H. pylori, in which regulation at the level of
      replication slippage (mutation), transcription and translation of the fucT2 gene 
      may all be involved.
FAU - Wang, G
AU  - Wang G
AD  - Department of Medical Microbiology and Immunology, University of Alberta,
      Edmonton, Canada.
FAU - Rasko, D A
AU  - Rasko DA
FAU - Sherburne, R
AU  - Sherburne R
FAU - Taylor, D E
AU  - Taylor DE
LA  - eng
SI  - GENBANK/AF076779
SI  - GENBANK/AF093828
SI  - GENBANK/AF093829
SI  - GENBANK/AF093830
SI  - GENBANK/AF093831
SI  - GENBANK/AF093832
SI  - GENBANK/AF093833
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Mol Microbiol
JT  - Molecular microbiology
JID - 8712028
RN  - 0 (DNA, Bacterial)
RN  - 0 (Lewis Blood-Group System)
RN  - 0 (Lewis X Antigen)
RN  - 0 (Lewis Y antigen)
RN  - EC 2.4.1.- (Fucosyltransferases)
RN  - EC 2.4.1.69 (galactoside 2-alpha-L-fucosyltransferase)
SB  - IM
MH  - Amino Acid Sequence
MH  - Base Sequence
MH  - DNA, Bacterial/genetics
MH  - Electrophoresis, Polyacrylamide Gel
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Fucosyltransferases/chemistry/*genetics/*metabolism
MH  - Helicobacter pylori/enzymology/*genetics
MH  - Humans
MH  - Immunoblotting
MH  - Lewis Blood-Group System/*biosynthesis
MH  - Lewis X Antigen/biosynthesis
MH  - Microscopy, Immunoelectron
MH  - Molecular Sequence Data
MH  - Mutagenesis, Insertional
MH  - Plasmids/genetics
MH  - Sequence Analysis, DNA
EDAT- 1999/03/30 00:00
MHDA- 1999/03/30 00:01
CRDT- 1999/03/30 00:00
PHST- 1999/03/30 00:00 [pubmed]
PHST- 1999/03/30 00:01 [medline]
PHST- 1999/03/30 00:00 [entrez]
PST - ppublish
SO  - Mol Microbiol. 1999 Feb;31(4):1265-74.