Contributions of genome sequencing to understanding the biology of Helicobacter pylori

Zm. Ge et De. Taylor, Contributions of genome sequencing to understanding the biology of Helicobacter pylori, ANN R MICRO, 53, 1999, pp. 353-387
Citations number
Categorie Soggetti
Journal title
ISSN journal
0066-4227 → ACNP
Year of publication
353 - 387
SICI code
About half of the world's population carries Helicobacter pylori, a gram-ne gative, spiral bacterium that colonizes the human stomach. The link between H. pylori and, ulceration as well as its association with the development of both gastric cancer and mucosa-associated lymphoid tissue lymphoma in hu mans is a serious public health concern. The publication of the genome sequ ences of two stains of H, pylori gives rise to direct evidence on the genet ic diversity reported previously with respect to gene organization and nucl eotide variability from strain to strain. The genome size of H. pylori stra in 26695 is 1,6697,867 bp and is 1,643,831 bp for strain J99. Approximately 89% of the predicted open reading frames are common to both of the strains , confirming H. pylori as a single species, A region containing similar to 45% of H. pylori strain-specific open reading frames, termed the plasticity zone, is present on the chromosomes, verifying that some strain variabilit y exists. Frequent alteration of nucleotides in the third position of the t riplet codons and various copies of insertion elements on the individual ch romosomes appear to contribute to distinct polymorphic fingerprints among s trains analyzed by restriction fragment length polymorphisms, random amplif ied polymorphic DNA method, and repetitive element-polymerase chain reactio n. Disordered chromosomal locations of some genes seen by pulsed-field gel electrophoresis are likely caused by rearrangement or inversion of certain segments in the genomes. Cloning and functional characterization of the gen es involved in acidic survival, vacuolating toxin, cag-pathogenicity island , motility, attachment to epithelial cells, natural transformation, and the biosynthesis of Lipopolysaccharides have considerably increased our unders tanding of the molecular genetic basis for the pathogenesis of H. pylori. T he homopolymeric nucleotide tracts and dinucleotide repeats, which potentia lly regulate the on- and off-status of the target genes by the strand-slipp ed mispairing mechanism, are often found in the genes encoding the outer-me mbrane proteins, in enzymes for lipopolysaccharide synthesis, and within DN A modification/restriction systems. Therefore, these genes mag. be involved in the H. pylori-host interaction.