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Restriction and Modification Systems.

Editors

In: Mobley HLT, Mendz GL, Hazell SL, editors.

Source

Helicobacter pylori: Physiology and Genetics. Washington (DC): ASM Press; 2001. Chapter 24.

Excerpt

Analyses of the genome sequences of strains 26695 and J99 have revealed that 6 to 7% of the coding capacity of each strain are strain-specific genes, and more than half of these genes with functional orthologs in other bacterial species were predicted to encode R-M enzymes (3, 30). This prediction was subsequently supported by studies of genetic variation among H. pylori strains (1), and essentially confirmed when eight different, type II/IIS restriction endonucleases were isolated from the two sequenced strains (Table 4). With the exception of Hpy991, which is unique to H. pylori, each of these restriction endonucleases is highly homologous to prototype restriction endonucleases from other bacterial species. In general, H. pylori R-M genes occupy discrete regions of the chromosome that exhibit the greatest degree of genetic variability between strains (4) and which are usually characterized by a lower (G + C)% content than the overall genome (3). Together, these observations strongly suggest that H. pylori acquired the majority of its R-M genes from other bacterial species through horizontal gene transfer. H. pylori apparently possesses a much greater number of R-M genes than other bacterial species whose genomes have been sequenced (29) and, as shown in Tables 4 and 5, many of these genes encode functional R-M proteins. It is unknown what, if any, selective advantage these numerous and diverse systems afford H. pylori in its natural environment. In an organism that is naturally competent for transformation by exogenous DNA, these systems may function in self/non-self recognition and protect against genomic adulteration by foreign DNA. Simultaneously, these same systems may promote homologous recombination of species-specific or closely related DNA, and thereby provide H. pylori a more rapid mechanism of genetic adaptation than de novo mutation. Rapid adaptation may be essential for an organism that colonizes a potentially hostile niche, such as the human stomach, and therefore necessary to sustain long-term infection. However, since H. pylori may readily acquire genes from its environment, it is also possible that once an R-M system establishes itself in the genome it assures its own perpetuation as a "selfish DNA element" by virtue of its DNA endonucleolytic and modifying properties (19) and therefore provides no particular benefit to its host cell. Finally, in addition to the various R-M systems demonstrated in H. pylori, there are several examples of specific methyltransferase expression in the absence of the cognate restriction endonuclease. This observation has led to speculation that H. pylori may use site-specific methylation for the regulation of gene transcription or DNA replication. The observations that M. HpyI methyltransferase function is conserved in all the strains examined (5, 33, 34) and that hpyIM transcription is regulated by gastric epithelial cell contact (13, 23) support the hypothesis that site-specific methylation may be involved in the control of expression of genes involved in virulence and/or host cell interactions.

Copyright © 2001, ASM Press.

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