Baek Jong Hwan, Chattoraj Dhruba K
Laboratory of Biochemistry and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
PLoS Genet. 2014 Feb 27;10(2):e1004184. doi: 10.1371/journal.pgen.1004184. eCollection 2014 Feb.
Control of chromosome replication involves a common set of regulators in eukaryotes, whereas bacteria with divided genomes use chromosome-specific regulators. How bacterial chromosomes might communicate for replication is not known. In Vibrio cholerae, which has two chromosomes (chrI and chrII), replication initiation is controlled by DnaA in chrI and by RctB in chrII. DnaA has binding sites at the chrI origin of replication as well as outside the origin. RctB likewise binds at the chrII origin and, as shown here, to external sites. The binding to the external sites in chrII inhibits chrII replication. A new kind of site was found in chrI that enhances chrII replication. Consistent with its enhancing activity, the chrI site increased RctB binding to those chrII origin sites that stimulate replication and decreased binding to other sites that inhibit replication. The differential effect on binding suggests that the new site remodels RctB. The chaperone-like activity of the site is supported by the finding that it could relieve the dependence of chrII replication on chaperone proteins DnaJ and DnaK. The presence of a site in chrI that specifically controls chrII replication suggests a mechanism for communication between the two chromosomes for replication.
在真核生物中，染色体复制的控制涉及一组共同的调节因子，而具有分开基因组的细菌则使用染色体特异性调节因子。细菌染色体如何进行复制通信尚不清楚。在具有两条染色体（chrI和chrII）的霍乱弧菌中，复制起始由chrI中的DnaA和chrII中的RctB控制。DnaA在chrI复制起点以及起点之外都有结合位点。同样，RctB在chrII起点以及此处所示的外部位点结合。与chrII外部位点的结合会抑制chrII复制。在chrI中发现了一种新型位点，它能增强chrII复制。与其增强活性一致，chrI位点增加了RctB与那些刺激复制的chrII起点位点的结合，并减少了与其他抑制复制位点的结合。对结合的差异影响表明新位点重塑了RctB。该位点类似伴侣蛋白的活性得到了以下发现的支持：它可以缓解chrII复制对伴侣蛋白DnaJ和DnaK的依赖。chrI中存在一个特异性控制chrII复制的位点，这提示了两条染色体之间进行复制通信的一种机制。
