二倍体人类淋巴母细胞中的表型滞后及对6-硫鸟嘌呤抗性的突变
Phenotypic lag and mutation to 6-thioguanine resistance in diploid human lymphoblasts.
作者信息
Thilly W G, Deluca J G, Hoppe H, Penman B W
出版信息
Mutat Res. 1978 Apr;50(1):137-44. doi: 10.1016/0027-5107(78)90068-4.
Mutants of a diploid human lymphoblast line resistant to 6-thioguanine (6TG) appear 6--16 generations after treatment with any of a diverse group of mutagents: methylnitrosourea (MNU), methylnitrosoguanidine (MNNG), ICR-191, 5-bromodeoxyuridine (BUdR). A hypothesis is advanced that expression of the 6-thioguanine-resistant state may require the removal of essentially all pre-existing hypoxanthine--guanine phosphoribosyl transferase (HGPRT) molecules via division, dilution, and protein turnover. Design of protocols for quantitative mutation assays requires attention to this phenomenon.
在用人的二倍体淋巴母细胞系进行实验时，用多种诱变剂（甲基亚硝基脲、甲基亚硝基胍、ICR - 191、5 - 溴脱氧尿苷）中的任何一种处理后，对6 - 硫鸟嘌呤（6TG）有抗性的突变体在6至16代后出现。提出了一种假说，即6 - 硫鸟嘌呤抗性状态的表达可能需要通过分裂、稀释和蛋白质周转基本上去除所有预先存在的次黄嘌呤 - 鸟嘌呤磷酸核糖转移酶（HGPRT）分子。定量突变试验方案的设计需要关注这一现象。
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