DNA amplification--deletion in a spontaneous mutation of the hamster aprt locus: structure and sequence of the novel joint.
DNA amplification--deletion in a spontaneous mutation of the hamster aprt locus: structure and sequence of the novel joint.
复制标题
DNA 扩增——仓鼠 aprt 基因座自发突变的缺失：新关节的结构和序列。
作者：
Josephine Nalbantoglu;M. Meuth
在腺嘌呤磷酸核糖转移酶（aprt）活性缺乏的中国仓鼠卵巢细胞中，发现一个突变体不仅存在aprt编码序列缺失，而且其余序列明显扩增。对携带新关节的HindIII片段进行了克隆和测序，揭示了复杂的基因重排。aprt位点上游至少9kb的缺失，伴随着新关节下游672 bp的侧链序列的反向重复。这个单位被放大三到四倍，一些序列的净结果是由于复制而增加了多达八倍的拷贝数。所涉及的序列的保真度被保留。我们提出了一个可以解释这种反向重复的模型。
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.