作者: Annie Kolb , Yi-Ping Wang , Zhe-Xian Tian , Quan-Sheng Li , Martin Buck
DOI: 10.1046/J.1365-2958.2001.02561.X
关键词: Biology 、 Glutamine synthetase 、 Regulon 、 Downregulation and upregulation 、 Promoter 、 Escherichia coli 、 Gene 、 cAMP receptor protein 、 Primer extension 、 Molecular biology
摘要: In Escherichia coli, glnA (encoding glutamine synthetase) is transcribed from two promoters (glnAp1 and glnAp2). The glnAp1 a sigma(70)-dependent promoter that activated by the cAMP receptor protein (CRP). Under nitrogen-deficient growth conditions, repressed NtrC-phosphate. downstream glnAp2 sigma(54)-dependent Here, we show expression affected different carbon sources CRP-cAMP complex inhibits activity. Primer extension KMnO4 footprinting analysis indicate inhibitory effect at transcriptional level in vivo. When NifA, similar observed. Site-directed mutagenesis deletion characterized putative CRP-binding sites located upstream region of are not essential for effect. strongly, 21-fold. By activating downregulating glnAp2, overall on an approximately fourfold reduction, which correlates with reduction gamma-glutamyl transferase activities cells. We propose therefore physiological role activation to partially compensate downregulation allowing low but non-negligible important genes it. A novel regulatory linkage between nitrogen regulons proposed.