# RepE Monomer–Dimer Equilibrium Shapes Replication and Autoregulatory Control of the F Plasmid

## TL;DR

This study shows how the balance between monomer and dimer forms of the RepE protein controls replication and gene regulation in the F plasmid.

## Contribution

The study reveals that both RepE monomers and dimers contribute to autoregulation, refining the F plasmid replication model.

## Key findings

- Plasmid copy number control aligns with the titration and loop formation models.
- RepE monomers act as active replication initiators.
- Both RepE monomers and dimers regulate repE gene expression.

## Abstract

Although the replication mechanism of the F plasmid and its regulatory strategies have been addressed in several studies, a comprehensive understanding of these processes remains incomplete. In this work, we present new observations that contribute to refining the current model of F plasmid replication control. In this work, the results indicate that plasmid copy number control in both the F plasmid and its derivatives is consistent with two previously proposed mechanisms: the titration model and the loop formation model. In both cases, the intracellular concentration and functional state of the RepE protein appear to play a central role. Consistent with earlier reports, the data of this study support the conclusion that the RepE monomer functions as the active replication initiator. Importantly, the transcriptional analyses suggest that not only RepE dimers but also monomers contribute to autoregulatory control of repE expression. These findings support a model in which the monomer–dimer equilibrium of RepE shapes both replication initiation and transcriptional autoregulation of the F plasmid.