Bezanson G S, Iyer V N
J Bacteriol. 1975 Jul;123(1):147-53. doi: 10.1128/jb.123.1.147-153.1975.
F-prime derivatives of the Escherichia coli strain CR34 bearing the thermosensitivity mutation dnaB43 display low levels of plasmid-determined superinfection inhibition in conjugational crosses at 30 C. Salt-mediated phenotypic suppression of this temperature sensitivity fails to restore normal levels of inhibition, indicating its alteration is not a secondary effect of dnaB43 a-tion on growth or deoxyribonucleic acid syntheiss. Superinfection inhibition is fully restored in mutant cells made merodiploid for the dnaB region by introduction of the F' dnaB-+ plasmid F134-1. dnaB43-bearing strains lysogenized with P1 phage contribution dnaB-analogue protein show eight to nine times more superinfection inhibition than do the same cells carrying P1 prophage repressed dnaB-analogue protein production. Taken together, this evidence suggests a direct causal relationship between dnaB43 and the altered superinfection inhibition phenotype.
携带热敏感突变dnaB43的大肠杆菌CR34菌株的F'衍生物在30℃的接合杂交中表现出低水平的质粒决定的超感染抑制。盐介导的这种温度敏感性的表型抑制未能恢复正常的抑制水平，表明其改变不是dnaB43对生长或脱氧核糖核酸合成作用的次要效应。通过引入F' dnaB +质粒F134 - 1，使dnaB区域成为部分二倍体的突变细胞中，超感染抑制完全恢复。用P1噬菌体溶源化的携带dnaB43的菌株，其产生dnaB类似蛋白时的超感染抑制比携带P1原噬菌体抑制dnaB类似蛋白产生的相同细胞高八到九倍。综上所述，这些证据表明dnaB43与改变的超感染抑制表型之间存在直接因果关系。
