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大肠杆菌 QseB/QseC 信号传导对于复制起始和细胞迁移的正确时间控制是必需的。

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

机构信息

State Key Laboratory of Reproductive Regulation & Breeding of Grassland Livestock, School of Life Sciences, Inner Mongolia University, Hohhot 010070, China.

State Key Laboratory of Reproductive Regulation & Breeding of Grassland Livestock, School of Life Sciences, Inner Mongolia University, Hohhot 010070, China; Department of Neurology, Inner Mongolia People's Hospital, Hohhot 010017, China.

出版信息

Gene. 2021 Mar 20;773:145374. doi: 10.1016/j.gene.2020.145374. Epub 2020 Dec 23.

DOI:10.1016/j.gene.2020.145374
PMID:33359126
Abstract

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.

摘要

大肠杆菌 QseB/QseC 信号调节超过 50 个编码鞭毛蛋白和与毒力相关蛋白的基因表达。在这里,我们发现 QseB/QseC 信号的缺失导致染色体复制的早期起始和 DnaA 的浓度升高,DnaA 是复制的起始因子。dnaA 启动子的上游区域包含三个潜在的 QseB 结合位点,这些结合位点的缺失增加了野生型细胞中 dnaA 基因的转录,但在缺乏 qseB/qseC 基因的细胞中没有增加,表明 QseB/QseC 信号通过 QseB 结合位点调节 dnaA 的表达。此外,还观察到 ΔqseBC 和 ΔqseB 细胞的细胞迁移增加,但细胞大小和生长速率没有增加,这些效应可以通过异位表达 QseBC 来逆转。此外,发现 QseB 与 DnaK 伴侣和 FtsZ 细胞分裂蛋白在体内相互作用,DnaK 的缺失或 FtsZ 的部分失活会降低细胞迁移能力。因此,我们得出结论,QseB/QseC 信号通过调节 DnaA 的表达来调节复制起始的时间,通过与 DnaK 和 FtsZ 蛋白相互作用来协调细胞迁移与细胞分裂。

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