Hutchinson F, Stein J
Mol Gen Genet. 1977 Mar 28;152(1):29-36. doi: 10.1007/BF00264936.
Mutagenesis by 5-bromouracil of lambda phage to clear plaque formers does not depend on the recA function of the host E. coli cell or on the red function of the phage. Pretreatment of the host cells with ultraviolet light does not affect bromouracil mutagenesis of the adsorbed phage. Mutagenesis by hydroxlamine to clear plaque formers takes place at a high level in recA- host cells, and is not changed by preirradiation of of rec+ (wild type) hosts with ultraviolet light. Thus, bromouracil and hydroxylamine appear to mutate lambda phage by a process which differs from that responsible for ultraviolet mutagenesis. Two characteristics of bromouracil mutagenesis--the nonlinear dependence of the number of mutants on bromouracil incorporation, and a high frequency of heterozygotes--fit in with Rydberg's (1977) picture of bromouracil mutagenesis as a consequence of base mispairing, with mismatch repair removing the mutations at low incorporation of the analog.
用5-溴尿嘧啶使λ噬菌体发生诱变以产生清晰噬菌斑的突变体，这并不依赖于宿主大肠杆菌细胞的recA功能或噬菌体的red功能。用紫外线对宿主细胞进行预处理不会影响吸附噬菌体的5-溴尿嘧啶诱变作用。用羟胺使λ噬菌体产生清晰噬菌斑突变体的诱变作用在recA-宿主细胞中高水平发生，并且rec+（野生型）宿主细胞经紫外线预照射后该诱变作用不变。因此，5-溴尿嘧啶和羟胺似乎通过一种不同于紫外线诱变的过程使λ噬菌体发生突变。5-溴尿嘧啶诱变的两个特征——突变体数量对5-溴尿嘧啶掺入的非线性依赖性以及高频率的杂合子——符合里德伯格（1977年）提出的5-溴尿嘧啶诱变是碱基错配结果的观点，即错配修复在类似物低掺入时会去除突变。
