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The broad-host-range plasmid pTF-FC2 requires a primase-like protein for autonomous replication in Escherichia coli

R A Dorrington1, S Bardien, D E Rawlings

  • 1Department of Microbiology, University of Cape Town, Rondebosch, South Africa.

Gene
|December 1, 1991
PubMed

Insights

A new 1239-bp fragment from plasmid pTF-FC2 enables autonomous replication. This fragment encodes a 40-kDa protein functioning as a primase, crucial for plasmid replication in various bacteria.

Area of Science:

  • Molecular Biology
  • Microbiology
  • Plasmid Biology

Background:

  • The minimum replication region of plasmid pTF-FC2 (3202-bp) cloned into pUC19 requires pUC19 vector functions for replication in Pseudomonas aeruginosa and Escherichia coli polA- mutants.
  • This dependency suggests a need for additional factors or functions not inherent to the minimal replicon fragment alone.

Purpose of the Study:

  • To identify the genetic element responsible for the autonomous replication of plasmid pTF-FC2.
  • To characterize the function of the identified replication element and its encoded protein.

Main Methods:

  • Plasmid construction and replication assays in bacterial hosts (Pseudomonas aeruginosa, Escherichia coli).
  • DNA sequencing and in vitro transcription/translation to analyze the identified fragment.
  • Homology searches against sequence databases.
  • Functional characterization using an M13 replication-deficient phage system.

Main Results:

  • An additional 1239-bp fragment from pTF-FC2 restored autonomous replication.
  • Sequence analysis revealed a single open reading frame encoding a 40-kDa polypeptide.
  • The 40-kDa protein exhibited limited homology to the RepB' primase of IncQ plasmid RSF1010.
  • The 40-kDa protein was confirmed to function as a primase for pTF-FC2 replication.

Conclusions:

  • The 1239-bp fragment contains the necessary genetic information for autonomous replication of pTF-FC2.
  • The 40-kDa protein encoded by this fragment acts as a primase, essential for initiating replication at the vegetative origin of pTF-FC2.
  • This finding contributes to understanding plasmid replication mechanisms and the development of novel cloning vectors.

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