The Escherichia coli QseB/QseC signaling is required for correct timing of replication initiation and cell motility

The Escherichia coli QseB/QseC signaling is required for correct timing of replication initiation and cell motility
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大肠杆菌 QseB/QseC 信号传导对于复制起始和细胞运动的正确计时是必需的

DOI:
10.1016/j.gene.2020.145374
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发表时间:
2021-01-11
期刊:
影响因子:
3.5
通讯作者:
Morigen
Morigen
中科院分区:
生物学3区
文献类型:
--
作者:
Wu, Dan;Baigalmaa, Luvsandorj;Morigen

文献摘要

相似文献

大肠杆菌线圈QseB/QseC信号通路调控超过50个编码鞭毛蛋白和毒力相关蛋白的基因的表达。我们发现,缺乏QseB/QseC信号通路导致染色体复制的早期启动和dna的高浓度,dna是复制的起始物。dnaA启动子上游区域包含三个潜在的QseB结合位点,缺乏这些结合位点会增加野生型细胞中dnaA基因的转录,而在缺乏QseB/ qseC基因的细胞中则不会,这表明QseB/ qseC信号通过QseB结合位点调节dnaA的表达。在Delta qseBC和Delta qseB细胞中也观察到细胞活力增加,但细胞大小和生长速度没有增加,这些影响被qseBC的异位表达逆转。此外,我们还发现QseB在体内与DnaK伴侣和FtsZ细胞分裂蛋白相互作用,缺乏DnaK或FtsZ部分失活会降低细胞的运动能力。因此,我们得出结论,QseB/QseC信号通过调节dna的表达来调节复制起始的时间,通过与DnaK和FtsZ蛋白的相互作用来协调细胞运动和细胞分裂。
The Escherichia coil 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 Delta qseBC and Delta qseB 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.