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AmpG,一种参与染色体β-内酰胺酶诱导的信号转导蛋白。

AmpG, a signal transducer in chromosomal beta-lactamase induction.

作者信息

Lindquist S, Weston-Hafer K, Schmidt H, Pul C, Korfmann G, Erickson J, Sanders C, Martin H H, Normark S

机构信息

Department of Microbiology, University of Umeå, Sweden.

出版信息

Mol Microbiol. 1993 Aug;9(4):703-15. doi: 10.1111/j.1365-2958.1993.tb01731.x.

Abstract

The chromosomal ampC beta-lactamase in Citrobacter freundii and Enterobacter cloacae is inducible by beta-lactam antibiotics. When an inducible ampC gene is introduced on a plasmid into Escherichia coli together with its transcriptional regulator ampR, the plasmid-borne beta-lactamase is still inducible. We have isolated mutants, containing alterations in a novel E. coli gene, ampG, in which a cloned C. freundii ampC gene is unable to respond to beta-lactam inducers. The ampG gene was cloned, sequenced and mapped to minute 9.6 on the E. coli chromosome. The deduced amino acid sequence predicted AmpG to be a 53 kDa, transmembrane protein, which we propose acts as a signal transducer or permease in the beta-lactamase induction system. Immediately upstream of ampG there is another 579-base-pair-long open reading frame (ORF) encoding a putative lipoprotein shown to be non-essential for beta-lactamase induction. We have found that ampG and this ORF form an operon, whose promoter is located in front of the ORF. Located closely upstream of the putative promoter is the morphogene bolA, which is transcribed in the opposite orientation. However, using transcription fusions, we have found that the ampG transcription is not regulated by bolA. In addition, we show that transcription is probably not regulated by either the starvation specific sigma factor RpoS, which controls bolA, or by AmpD the negative regulator for ampC transcription.

摘要

弗氏柠檬酸杆菌和阴沟肠杆菌中的染色体AmpCβ-内酰胺酶可被β-内酰胺抗生素诱导。当一个可诱导的ampC基因与其转录调节因子ampR一起通过质粒导入大肠杆菌时,质粒携带的β-内酰胺酶仍可被诱导。我们分离出了一些突变体,这些突变体在一个新的大肠杆菌基因ampG中发生了改变,在这些突变体中,克隆的弗氏柠檬酸杆菌ampC基因无法对β-内酰胺诱导剂作出反应。ampG基因被克隆、测序并定位到大肠杆菌染色体的9.6分钟处。推导的氨基酸序列预测AmpG是一种53 kDa的跨膜蛋白,我们认为它在β-内酰胺酶诱导系统中作为信号转导器或通透酶发挥作用。在ampG的紧邻上游有另一个579个碱基对长的开放阅读框(ORF),其编码一种假定的脂蛋白,已证明该脂蛋白对β-内酰胺酶诱导并非必需。我们发现ampG和这个ORF形成一个操纵子,其启动子位于ORF的前面。在假定启动子的紧邻上游是形态发生基因bolA,它以相反的方向转录。然而,通过转录融合,我们发现ampG的转录不受bolA的调控。此外,我们表明转录可能既不受控制bolA的饥饿特异性σ因子RpoS的调控,也不受ampC转录的负调节因子AmpD的调控。

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