Sclafani R A, Wechsler J A, Schuster H
Mol Gen Genet. 1981;182(1):112-8. doi: 10.1007/BF00422776.
Exploitation of the ability of the ban protein encoded by phage P1 to compensate for dnaB-defective host mutations, allowed the isolation of dnaB::Tn10 insertion mutations. The presence of P1bac prophage was required for survival of dnaB::Tn10 mutants, and such lysogens were cryosensitive. The insertions were shown to map in dnaB by transduction and this was confirmed by complementation analysis. The dnaB::Tn10 (P1bac) strains were non-permissive for lambda growth but did support the growth of lambda-dnaB+ specialized transducing phage. No antigenically active dnaB product could be detected by immunologic assays using either of two methods. In addition, it was shown that the observe cryosensitivity of P1bac suppression was a direct result of reversible inactivation of the ban protein at low temperature.
利用噬菌体P1编码的ban蛋白补偿dnaB缺陷型宿主突变的能力，得以分离出dnaB::Tn10插入突变。dnaB::Tn10突变体的存活需要P1bac原噬菌体的存在，且此类溶原菌对低温敏感。通过转导表明插入位点在dnaB中，这通过互补分析得到了证实。dnaB::Tn10（P1bac）菌株不允许λ噬菌体生长，但确实支持λ-dnaB+特异性转导噬菌体的生长。使用两种方法中的任何一种进行免疫测定，均未检测到具有抗原活性的dnaB产物。此外，研究表明观察到的P1bac抑制的低温敏感性是低温下ban蛋白可逆失活的直接结果。
