Shcherbakova P V, Pavlov Y I
Department of Genetics, State University of Sankt-Petersburg, Russia.
Mutagenesis. 1993 Sep;8(5):417-21. doi: 10.1093/mutage/8.5.417.
The mutational specificity of the base analog 6-N-hydroxylaminopurine (HAP) was studied in the URA3 gene of the yeast Saccharomyces cerevisiae. Twenty-nine independent HAP-induced ura3 mutations were sequenced. GC-->AT transitions were found most frequently (21 out of 29) while AT-->GC transitions were less abundant (five out of 29). Three GC-->TA transversions were also detected. Two interesting features of DNA context were revealed for transition mutations. One third of the transitions occurred at one site within short direct imperfect repeats converting them to perfect repeats. A model involving complementary interaction of imperfect repeats is proposed to explain the origin of these mutations. Nearly all of the rest of the GC-->AT as well as the AT-->GC transitions were found in the runs of several identical base pairs, predominantly in the middle or at the 3' template nucleotide of (G)n and (A)n runs.
在酿酒酵母的URA3基因中研究了碱基类似物6-N-羟基氨基嘌呤（HAP）的突变特异性。对29个独立的HAP诱导的ura3突变进行了测序。发现GC→AT转换最为频繁（29个中有21个），而AT→GC转换则较少（29个中有5个）。还检测到3个GC→TA颠换。对于转换突变，揭示了DNA上下文的两个有趣特征。三分之一的转换发生在短的直接不完全重复序列中的一个位点，将它们转换为完美重复序列。提出了一个涉及不完全重复序列互补相互作用的模型来解释这些突变的起源。几乎所有其余的GC→AT以及AT→GC转换都出现在几个相同碱基对的序列中，主要在（G）n和（A）n序列的中间或3'模板核苷酸处。
