Konevega L V, Kalinin V L
Genetika. 1985 Jul;21(7):1105-10.
Survival of phage lambda cI857 inactivated by bisulfite (pH 5.6, 37 degrees C) is higher (the dose modification factor approx. 1.2) and frequency of bisulfite-induced c-mutations 2-4-fold lower on the lawn of the wild-type strain ung+, as compared to ung-1 mutant deficient in uracil-DNA glycosylase. Irradiation of host cells by a moderate UV dose inducing SOS repair system enhances the frequency of bisulfite-induced c-mutations 2-3-fold in the wild-type (ung+) host, but not in the ung-1 mutant. It is suggested that W-mutagenesis in bisulfite-treated lambda phage in the ung+ cells is due to SOS repair of apyrimidinic sites which are produced during excision of uracil residues, the products of cytosine deamination.
在亚硫酸氢盐（pH 5.6，37℃）作用下失活的λ噬菌体cI857，在野生型ung +菌株的菌苔上存活率更高（剂量修正因子约为1.2），且亚硫酸氢盐诱导的c突变频率比缺乏尿嘧啶-DNA糖基化酶的ung-1突变体低2至4倍。适度紫外线剂量照射宿主细胞以诱导SOS修复系统，可使野生型（ung +）宿主中亚硫酸氢盐诱导的c突变频率提高2至3倍，但在ung-1突变体中则不会。这表明在ung +细胞中，经亚硫酸氢盐处理的λ噬菌体中的W诱变是由于尿嘧啶残基切除过程中产生的无嘧啶位点的SOS修复，尿嘧啶残基是胞嘧啶脱氨的产物。
