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Related Experiment Videos

Control of P1 plasmid replication by iterons

A L Abeles1, L D Reaves, B Youngren-Grimes

  • 1Laboratory of Chromosome Biology, ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201, USA.

Molecular Microbiology
|December 1, 1995
PubMed
Summary

This study reveals that plasmid P1 copy number control involves dynamic interactions between incA and oriR loci. Individual incA units randomly contact origin sites, regulating replication initiation.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Plasmid P1 copy number is regulated by the incA locus interacting with the replication origin (oriR).
  • Both loci contain iteron sequences that bind the P1 RepA protein, mediating regulatory contacts.

Purpose of the Study:

  • To investigate the mechanism of plasmid P1 replication control by examining two models of incA-oriR interaction.
  • To determine whether incA-oriR complex formation is stable or dynamic.

Main Methods:

  • Construction of synthetic incA iteron arrays with varied iteron numbers, sequences, and spacing.
  • In vitro and in vivo assays to test regulatory models.

Main Results:

  • Data strongly favor a model where individual incA iterons act as freely diffusing units.

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  • These units dynamically contact origin iterons in a random fashion.
  • The origin iterons function as regulatory targets but not effectors.

    • Conclusions:

    • A model for replication control based on random, dynamic contacts between incA and origin iterons is proposed.
    • This mechanism ensures cell-cycle coordinated replication in dividing cells.