Paterson Laboratories, Christie Hospital and Holt Radium Institute, Manchester M20 9BX, UK.
Carcinogenesis. 1980 Feb;1(2):189-98. doi: 10.1093/carcin/1.2.189.
A spontaneous TG(R) HAT(s) V79 mutant had an HGPRT specific activity of less than 5% that of the wild type. Only two spontaneous revertants were recovered from more than 10(8) mutant cells screened. However, HAT resistant clones were recovered, after EMS mutagenesis at a frequency of 4.5 x 10(-6) and at a lower frequency from u.v. irradiated mutant cells. Of more than 400 clones tested, over 90% had regained a HAT(R) TG(s) HGPRT(+) revertant phenotype. Nine of these revertants that were further characterised had HGPRT specific activities within the wild type range and showed wild type electrophoretic mobility. These data suggest that the original HGPRT(-) phenotype was of a mutational rather than an adaptational origin.
自发的 TG(R) HAT(s) V79 突变体的 HGPRT 比活度低于野生型的 5%。从筛选的 10(8)个以上突变细胞中仅回收了两个自发回复突变体。然而,在用 EMS 诱变以 4.5 x 10(-6)的频率和从 u.v. 照射的突变细胞以较低频率处理后,回收了 HAT 抗性克隆。在测试的 400 多个克隆中,超过 90%的克隆恢复了 HAT(R) TG(s) HGPRT(+)回复突变表型。对其中 9 个进一步表征的回复突变体的 HGPRT 比活度在野生型范围内,并表现出野生型电泳迁移率。这些数据表明,最初的 HGPRT(-)表型是突变而不是适应性起源。