Bacterial plasmids are stabilized by a number of different mechanisms.
Here we describe the molecular aspects of a group of plasmid-encoded
gene systems called the proteic killer gene systems. These systems med
iate plasmid maintenance by selectively killing plasmid-free cells (po
st-segregational killing or plasmid addiction). The group includes ccd
of F, parD/ pem of R1/R100, parDE of RP4/RK2, and phd/doc of P1. All
of these systems encode a stable toxin and an unstable antidote. The a
ntidotes prevent the lethal action of their cognate toxins by forming
tight complexes with them. The antidotes are degraded by cellular prot
eases. Thus, the different decay rates of the toxins and antidotes see
m to be the molecular basis of toxin activation in plasmid-free cells.
The operons encoding the toxins and antidotes are autoregulated at th
e level of transcription either by a complex formed by the toxins and
the cognate antidotes or by the antidote alone. The cellular targets o
f the killer proteins have been determined to be DNA gyrase in the cas
e of ccd of F and DnaB in the case of parD of R1. Surprisingly, the Es
cherichia coil chromosome encodes at least two of these peculiar gene
systems.