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FEMS Microbiol Lett. 2002 Mar 5;208(2):295-301.

Inactivation of a Helicobacter pylori DNA methyltransferase alters dnaK operon expression following host-cell adherence.

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1
Department of Medicine, Division of Infectious Diseases, A3310, MCN, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. john.donahue@mcmail.vanderbilt.edu

Abstract

The Helicobacter pylori hpyIM gene encodes a type II DNA methyltransferase that is highly conserved among strains. To investigate the potential role of M.HpyI methyltransferase activity in controlling gene expression in H. pylori, we analyzed gene transcription profiles in wild-type strain J166 and an isogenic hpyIM mutant strain using gene arrays. This analysis showed that the expression of a majority of genes was unaffected by hpyIM mutation, especially in exponential phase cultures. However, in stationary phase cultures and in cells adherent to AGS gastric epithelial cells in vitro, loss of hpyIM function altered the expression of the stress-responsive dnaK operon. Complementation of the hpyIM mutation using a shuttle plasmid encoding a wild-type copy of the gene re-established the wild-type pattern of dnaK operon expression. These data suggested that hpyIM, encoding a DNA methyltransferase, may have a role in H. pylori physiology that supersedes its original function in a type II restriction-modification system.

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