Parry G, Bartholomew J C, Bissell M J
Nature. 1980 Dec 25;288(5792):720-2. doi: 10.1038/288720a0.
We report here a study of the mechanisms leading to loss of growth control in chicken embryo fibroblasts transformed by Rous sarcoma virus (RSV). We have been particularly concerned with the role of the src gene in this process, and have used RSV mutants temperature sensitive (ts) for transformation to investigate the nature of the growth regulatory lesion. The two principal findings were (1) the stationary phase of the cell cycle (G1) in chick embryo fibroblasts seems to have two distinct regulatory compartments (using the terminology of Brooks et al. we refer to these as 'Q' and 'A' states). When rendered stationary at 41.5 degrees C by serum deprivation, normal cells enter a Q state, but cells infected with the ts-mutant occupy an A state. (2) Whereas normal cells can occupy either state depending on culture conditions, the ts-infected cells, at 41.5 degrees C, do not seem to enter Q even though a known src gene product, a kinase, is reported to be inactive at this temperature. We discuss the possibility that viral factors other than the active src protein kinase influence growth control in infected cultures.
我们在此报告一项关于劳斯肉瘤病毒（RSV）转化的鸡胚成纤维细胞生长控制丧失机制的研究。我们特别关注src基因在此过程中的作用，并使用对转化温度敏感（ts）的RSV突变体来研究生长调节损伤的本质。两个主要发现是：（1）鸡胚成纤维细胞细胞周期的静止期（G1）似乎有两个不同的调节区室（使用布鲁克斯等人的术语，我们将其称为“Q”和“A”状态）。当通过血清剥夺在41.5摄氏度下使其静止时，正常细胞进入Q状态，但感染ts突变体的细胞占据A状态。（2）正常细胞可根据培养条件处于任何一种状态，而在41.5摄氏度下，感染ts的细胞似乎不会进入Q状态，尽管据报道一种已知的src基因产物，即一种激酶，在此温度下无活性。我们讨论了除活性src蛋白激酶之外的病毒因子影响感染培养物中生长控制的可能性。
