Abstract: Bacteria display a variety of mechanisms to control plasmid conjugation. Among them,
fertility inhibition (FI) systems prevent conjugation of co-resident plasmids within donor
cells. Analysis of the mechanisms of inhibition between conjugative plasmids could
provide new alternatives to fight antibiotic resistance dissemination. In this work, inhibition
of conjugation of broad host range IncW plasmids was analyzed in the presence of a
set of co-resident plasmids. Strong FI systems against plasmid R388 conjugation were
found in IncF/MOBF12 as well as in IncI/MOBP12 plasmids, represented by plasmids
F and R64, respectively. In both cases, the responsible gene was pifC, known also
to be involved in FI of IncP plasmids and Agrobacterium T-DNA transfer to plant
cells. It was also discovered that the R388 gene osa, which affects T-DNA transfer,
also prevented conjugation of IncP-1/MOBP11 plasmids represented by plasmids RP4
and R751. Conjugation experiments of different mobilizable plasmids, helped by either
FI-susceptible or FI-resistant transfer systems, demonstrated that the conjugative
component affected by both PifC and Osa was the type IV conjugative coupling protein.
In addition, in silico analysis of FI proteins suggests that they represent recent acquisitions
of conjugative plasmids, i.e., are not shared by members of the same plasmid species.
This implies that FI are rapidly-moving accessory genes, possibly acting on evolutionary
fights between plasmids for the colonization of specific hosts.
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