Abstract
kis-kid, the auxiliary maintenance system of plasmid R1 and copB, the auxiliary copy number control gene of this plasmid, contribute to increase plasmid replication efficiency in cells with lower than average copy number. It is thought that Kis antitoxin levels decrease in these cells and that this acts as the switch that activates the Kid toxin; activated Kid toxin reduces copB-mRNA levels and this increases RepA levels that increases plasmid copy number. In support of this model we now report that: (i) the Kis antitoxin levels do decrease in cells containing a mini-R1 plasmid carrying a repA mutation that reduces plasmid copy number; (ii) kid-dependent replication rescue is abolished in cells in which the Kis antitoxin levels or the CopB levels are increased. Unexpectedly we found that this coordination significantly increases both the copy number of the repA mutant and of the wt mini-R1 plasmid. This indicates that the coordination between plasmid replication functions and kis-kid system contributes significantly to control plasmid R1 replication.
Highlights
Plasmid R1 is an antibiotic resistance plasmid of enteric bacteria that has contributed important insights into plasmid replication and its control as well as into the regulation and role of auxiliary plasmid maintenance systems [1]
We reported recently that increasing in trans the Kis antitoxin levels suppressed the “interference” phenotype; this suggested that Kis antitoxin levels could act as the switch connecting the replication and kis-kid toxin-antitoxin maintenance functions [22]
The results reported here support the role of Kis antitoxin as the switch that couples replication functions and the kis-kid maintenance system; they support the proposal that a Kid-dependent decrease in the CopB levels increases plasmid replication efficiency
Summary
Plasmid R1 is an antibiotic resistance plasmid of enteric bacteria that has contributed important insights into plasmid replication and its control as well as into the regulation and role of auxiliary plasmid maintenance systems [1]. Its replication is initiated due to specific interactions of a rate limiting protein, RepA, at oriR1, the origin of replication [2]. The frequency of this process is regulated by the copy number control genes copA and copB. CopA, the key regulator gene, codes an unstable antisense RNA, CopA, that inhibits at the posttranscriptional level the synthesis of RepA. CopA RNA targets the polycistronic copB-repA mRNA at copT, its complementary sequence, and inhibits translation of the tap orf which is needed for RepA translation [3,4]. Inactivation of copA leads to uncontrolled amplification of the plasmid or run-away replication [5]
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