During bacterial cell division, chromosomal DNA must be precisely replicated and then correctly segregated. During replication, DNA may suffer damage by various endogenous (e.g., ROS) or exogenous (e.g., nucleotide analogs, irradiation) agents. The damage leads to formation of single strand gaps and double strand breaks, which may collapse the replication fork. To re-initiate replication, the stopped replication forks undergo recombination-dependent repair by several pathways. The Recombination Dependent Repair (RDR) of replication forks may lead to the formation of chromosome dimers, which need to be resolved by XerCD recombination into monomers for efficient segregation. In order to ensure correct replication and to coordinate chromosome segregation with cell division, bacteria employ various nucleoid-associated proteins, like MukBEF, SeqA, MatP. SeqA binds to the GATC sites and hold the DNA apart, thereby decreasing the chances of intersister homologous recombination. Excess SeqA prevents the over-initiation of replication at OriC by sequestration and may also inhibit early chromosome segregation in order to ensure that both daughter cells have equal DNA content at the time of cell division. Our lab has previously characterized a peptide "wrwycr" that binds Holliday Junctions and prevents their resolution. We have used this peptide as a tool to study homologous recombination in vivo in Salmonella by following the trapped Holliday Junctions in response to excess DNA damages created by AZT (DNA damaging agent). Apart from undergoing DNA repair by RDR and completing replication, DNA should also undergo efficient segregation for proper cell division. Our hypothesis was that there is a constant competition between recombination processes and chromosome segregation mechanisms.