Plasmid pT181 replication is decreased at high levels of RepC per plasmid copy.
The replication of staphylococcal plasmid pT181 is indirectly controlled at the level of the synthesis of its replication initiator, RepC. As a result, high levels of RepC synthesis per plasmid copy were expected to lead to autocatalytic plasmid replication, which secondarily would affect host physiology. Surprisingly, RepC overexpression was found to lead to a rapid decrease in pT181 copy number and replication rate. These effects depended on the ratio of RepC to the pT181 replication origin rather than on the absolute amount of RepC in the cell. In a wild-type host, the increase in RepC/plasmid copy also inhibited chromosome replication and cell division. The changes in host physiology did not play any role in the decrease in pT181 replication caused by RepC overexpression since pT181 replication responded in the same way in a host mutant insensitive to the effects of RepC induction. These results suggest that pT181, the prototype of an entire class of plasmids from Gram-positive bacteria, responds to overexpression of its replication initiator by a decrease in plasmid replication.
Iordanescu
S
S
Public Health Research Institute, New York, New York 10016, USA.
D001426:Bacterial Proteins / Q000235:genetics*; D002455:Cell Division; D004261:DNA Replication; D004269:DNA, Bacterial / Q000235:genetics*; D015964:Gene Expression Regulation, Bacterial; D010957:Plasmids / Q000235:genetics*; D012093:Replicon; D013211:Staphylococcus aureus / Q000235:genetics / Q000502:physiology*
D001426:Bacterial Proteins; D004269:DNA, Bacterial; C043650:RepC protein, Staphylococcus aureus