Expression of the Uhp Sugar-Phosphate Transport System of Escherichia coli
Expression of the Uhp Sugar-Phosphate Transport System of Escherichia coli
复制标题
大肠杆菌超高压糖磷酸转运系统的表达
DOI：
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发表时间：
1995
期刊：
影响因子：
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通讯作者：
R. Kadner
中科院分区：
文献类型：
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作者：
R. Kadner
本章综述了Uhp系统的调节，这是一种糖-磷酸转运蛋白，其表达由外部葡萄糖6-磷酸（Glu 6P）诱导。在许多革兰氏阳性和革兰氏阴性细菌中存在有机磷转运系统，这表明它们的有机磷底物是广泛可用的。在大肠杆菌或鼠伤寒沙门氏菌中分析了几种有机磷转运系统。UhpT的表达也作为OxyR过氧化物反应系统的一部分发生。正如预期的那样，uhpA的缺失导致可检测的uhpT表达的完全缺失。如果截短的变体保留uhpA的阻遏，但缺乏激活uhpT转录的能力，则解释了显性负性行为，类似于LuxR中的情况。接头取代突变（其中-64区域中的天然序列转化为NcoI限制性位点）降低或消除启动子功能，这取决于取代的位置和改变的碱基对残基的数量。已发现分解代谢物基因激活蛋白（CAP）的几个表面暴露区域对于CAP依赖性启动子的转录激活是必需的，所述启动子不需要其他转录激活蛋白的作用。不直接通过糖酵解代谢的糖磷酸盐也抑制这些细胞的生长，但不引起细胞杀伤或甲基乙二醛的产生。
This chapter reviews the regulation of the Uhp system, which is a sugar-phosphate transport protein whose expression is induced by external glucose 6-phosphate (Glu6P). The presence of organophosphate transport systems in many gram-positive and gram-negative bacteria suggests that their organophosphate substrates are widely available. Several organophosphate transport systems have been analyzed in Escherichia coli or Salmonella typhimurium. Expression of UhpT also occurs as part of the OxyR peroxide response system. As expected, loss of uhpA resulted in complete loss of detectable uhpT expression. The dominant negative behavior is explained if the truncated variants retain repression of uhpA but lack the ability to activate transcription of uhpT, analogous to the situation in LuxR. Linker substitution mutations in which the native sequences in the -64 region are converted to an NcoI restriction site reduced or eliminated promoter function, depending on the location of the substitution and the number of base pair residues that were changed. Several surface-exposed regions of the catabolite gene activator protein (CAP) have been found to be necessary for transcription activation at CAP-dependent promoters that do not require the action of other transcription activator proteins. Sugar phosphates that are not directly metabolized by glycolysis also inhibit growth of those cells but do not elicit cell killing or methylglyoxal production.
影响因子：
2.9
作者：
VOLZ, K
通讯作者：
VOLZ, K