Investigations into the genetic determinants for incompatibility of miniplasmids and hybrid replicons constructed from wild type and mutant R1 revealed the presence of an incompatibility function at the junction of two small PstI fragments. These two fragments were not distinguished in earlier exper
Isolation and characterization of new copy mutants of plasmid R1, and identification of a polypeptide involved in copy number control
✍ Scribed by Molin, Søren ;Stougaard, Peter ;Light, Janice ;Nordström, Marie ;Nordström, Kurt
- Publisher
- Springer
- Year
- 1981
- Tongue
- English
- Weight
- 716 KB
- Volume
- 181
- Category
- Article
- ISSN
- 0026-8925
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✦ Synopsis
Site-specific deletions and insertions in the replication region of plasmid R1 have generated a new class of copy mutants that are present in the cell with 10-15-fold increased copy number. All mutations described inactivate a copy number control gene which is distinct from another cop inc gene that was identified previously (Molin and Nordström 1980). Insertion of the lac operon lacking the normal lac promoter has been used to determine the direction of transcription of this cop gene. The mutants may all be complemented by wild-type plasmid derivatives and are thus recessive. In incompatibility tests with wild-type R1 plasmids, these mutants are indistinguishable from the wild-type plasmid. It therefore seems that this cop function does not play an important role for the incompatibility function. A polypeptide, molecular weight 11,000, has been identified as being the product of this cop gene.
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