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The mutH gene regulates the replication and methylation of the pMB1 origin

D W Russell1, K Horiuchi

  • 1Laboratory of Genetics, Rockefeller University, New York, New York 10021.

Journal of Bacteriology
|May 1, 1991
PubMed

Insights

The mismatch repair protein MutH partially hinders pMB1 plasmid replication when hemimethylated at dam sites. MutH does not affect oriC replication, suggesting a coordinated DNA repair and replication control mechanism.

Area of Science:

  • Molecular Biology
  • Genetics
  • Microbiology

Background:

  • DNA methylation regulates prokaryotic replication origins.
  • Hemimethylation at dam (GATC) sites impairs replication of Escherichia coli oriC and pMB1 plasmid origins.
  • The mismatch repair protein MutH recognizes hemimethylated dam sites.

Purpose of the Study:

  • Investigate the role of the MutH protein in the replication of prokaryotic origins, specifically oriC and pMB1.
  • Determine if MutH contributes to the poor replication of hemimethylated origins.

Main Methods:

  • Investigated the effect of the mutH gene product on the replication efficiency of hemimethylated pMB1 and oriC origins.
  • Analyzed methylation levels at individual dam sites.
  • Examined MutH protein binding to specific DNA sequences.

Main Results:

  • The mutH gene product was found to be partially responsible for the poor replication of the pMB1 origin when hemimethylated.
  • MutH had no significant effect on the replication of the oriC origin.
  • MutH protein likely binds to an inverted repeat within the pMB1 replication primer promoter.

Conclusions:

  • MutH plays a role in regulating pMB1 plasmid replication, particularly under hemimethylated conditions.
  • The findings suggest a novel mechanism for coordinated control between DNA repair pathways (involving MutH) and DNA replication.
  • This study highlights the differential impact of DNA methylation and repair proteins on distinct replication origins.

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