Anderson D D, Beckmann R P, Harms E H, Nakamura K, Weber M J
J Virol. 1981 Jan;37(1):445-58. doi: 10.1128/JVI.37.1.445-458.1981.
We have isolated mutants of Rous sarcoma virus from an unmutagenized stock of the Schmidt-Ruppin strain of Rous sarcoma virus. These mutants induce only a "partial" transformation, and the transformation properties induced show unusual properties or combinations. Cells infected with mutant CU2 have a unique "blebby" morphology, have lost surface fibronectin, form very small colonies in soft agar, and are nearly normal with respect to adhesiveness and hexose transport. Cells infected with mutant tsCU11 have a nearly normal morphology, but grow well in soft agar. Cells infected with mutant CU12 have a fusiform morphology, intermediate levels of hexose transport and fibronectin, and form very large colonies in soft agar. Because the appearance of the different parameters of transformation is dissociated in these mutant-infected cells, these data are interpreted as supporting a model in which the transforming protein pp60src interacts with more than one primary target in generating the transformed phenotype. All of the mutants display levels of pp60src kinase activity less than that of the wild type. In the case of mutant CU12, the lower kinase activity is in part a consequence of a lower steady-state amount of pp60src inside the cell.
我们从劳斯肉瘤病毒施密特 - 鲁平株未经诱变处理的病毒株中分离出了突变体。这些突变体仅诱导“部分”转化，且所诱导的转化特性表现出异常特性或组合。感染突变体CU2的细胞具有独特的“泡状”形态，表面纤连蛋白缺失，在软琼脂中形成非常小的菌落，并且在黏附性和己糖转运方面几乎正常。感染突变体tsCU11的细胞形态近乎正常，但在软琼脂中生长良好。感染突变体CU12的细胞呈梭形形态，己糖转运和纤连蛋白水平中等，并且在软琼脂中形成非常大的菌落。由于在这些感染突变体的细胞中转化的不同参数的出现是分离的，这些数据被解释为支持一种模型，即在产生转化表型的过程中，转化蛋白pp60src与不止一个主要靶点相互作用。所有突变体的pp60src激酶活性水平均低于野生型。就突变体CU12而言，较低的激酶活性部分是细胞内pp60src稳态量较低的结果。
