A single parS sequence from the cluster of four sites closest to oriC is necessary and sufficient for proper chromosome segregation in XXXX .

@entity5175 @entity796 @entity71306 @entity4334 @entity71305
Among the mechanisms that control chromosome segregation in bacteria are highly-conserved partitioning systems comprising three components: @entity71305 protein (a deviant Walker-type ATPase), @entity71306 protein (a DNA-binding element) and multiple cis-acting palindromic centromere-like sequences, designated parS. Ten putative parS sites have been identified in the @entity5175 genome, four localized in close proximity of oriC and six, diverged by more than one @entity4334 from a perfect palindromic sequence, dispersed along the chromosome. Here, we constructed and analyzed @entity796 mutants deprived of each single parS sequence and their different combinations. The analysis included evaluation of a set of phenotypic features, chromosome segregation, and @entity71306 localization in the cells. It was found that @entity71306 binds specifically to all ten parS sites, although with different affinities. The @entity796 parS mutant with all ten parS sites modified (parSnull) is viable however it demonstrates the phenotype characteristic for parAnull or parBnull mutants: slightly slower growth rate, high frequency of anucleate cells, and defects in motility. The genomic position and sequence of parS determine its role in @entity796 biology. It transpired that any one of the four parS sites proximal to oriC (parS1 to parS4), which are bound by @entity71306 with the highest affinity, is necessary and sufficient for the parABS role in chromosome partitioning. When all these four sites are mutated simultaneously, the strain shows the parSnull phenotype, which indicates that none of the remaining six parS sites can substitute for these four oriC-proximal sites in this function. A single ectopic parS2 (inserted opposite oriC in the parSnull mutant) facilitates @entity71306 organization into regularly spaced condensed foci and reverses some of the mutant phenotypes but is not sufficient for accurate chromosome segregation.
