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Release of initiation control by a mutational alteration in the R6K pi protein required for plasmid DNA replication

Insights

A mutation in the pi protein of plasmid R6K (cos405) increases its copy number in E. coli. This suggests the pi protein regulates plasmid replication initiation frequency.

Area of Science:

  • Molecular Biology
  • Microbiology
  • Genetics

Background:

  • Plasmid R6K is a naturally occurring antibiotic resistance plasmid.
  • Plasmid pRK419, a derivative of R6K, contains the pir gene encoding the pi initiation protein and R6K replication origins.
  • The pir gene product is essential for R6K replication initiation.

Purpose of the Study:

  • To investigate the function of the pi initiation protein in plasmid R6K replication.
  • To characterize a mutation (cos405) affecting plasmid copy number.

Main Methods:

  • Plasmid manipulation and propagation in Escherichia coli.
  • Temperature shift experiments to assess copy number variations.
  • Complementation assays to determine mutation location.
  • Nucleotide sequencing to identify the specific mutation.

Main Results:

  • The cos405 mutation in pRK419 leads to increased plasmid copy number in E. coli at 42°C, with a more significant increase at 30°C.
  • The mutant phenotype was suppressed by providing wild-type pi protein in trans, confirming the mutation is in the pir gene.
  • Sequence analysis revealed a single amino acid substitution (Gly81Asp) in the pi protein.

Conclusions:

  • The cos405 mutation affects the pi protein's function.
  • The pi protein is involved in the negative control of R6K replication initiation frequency, beyond its essential role in initiation.
  • This finding provides new insights into the regulatory mechanisms of plasmid replication.

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