Vinella D, Cashel M, D'Ari R
Institut Jacques Monod (CNRS, Université Paris 7, Université Paris 6), 75251 Paris Cedex 05, France.
Genetics. 2000 Dec;156(4):1483-92. doi: 10.1093/genetics/156.4.1483.
Rapidly growing Escherichia coli is unable to divide in the presence of the antibiotic mecillinam, whose direct target is penicillin-binding protein 2 (PBP2), responsible for the elongation of the cylindrical portion of the cell wall. Division can be restored in the absence of PBP2 activity by increasing the concentration of the cell division proteins FtsQ, FtsA, and FtsZ. We tried to identify regulators of the ftsQ-ftsA-ftsZ operon among mecillinam-resistant mutants, which include strains overexpressing these genes. By insertional mutagenesis with mini-Tn10 elements, we selected for insertions that conferred mecillinam resistance. Among 15 such mutants, 7 suppressed the thermosensitivity of the ftsZ84(Ts) mutant, strongly suggesting that they had increased FtsZ activity. In all 7 cases, however, the mutants resulted from a duplication of the ftsQAZ region. These duplications seemed to result from multiple events, suggesting that no simple insertional inactivation can result in a mutant with sufficiently amplified ftsQAZ expression to confer mecillinam resistance. The structure of the duplications suggests a general method for constructing directed duplications of precise sequences.
快速生长的大肠杆菌在抗生素美西林存在的情况下无法分裂,美西林的直接靶点是青霉素结合蛋白2(PBP2),它负责细胞壁圆柱形部分的延伸。通过增加细胞分裂蛋白FtsQ、FtsA和FtsZ的浓度,在没有PBP2活性的情况下可以恢复分裂。我们试图在耐美西林突变体中鉴定ftsQ-ftsA-ftsZ操纵子的调节因子,其中包括过表达这些基因的菌株。通过用mini-Tn10元件进行插入诱变,我们筛选出赋予美西林抗性的插入。在15个这样的突变体中,7个抑制了ftsZ84(Ts)突变体的温度敏感性,强烈表明它们具有增强的FtsZ活性。然而,在所有7个案例中,突变体是由ftsQAZ区域的重复产生的。这些重复似乎是由多个事件导致的,这表明没有简单的插入失活能够产生一个具有足够扩增的ftsQAZ表达以赋予美西林抗性的突变体。重复的结构提示了一种构建精确序列定向重复的通用方法。