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苄基衍生物对大肠杆菌中阿拉伯糖操纵子和乳糖操纵子启动子转录的促进作用:代谢物基因调控(MGR)

Benzyl derivative facilitation of transcription in Escherichia coli at the ara and lac operon promoters: metabolite gene regulation (MGR).

作者信息

Kline E L, West R W, Ink B S, Kline P M, Rodriguez R L

出版信息

Mol Gen Genet. 1984;193(2):340-8. doi: 10.1007/BF00330691.

Abstract

A number of benzyl derivatives have been tested for their ability to induce the expression of the araBAD operon in an Escherichia coli K-12 strain. Those derivatives shown to be stimulatory include: benzoic acid (BA), para-amino benzoic acid (PABA), para-hydroxy benzoic acid (PHBA), ortho-amino benzoic acid (OABA), 3-hydroxy-4-methoxy phenylethylamine (MTA), and 4-hydroxy-3-methoxyphenol acetic acid (HVA). The araC gene product was necessary to facilitate the induction. To further characterize if the inductive effect was mediated at the level of transcription, an araBAD-tetracycline resistant (Tcr) operon fusion plasmid (pAP-B) was employed. Benzyl derivatives which induce expression of the araBAD operon in situ also induced a Tcr phenotype with pAP-B. Both indole acetic acid (IAA) and imidazole (IM), which were previously shown to circumvent the necessity for cAMP in the induction of the araBAD operon, also induced a Tcr phenotype with pAP-B. Induction of lac or other cAMP responding operons with the inducing molecules at the chromosomal level was not detectable when assessed by carbon utilization. However, a lacZYA-Tcr operon fusion plasmid (pLPI) did respond to IAA and several of the inducing benzyl derivatives. Catabolite repression of chromosomal araBAD expression was reversed when the exogenous concentration of OABA was elevated. Similar effects on the Tcr phenotypes conferred by pAP-B and pLP1 were observed when OABA or several other inducing benzyl derivatives were present exogenously.

摘要

已对多种苄基衍生物诱导大肠杆菌K-12菌株中araBAD操纵子表达的能力进行了测试。显示具有刺激作用的那些衍生物包括:苯甲酸(BA)、对氨基苯甲酸(PABA)、对羟基苯甲酸(PHBA)、邻氨基苯甲酸(OABA)、3-羟基-4-甲氧基苯乙胺(MTA)和4-羟基-3-甲氧基苯酚乙酸(HVA)。araC基因产物对于促进诱导是必需的。为了进一步表征诱导作用是否在转录水平介导,使用了一种araBAD-四环素抗性(Tcr)操纵子融合质粒(pAP-B)。在原位诱导araBAD操纵子表达的苄基衍生物也用pAP-B诱导出Tcr表型。吲哚乙酸(IAA)和咪唑(IM),先前已证明它们在araBAD操纵子的诱导中可规避对cAMP的需求,也用pAP-B诱导出Tcr表型。当通过碳利用评估时,在染色体水平用诱导分子诱导lac或其他cAMP响应操纵子未检测到。然而,一个lacZYA-Tcr操纵子融合质粒(pLPI)确实对IAA和几种诱导性苄基衍生物有反应。当外源性OABA浓度升高时,染色体araBAD表达的分解代谢物阻遏被逆转。当外源性存在OABA或其他几种诱导性苄基衍生物时,观察到对pAP-B和pLP1赋予的Tcr表型有类似影响。

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