In order to understand mechanisms by which unit-copy bacterial plasmids are stably inherited, we seek to identify and characterize functions of the host that are directly implicated in the maintenance processes. In the period of this report our recently established laboratory has succeeded in resolving contradictory evidence concerning the participation of the dnaA protein of Escherichia coli in maintaining the 90 kb P1 plasmid. It has previously been found that a well-characterized plasmid replicon isolated from P1 carries two copies of a dnaA protein binding site, but appears unaffected in its replication by a mutant allele of dnaA that does not satisfy the dnaA requirement of the E. coli origin of DNA replication. We report here that this P1 replicon cannot do wihout dnaA protein entirely. On the other hand, a presumably different P1 plasmid replicon, which remains to be isolated and characterized, can integratively suppress a null mutation in the dnaA gene. We suggest that P1 carries both dnaA dependent and dnaA-independent plasmid replicons. The biological significance of the pressence of replicons with differing host-function requirements in so simple an organism as P1 remains to be determined.

Agency
National Institute of Health (NIH)
Institute
Division of Cancer Biology And Diagnosis (NCI)
Type
Intramural Research (Z01)
Project #
1Z01CB005267-01
Application #
4691804
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
1
Fiscal Year
1985
Total Cost
Indirect Cost
Name
Cancer Biology and Diagnosis
Department
Type
DUNS #
City
State
Country
United States
Zip Code