Early onset of septal FtsK localization allows for efficient DNA segregation in SMC-deleted strains.

Structural maintenance of chromosomes (SMC) are ubiquitously distributed proteins involved in chromosome organization. Deletion of causes severe growth phenotypes in many organisms. Surprisingly, can be deleted in , a member of the phylum, without any apparent growth phenotype. SMC in is loaded in a ParB-dependent fashion to the chromosome and functions in replichore cohesion. The unexpected absence of a growth phenotype in the mutant prompted us to screen for synthetic interactions within . We generated a high-density Tn5 library from wild-type and -deleted strains. Transposon sequencing data revealed that the DNA translocase FtsK is essential in an -deletion strain. In wild-type cells, FtsK localized to the septa and cell poles, showing polar enrichment during the earlier stages of the life cycle and relocating to the septum in the later stages. However, deletion of resulted in an earlier onset of pole-to-septum FtsK relocation, suggesting that prolonged FtsK complex activity is both required and sufficient to compensate for the absence of SMC, thus achieving efficient chromosome segregation in . Deletion of ParB increases SMC and FtsK mobility. While the change in SMC dynamics aligns with previous data showing ParB's role in SMC loading on DNA, the change in FtsK mobility suggests defects in chromosome segregation. Based on our data, we propose an efficient mechanism for reliable DNA segregation in the absence of replichore arm cohesion in mutant cells.IMPORTANCEFaithful DNA segregation is of fundamental importance for life. Bacteria have developed efficient systems to coordinate chromosome compaction, DNA segregation, and cell division. A key factor in DNA compaction is the SMC complex that is found to be essential in many bacteria. In members of the is dispensable, but the reason for the lack of an phenotype in these bacteria remained unclear. We show here that the divisome-associated DNA pump FtsK can compensate for SMC loss and the subsequent loss in correct chromosome organization. In cells with distorted chromosomes, FtsK is recruited and stabilized earlier to the septum, allowing for DNA segregation for a larger part of the cell cycle, until chromosomes are segregated.