Participation of the purine repressor in control of the carbamoylphosphate synthetase operon in Salmonella typhimurium.
Participation of the purine repressor in control of the carbamoylphosphate synthetase operon in Salmonella typhimurium.
复制标题
嘌呤阻遏物参与鼠伤寒沙门氏菌中氨基甲酰磷酸合成酶操纵子的控制。
DOI：
10.1111/j.1365-2958.1995.mmi_17050981.x
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发表时间：
1995
影响因子：
3.6
通讯作者：
Abdelal,AT
中科院分区：
文献类型：
--
作者：
Lu,CD;Katzif,S;Abdelal,AT
先前的研究表明，鼠伤寒沙门氏菌的carAB操纵子是由串联启动子P1和P2转录的，它们分别由嘧啶和精氨酸负控制。本文报道的结果表明，嘌呤也负调控carAB的表达，而这种作用在apurR：：Tn10衍生物中不存在。引物延伸实验确定嘌呤效应在P1发挥作用，从而将该启动子重新定义为对嘌呤和嘧啶敏感。凝胶阻滞实验以及DNA酶I和预甲基化足迹的结果表明，嘌呤阻遏物与P1上游85 bp的PUR盒相互作用。通过定点突变修饰该PUR盒消除了阿卡拉：：lacZ融合中嘌呤的抑制，证实了该盒在carAB表达的体内嘌呤控制中发挥作用。
Previous work has shown that thecarABoperon ofSalmonella typhimuriumis transcribed from tandem promoters, P1 and P2, that are negatively controlled by pyrimidines and arginine, respectively. The results reported here show that purines also negatively control expression ofcarABand that this effect is absent in apurR::Tn10derivative. Primer‐extension experiments established that the purine effect is exerted at P1, thus redefining this promoter as sensitive to both purines and pyrimidines. The results of gel‐retardation experiments as well as DNase I and premethylation footprintings indicate that the purine repressor interacts with a PUR box 85 bp upstream of P1. Modification of this PUR box by site‐directed mutagenesis abolishes the repression by purines in acarA::lacZfusion, confirming that this box functionsin vivoin purine control ofcarABexpression.