Tyson K L, Bell A I, Cole J A, Busby S J
School of Biochemistry, University of Birmingham, UK.
Mol Microbiol. 1993 Jan;7(1):151-7. doi: 10.1111/j.1365-2958.1993.tb01106.x.
Transcription initiation at the Escherichia coli nirB promoter is induced by anaerobic growth and further increased by the presence of nitrite or nitrate in the growth medium. Expression from this promoter is totally dependent on the transcription factor, FNR, which binds between positions -52 and -30 upstream of the transcription startsite. The 20 base pairs from position -79 to -60 contain an inverted repeat of two 10-base sequence elements that are related to sequences at the NarL-binding site at the E. coli narG promoter. Comparison of these, and sequence elements at other promoters regulated by NarL, suggests a consensus NarL-binding sequence. Mutations in the putative NarL-binding site at the nirB promoter decrease FNR-dependent anaerobic induction, suggesting that NarL acts as a helper to FNR during transcription activation. These mutations also suppress induction by nitrite: single mutations at symmetry-related positions have similar effects, whilst double mutations have more severe effects, probably because two NarL subunits bind to the inverted repeat. Disruption of narL decreases nitrite induction of the nirB promoter whilst not suppressing induction by nitrate, suggesting that there may be a second nitrate-responsive factor. Nitrate induction was, however, suppressed by double mutations at symmetry-related positions in the NarL-binding site, suggesting that this putative second factor may bind to sequences similar to those recognized by NarL.
大肠杆菌nirB启动子的转录起始由厌氧生长诱导,并且在生长培养基中存在亚硝酸盐或硝酸盐时会进一步增强。该启动子的表达完全依赖于转录因子FNR,FNR结合在转录起始位点上游-52至-30位之间。从-79至-60位的20个碱基对包含两个10碱基序列元件的反向重复,这些元件与大肠杆菌narG启动子处NarL结合位点的序列相关。对这些以及由NarL调控的其他启动子处的序列元件进行比较,得出了一个共有NarL结合序列。nirB启动子处假定的NarL结合位点发生突变会降低FNR依赖性厌氧诱导,这表明在转录激活过程中,NarL作为FNR的辅助因子发挥作用。这些突变也抑制了亚硝酸盐的诱导作用:对称相关位置的单突变具有相似的效果,而双突变具有更严重的影响,这可能是因为两个NarL亚基结合到反向重复序列上。narL的缺失降低了nirB启动子的亚硝酸盐诱导作用,但不抑制硝酸盐的诱导作用,这表明可能存在第二个硝酸盐反应因子。然而,NarL结合位点对称相关位置的双突变抑制了硝酸盐诱导,这表明这个假定的第二个因子可能结合到与NarL识别的序列相似的序列上。