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

John P Donahue1, Dawn A Israel, Victor J Torres

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

Insights

The Helicobacter pylori hpyIM gene, encoding a DNA methyltransferase, influences stress-responsive gene expression, particularly the dnaK operon, in stationary and adherent phases. This suggests a broader physiological role beyond DNA modification.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Helicobacter pylori is a significant human pathogen.
  • The hpyIM gene encodes a type II DNA methyltransferase, conserved across H. pylori strains.
  • The function of M.HpyI methyltransferase in H. pylori gene regulation is not fully understood.

Purpose of the Study:

  • To investigate the role of M.HpyI methyltransferase activity in controlling gene expression in H. pylori.
  • To analyze the impact of hpyIM gene mutation on H. pylori transcription profiles.

Main Methods:

  • Gene expression profiling using gene arrays.
  • Comparison of wild-type strain J166 and an isogenic hpyIM mutant strain.
  • Analysis of gene expression in exponential and stationary phases, and in adherent cells.

Main Results:

  • The hpyIM mutation did not significantly affect the expression of most genes, especially in exponential phase.
  • Loss of hpyIM function altered the expression of the stress-responsive dnaK operon in stationary phase and adherent cells.
  • Complementation restored the wild-type dnaK operon expression pattern.

Conclusions:

  • The hpyIM gene product, M.HpyI DNA methyltransferase, plays a role in H. pylori physiology.
  • This role extends beyond its function in a type II restriction-modification system, impacting stress response gene regulation.

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