Seeto Shona, Notley-McRobb Lucinda, Ferenci Thomas
School of Molecular and Microbial Biosciences, G08, University of Sydney, Sydney, NSW 2006, Australia.
Res Microbiol. 2004 Apr;155(3):211-5. doi: 10.1016/j.resmic.2003.11.011.
The ptsG gene encodes the high-affinity glucose receptor component of the PEP:glucose phosphotransferase system. PtsG is the major glucose transporter in Escherichia coli under glucose-excess conditions but its regulation under glucose limitation or anaerobiosis is poorly defined. Using a ptsG-lacZ transcriptional fusion, ptsG expression was found to peak with low (micromolar) external glucose levels in glucose-limited chemostats, so PtsG is primed to contribute to glucose scavenging under hunger response conditions. This regulatory pattern was confirmed using methyl- alpha-glucoside transport assays of PtsG-dependent transport. The regulation of ptsG by cAMP contributed to the optimal expression with micromolar glucose but ptsG was actually repressed to levels below that in glucose-excess batch cultures at very slow growth rates and submicromolar glucose concentrations. RpoS contributed to repression of ptsG in slow-growing bacteria but not under glucose-excess conditions. Also, Mlc increasingly contributed to the repression of ptsG at residual glucose concentrations too low to saturate PtsG. A similar pattern of ptsG regulation was observed in anaerobic cultures with either glucose-excess or glucose-limiting situations.
ptsG基因编码磷酸烯醇式丙酮酸:葡萄糖磷酸转移酶系统的高亲和力葡萄糖受体成分。在葡萄糖过量条件下,PtsG是大肠杆菌中的主要葡萄糖转运蛋白,但其在葡萄糖限制或厌氧条件下的调控尚不清楚。使用ptsG - lacZ转录融合,发现在葡萄糖限制的恒化器中,ptsG表达在低(微摩尔)外部葡萄糖水平时达到峰值,因此PtsG准备好在饥饿反应条件下促进葡萄糖清除。使用依赖PtsG转运的甲基 - α - 葡萄糖苷转运试验证实了这种调控模式。cAMP对ptsG的调控有助于在微摩尔葡萄糖水平下实现最佳表达,但在非常缓慢的生长速率和亚微摩尔葡萄糖浓度下,ptsG实际上被抑制到低于葡萄糖过量分批培养中的水平。RpoS在生长缓慢的细菌中有助于ptsG的抑制,但在葡萄糖过量条件下则不然。此外,在残余葡萄糖浓度过低而无法使PtsG饱和时,Mlc对ptsG抑制的作用越来越大。在葡萄糖过量或葡萄糖限制的厌氧培养物中观察到类似的ptsG调控模式。