Miyada C G, Sheppard D E, Wilcox G
J Bacteriol. 1983 Nov;156(2):765-72. doi: 10.1128/jb.156.2.765-772.1983.
Five mutations that result in reduced expression of the araBAD operon were cloned onto the plasmid pBR322. The position of each mutation was determined by DNA sequence analysis. Three of the mutations were located in the RNA polymerase binding site of the araBAD promoter. The first, ara-1016, was a one-base-pair deletion at position -35; the second, ara-1036, was a transversion at position -13; the third, ara-1027, was a nine-base-pair deletion from +5 to +13. S1 nuclease mapping showed that mutations ara-1016 and ara-1036 greatly reduced transcription and that mutation ara-1027 had little, if any, effect on transcription. Two other mutations resulted from the transposition of the insertion element, IS1, downstream from the transcriptional start site of the operon. Molecular mechanisms for all of the mutations are discussed.
导致阿拉伯糖操纵子（araBAD operon）表达降低的五个突变被克隆到质粒pBR322上。通过DNA序列分析确定了每个突变的位置。其中三个突变位于araBAD启动子的RNA聚合酶结合位点。第一个突变ara - 1016在 - 35位发生了一个碱基对的缺失；第二个突变ara - 1036在 - 13位发生了一个颠换；第三个突变ara - 1027在 + 5到 + 13位有一个九个碱基对的缺失。S1核酸酶图谱分析表明，突变ara - 1016和ara - 1036极大地降低了转录，而突变ara - 1027对转录几乎没有影响（如果有影响的话也很小）。另外两个突变是由于插入元件IS1转座到操纵子转录起始位点下游所致。文中讨论了所有突变的分子机制。
