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Copy Number Control and Incompatibility of incFII R Plasmids

  • Robert H. Rownd
  • Alan M. Easton
  • Padmini Sampathkumar

Abstract

Bacterial plasmids are stably inherited even when present in low copy number in host cells. Thus, plasmid inheritance must be controlled by a mechanism which ensures that these extrachromosomal elements are replicated during each cell division cycle and that at least one copy is segregated to each daughter cell at division. The molecular nature of the control of plasmid replication and segregation is presently not understood in any detail. Most available data are consistent with the negative control mechanism proposed by Pritchard (1978). This repressor dilution model postulates that an inhibitor or repressor specified by a gene on a replicon interacts with a specific receptor on the DNA to control the frequency of initiation of replication. This model can account for the control of plasmid copy number and also for the inability of two plasmids which share the same replication control mechanism to coexist stably in descendants of the same host cell (incompatibility). Mutations in either the repressor molecule or its binding site could lead to less stringent control so that plasmid copy number would be increased. A number of plasmid copy number mutants have been isolated and many, but not all, have been found to have altered incompatibility properties (Uhlin and Nordstrom, 1975; Miki et al., 1980; Rownd et al., 1980).

Keywords

Plasmid Copy Number Chloramphenicol Acetyl Transferase Donor Plasmid Replicator Fragment Repressor Molecule 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1981

Authors and Affiliations

  • Robert H. Rownd
    • 1
  • Alan M. Easton
    • 1
  • Padmini Sampathkumar
    • 1
  1. 1.Laboratory of Molecular Biology and Department of BiochemistryUniversity of WisconsinMadisonUSA

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