Rønning O W, Lindmo T, Pettersen E O, Seglen P O
J Cell Physiol. 1981 Dec;109(3):411-8. doi: 10.1002/jcp.1041090306.
The cell cycle kinetics of NHIK 3025 cells, synchronized by mitotic selection, was studied in the presence of cycloheximide at concentrations (0.125-1.25 microM) which inhibited protein synthesis partially and slowed down the rate of cell cycle traverse. The median cell cycle duration was equal to the protein doubling time in both the control cells and in the cycloheximide-treated cultures at all drug concentrations. This conclusion was valid whether protein synthesis was continuously depressed by cycloheximide throughout the entire cell cycle, or temporarily inhibited during shorter periods at various stages of the cell cycle. These results may indicate that cell division does not take place before the cell has reached a critical size, or has completed a protein accumulation-dependent sequence of events. When present throughout the cell cycle, cycloheximide increased the median G1 duration proportionally to the total cell cycle prolongation. However, the entry of cells into S, once initiated, proceeded at an almost unaffected rate even at cycloheximide concentrations which reduced the rate of protein synthesis 50%. The onset of DNA synthesis seemed to take place in the cycloheximide-treated cells at a time when the protein content was lower than in the control cells. This might suggest that DNA synthesis in NHIK 3025 cells is not initiated at a critical cell mass.
采用有丝分裂选择法使NHIK 3025细胞同步化，在存在不同浓度（0.125 - 1.25微摩尔）环己酰亚胺的情况下研究其细胞周期动力学，这些浓度可部分抑制蛋白质合成并减缓细胞周期进程速率。在所有药物浓度下，对照细胞以及经环己酰亚胺处理的培养物中，细胞周期的中位数时长均等于蛋白质加倍时间。无论在整个细胞周期中环己酰亚胺持续抑制蛋白质合成，还是在细胞周期不同阶段短时间内暂时抑制蛋白质合成，该结论均成立。这些结果可能表明，细胞在达到临界大小或完成依赖蛋白质积累的一系列事件之前不会发生分裂。当在整个细胞周期中存在时，环己酰亚胺使G1期的中位数时长与总细胞周期延长成比例增加。然而，细胞一旦开始进入S期，即使在环己酰亚胺浓度降低蛋白质合成速率达50%的情况下，其进程速率几乎不受影响。在经环己酰亚胺处理的细胞中，DNA合成开始时蛋白质含量似乎低于对照细胞。这可能表明NHIK 3025细胞中的DNA合成并非在临界细胞质量时启动。
