Condensin—an SMC-kleisin complex—is essential for efficient segregation of sister chromatids in eukaryotes [ 1–4]. In Escherichia coli and Bacillus subtilis, deletion of condensin subunits results in severe growth phenotypes and the accumulation of cells lacking nucleoids [ 5, 6]. In many other bacteria and under slow growth conditions, however, the reported phenotypes are much milder or virtually absent [ 7–10]. This raises the question of what role prokaryotic condensin might play during chromosome segregation under various growth conditions. In B. subtilis and Streptococcus pneumoniae, condensin complexes are enriched on the circular chromosome near the single origin of replication by ParB proteins bound to parS sequences [ 11, 12]. Using conditional alleles of condensin in B. subtilis, we demonstrate that depletion of its activity results in an immediate and severe defect in the partitioning of replication origins. Multiple copies of the chromosome remain unsegregated at or near the origin of replication. Surprisingly, the growth and chromosome segregation defects in rich medium are suppressed by a reduction of replication fork velocity but not by partial inhibition of translation or transcription. Prokaryotic condensin likely prevents the formation of sister DNA interconnections at the replication fork or promotes their resolution behind the fork.
Smc-ScpAB inactivation causes a severe chromosome segregation defect in B. subtilis
Replication origins remain interconnected in the absence of prokaryotic condensin
Defects in chromosome segregation are highly dependent on growth conditions
Reduction of replication fork velocity rescues segregation of replication origins
Gruber et al. show that conditional inactivation of prokaryotic condensin in B. subtilis results in immediate and severe defects in chromosome segregation under conditions promoting fast growth. The separation of replication origins is blocked in the absence of Smc-ScpAB but can be rescued by artificial reduction of replication fork speed.