Dorado G, Steingrimsdottir H, Arlett C F, Lehmann A R
MRC Cell Mutation Unit, University of Sussex, Falmer, Brighton, U.K.
J Mol Biol. 1991 Jan 20;217(2):217-22. doi: 10.1016/0022-2836(91)90533-c.
We have isolated and characterized 47 ultraviolet light-induced hprt mutants from a simian virus 40-transformed excision-repair-deficient xeroderma pigmentosum cell line (complementation group A). Twenty-one independent mutations were found, of which the majority were point mutations. Eleven of these were identified as base changes, nine of which could be attributed to ultraviolet damage on the transcribed DNA strand. Both transitions and transversions were found among the single base changes. A large proportion of the mutations (13/21) resulted in aberrant splicing of the hprt gene, suggesting that the target size for mutations resulting in aberrant splicing must be quite large. A small number of spontaneous mutations were identified, most of which were large deletions. Our data provide a spectrum for the intrinsic mutations resulting from ultraviolet damage in human cells in the absence of repair.
我们从一株猿猴病毒40转化的、切除修复缺陷的着色性干皮病细胞系(互补组A)中分离并鉴定了47个紫外线诱导的次黄嘌呤磷酸核糖转移酶(hprt)突变体。发现了21个独立的突变,其中大多数是点突变。其中11个被鉴定为碱基变化,其中9个可归因于转录DNA链上的紫外线损伤。在单碱基变化中发现了转换和颠换。很大一部分突变(13/21)导致hprt基因的异常剪接,这表明导致异常剪接的突变靶标大小一定相当大。鉴定出少量自发突变,其中大多数是大的缺失。我们的数据提供了在没有修复的情况下人类细胞中紫外线损伤导致的内在突变谱。