The Escherichia coli QseB/QseC signaling regulates expressions of more than 50 genes encoding flagellar proteins and proteins associated with virulence. Here we found that absence of the QseB/QseC signaling led to an early initiation of chromosomal replication and higher concentration of DnaA which is initiator for replication. The upstream region of dnaA promoter contains three potential QseB binding sites and absence of these binding sites increased transcription of the dnaA gene in wild-type cells but not in the cells lacking the qseB/qseC genes, showing that the QseB/QseC signaling regulates dnaA expression through the QseB binding sites. Also increased cell motility but neither cell size nor growth rate in ΔqseBC and ΔqseB cells was observed and these effects were reversed by ectopic expression of QseBC. Further, it was found that QseB interacted with the DnaK chaperone and FtsZ cell division protein in vivo, and absence of DnaK or partial inactivation of FtsZ decreased cell motility. Thus, we conclude that the QseB/QseC signaling modulates timing of replication initiation by regulating expression of DnaA, coordinates cell motility with cell division through interacting with the DnaK and FtsZ protein.

的大肠杆菌QseB / QseC的信号传导调节的编码与毒力相关的鞭毛蛋白和蛋白超过50个基因的表达。在这里，我们发现QseB / QseC信号的缺失导致染色体复制的早期启动和更高浓度的DnaA，它是复制的发起者。dnaA启动子的上游区域包含三个潜在的QseB结合位点，而这些结合位点的缺失增加了野生型细胞中dnaA基因的转录，但缺少qseB / qseC基因的细胞中却没有，表明QseB / QseC信号调节了dnaA通过QseB结合位点表达。还观察到ΔqseBC和ΔqseB细胞的细胞运动性增加，但未观察到细胞大小或生长速率，并且通过异位表达QseBC逆转了这些作用。此外，发现QseB在体内与DnaK伴侣和FtsZ细胞分裂蛋白相互作用，而DnaK的缺乏或FtsZ的部分失活会降低细胞运动性。因此，我们得出结论，QseB / QseC信号传导通过调节DnaA的表达来调节复制起始的时间，通过与DnaK和FtsZ蛋白质相互作用来协调细胞分裂的细胞运动能力。