Croce C M, Bakay B, Nyhan W L, Koprowski H
Proc Natl Acad Sci U S A. 1973 Sep;70(9):2590-4. doi: 10.1073/pnas.70.9.2590.
Fusion of hypoxanthine phosphoribosyltransferase (HPRT)(-) rat hepatoma cells with HPRT(+) human fibroblasts yielded hybrid clones that grew in HAT selective medium and contained all the rat chromosomes and one to nine human chromosomes. Among the retained chromosomes was the human X chromosome. In all clones backselected in medium containing 8-azaguanine, human X chromosome was absent. Electrophoretic analysis revealed that, without exception, hybrid clones growing in HAT medium had an active HPRT enzyme, either human or rat, or both. When these clones were backselected in 8-azaguanine, they did not show HPRT enzyme activity. Hybrids that contained the human X chromosome also had human glucose-6-phosphate dehydrogenase. The observed reexpression of rat HPRT in hybrid cells derived from HPRT(-) rat cells suggests that a genetic factor from the human cell determined the expression of the rat structural gene for HPRT.
次黄嘌呤磷酸核糖基转移酶（HPRT）缺陷型大鼠肝癌细胞与HPRT阳性的人成纤维细胞融合，产生了能在HAT选择培养基中生长的杂交克隆，这些克隆包含所有大鼠染色体和1至9条人类染色体。保留的染色体中包括人类X染色体。在含8-氮杂鸟嘌呤的培养基中进行回选的所有克隆中，人类X染色体均不存在。电泳分析表明，无一例外，在HAT培养基中生长的杂交克隆具有活性HPRT酶，要么是人类的，要么是大鼠的，或者两者都有。当这些克隆在8-氮杂鸟嘌呤中进行回选时，它们未表现出HPRT酶活性。含有人类X染色体的杂交细胞也具有人类葡萄糖-6-磷酸脱氢酶。在源自HPRT缺陷型大鼠细胞的杂交细胞中观察到大鼠HPRT的重新表达，这表明来自人类细胞的一个遗传因子决定了大鼠HPRT结构基因的表达。
