Armel P, Williams G M
American Health Foundation, Valhalla, NY 10595.
Mutat Res. 1988 Nov;202(1):147-53. doi: 10.1016/0027-5107(88)90176-5.
The molecular nature of mutations in 6-thioguanine-resistant hypoxanthine/guanine phosphoribosyl transferase (HGPRT)-deficient clones of an adult rat liver (ARL) epithelial cell line mutated by benzo[a]pyrene or aflatoxin B1 was studied. DNA from these clones or spontaneous HGPRT-deficient mutants was subjected to Southern blotting using an HGPRT probe following DNA digestion with the restriction enzymes BamH1, EcoR1, HindIII or XbaI. With either the chemically induced or spontaneous mutants, no difference in restriction fragment pattern was observed between any of the mutants and their wild-type parent. However, differences were found between two lines ARL 6 and ARL 14 and the lines ARL 18, ARL 19 and DNA from Fischer rat hepatocytes. Although the variants did not display loss of HGPRT activity. It is suggested that deletion or loss of a pseudogene sequence could be the basis for the alterations in restriction fragment patterns.
对经苯并[a]芘或黄曲霉毒素B1诱变的成年大鼠肝脏(ARL)上皮细胞系的6-硫鸟嘌呤抗性次黄嘌呤/鸟嘌呤磷酸核糖转移酶(HGPRT)缺陷型克隆中的突变分子性质进行了研究。在用限制性内切酶BamH1、EcoR1、HindIII或XbaI消化DNA后,使用HGPRT探针,对这些克隆或自发HGPRT缺陷型突变体的DNA进行Southern印迹分析。无论是化学诱导突变体还是自发突变体,在任何突变体与其野生型亲本之间均未观察到限制性片段模式的差异。然而,在两条细胞系ARL 6和ARL 14与细胞系ARL 18、ARL 19以及Fischer大鼠肝细胞的DNA之间发现了差异。尽管这些变体并未表现出HGPRT活性的丧失。据推测,假基因序列的缺失或丢失可能是限制性片段模式改变的基础。