Nalbantoglu J, Meuth M
Nucleic Acids Res. 1986 Nov 11;14(21):8361-71. doi: 10.1093/nar/14.21.8361.
In a collection of spontaneous mutants of Chinese hamster ovary cells selected for deficiency in adenine phosphoribosyl transferase (aprt) activity, one was detected having not only a deletion of aprt coding sequences but also an apparent amplification of remaining sequences. The HindIII fragment bearing the novel joint was cloned and sequenced revealing a complex gene rearrangement. A deletion of at least 9 kb extending upstream from the aprt locus is accompanied by an inverted duplication of flanking sequences 672 bp downstream from the novel joint. This unit is amplified three to four times with the net result of some sequences being increased as much as eight fold in copy number because of the duplication. The fidelity of the sequences involved is preserved. We propose a model which could account for this inverted duplication.
在一组为腺嘌呤磷酸核糖转移酶（aprt）活性缺陷而选择的中国仓鼠卵巢细胞自发突变体中，检测到一个不仅缺失了aprt编码序列，而且剩余序列明显扩增。携带新连接点的HindIII片段被克隆并测序，揭示了一个复杂的基因重排。从aprt基因座上游至少延伸9 kb的缺失伴随着新连接点下游672 bp侧翼序列的反向重复。这个单元扩增了三到四倍，由于重复，一些序列的净结果是拷贝数增加了八倍。所涉及序列的保真度得以保留。我们提出了一个可以解释这种反向重复的模型。
