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Marker frequency analysis of the  Escherichia coli recB  mutant chromosome has revealed a deficit of DNA in a specific zone of the terminus, centred on the  dif/TerC  region. Using fluorescence microscopy of a marked chromosomal site, we show that the  dif  region is lost after replication completion, at the time of cell division, in one daughter cell only, and that the phenomenon is transmitted to progeny. Analysis by marker frequency and microscopy shows that the position of DNA loss is not defined by the replication fork merging point since it still occurs in the  dif/TerC  region when the replication fork trap is displaced in strains harbouring ectopic  Ter  sites. Terminus DNA loss in the  recB  mutant is also independent of dimer resolution by XerCD at  dif  and of Topo IV action close to  dif . It occurs in the terminus region, at the point of inversion of the GC skew, which is also the point of convergence of specific sequence motifs like KOPS and Chi sites, regardless of whether the convergence of GC skew is at  dif  (wild-type) or a newly created sequence. In the absence of FtsK-driven DNA translocation, terminus DNA loss is less precisely targeted to the KOPS convergence sequence, but occurs at a similar frequency and follows the same pattern as in FtsK +  cells. Importantly, using  ftsIts ,  ftsAts  division mutants and cephalexin treated cells, we show that DNA loss of the  dif  region in the  recB  mutant is decreased by the inactivation of cell division. We propose that it results from septum-induced chromosome breakage, and largely contributes to the low viability of the  recB  mutant.

Division-induced DNA double strand breaks in the chromosome terminus region of Escherichia coli lacking RecBCD DNA repair enzyme