Patterson D
Somatic Cell Genet. 1975 Jan;1(1):91-110. doi: 10.1007/BF01538734.
Purine biosynthesis was studied in 8 mutants of Chinese hamster cells which require purines for growth and in wild-type cells which do not show this nutritional requirement. Of these, 6 mutants, ade-B, ade-D, ade-E, ade-F, GAT-, and AT-, were shown to accumulate metabolic intermediates not accumulated by wild-type cells. These intermediates were shown to be compounds unique to the adenylic acid biosynthetic pathway by the following criteria: (a) their radioisotopic labeling properties, (b) their response to agents which specifically inhibit known enzymatic steps in the pathway, (c) their chromatographic properties, and (d) spectrophotometric analysis. Two mutants, ade-A and ade-C, accumulate no detectable compounds not accumulated by the wild type. These 2 mutants are believed to be defective in steps very early in the purine biosynthetic pathway. The sites of the defects in the other mutants are proposed, and the usefulness of these mutants is discussed.
在中国仓鼠细胞的8个突变体和野生型细胞中研究了嘌呤生物合成。这些突变体需要嘌呤才能生长，而野生型细胞则无此营养需求。其中，6个突变体ade-B、ade-D、ade-E、ade-F、GAT-和AT-被证明会积累野生型细胞不积累的代谢中间体。通过以下标准表明这些中间体是腺苷酸生物合成途径特有的化合物：（a）它们的放射性同位素标记特性；（b）它们对特异性抑制该途径中已知酶促步骤的试剂的反应；（c）它们的色谱特性；（d）分光光度分析。两个突变体ade-A和ade-C不积累野生型细胞未积累的可检测化合物。据信这两个突变体在嘌呤生物合成途径非常早期的步骤中存在缺陷。提出了其他突变体的缺陷位点，并讨论了这些突变体的用途。
