Kimura H, Higuchi H, Iyehara-Ogawa H, Kato T
Department of Experimental Radiology, Shiga University of Medical Science, Japan.
Radiat Res. 1993 May;134(2):202-8.
Sequences of 38 independent X-ray-induced mutations in a cDNA of the human hypoxanthine phosphoribosyltransferase (hprt) gene were analyzed after it was integrated into mammalian chromosomes as part of a shuttle vector. There were 15 base substitutions (39%), 9 frameshifts (24%), 11 deletions (29%), and 3 other mutations (8%) of two kinds. Radiation-induced mutations were found throughout the coding region of the gene. Base substitution mutations occurred more often at A:T sites than at G:C sites, and there were more transversions than transitions. Most of the frameshifts and deletions had short direct repeats or a run of several identical bases at the site of the mutation. A slippage misalignment mechanism, suggested previously, can account for the generation of these classes of mutations. The kinds, distribution, and possible mechanism of X-ray-induced mutations were similar to those of spontaneous mutations.
将人次黄嘌呤磷酸核糖转移酶(hprt)基因的cDNA作为穿梭载体的一部分整合到哺乳动物染色体中后,对38个独立的X射线诱导突变的序列进行了分析。有15个碱基替换(39%)、9个移码突变(24%)、11个缺失(29%)以及另外两种类型的3个突变(8%)。在该基因的整个编码区域都发现了辐射诱导的突变。碱基替换突变在A:T位点比在G:C位点更常发生,并且颠换比转换更多。大多数移码突变和缺失在突变位点有短的直接重复序列或几个相同碱基的连续排列。先前提出的滑动错配机制可以解释这些类型突变的产生。X射线诱导突变的种类、分布和可能机制与自发突变相似。