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Structural maintenance of chromosomes (SMC) are ubiquitously distributed proteins involved in chromosome organization. Deletion of smc causes severe growth phenotypes in many organisms. Surprisingly, smc can be deleted in Corynebacterium glutamicum , a member of the Actinomycetota phylum, without any apparent growth phenotype. SMC in C. glutamicum is loaded in a ParB-dependent fashion to the chromosome and functions in replichore cohesion. The unexpected absence of a growth phenotype in the smc mutant prompted us to screen for synthetic interactions within C. glutamicum . We generated a high-density Tn5 library from wild-type and smc -deleted C. glutamicum strains. Transposon sequencing data revealed that the DNA translocase FtsK is essential in an smc -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 smc 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 C. glutamicum . 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 smc 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 Actinomycetota, smc is dispensable, but the reason for the lack of an smc 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.