Differential effect of ionizing radiation on the expression of cyclin A and cyclin B in HeLa cells.
Differential effect of ionizing radiation on the expression of cyclin A and cyclin B in HeLa cells.
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发表时间：
1993-03
期刊：
影响因子：
11.2
通讯作者：
R. Muschel;Hong Bing Zhang;W. Mckenna
中科院分区：
文献类型：
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作者：
R. Muschel;Hong Bing Zhang;W. Mckenna
电离辐射诱导真核细胞G2期延迟。由于有丝分裂周期素需要触发从G2到有丝分裂的过渡，我们选择在HeLa细胞照射后研究它们的表达。在正常周期的HeLa细胞中，细胞周期蛋白A和B的mRNA和蛋白水平在G2/M期急剧上升，并随着有丝分裂的完成而迅速下降。在S/G2交界处cyclin A mRNA的上升略早于cyclin B mRNA的上升。尽管这些分子的表达峰重叠，但细胞周期蛋白A mRNA和蛋白在细胞周期蛋白B之前减少。在S中照射后，细胞周期蛋白A mRNA和蛋白水平以与对照相同的动力学上升，但最终超过了对照人群中观察到的水平。细胞周期蛋白A的mRNA和蛋白水平在整个G2延迟辐射诱导保持高水平。与此相反，细胞周期蛋白B的mRNA和蛋白水平并没有上升，因为辐射的细胞进入G2/M。只有在受照射的细胞从G2/M期退出之前，细胞周期蛋白B的水平才达到未受照射的对照组中所见的水平。细胞周期蛋白B mRNA和蛋白表达的下降与辐射剂量成反比。这些数据表明，导致G2延迟的照射似乎在细胞周期蛋白A产生之后但在细胞周期蛋白B可以完全表达之前的某个点阻断细胞，并且细胞不会从延迟中退出，直到细胞周期蛋白B再次表达。因此，细胞周期蛋白A和细胞周期蛋白B表达对辐射的反应不同，细胞周期蛋白A与对照组同时升高，甚至比对照组中观察到的水平更高，而细胞周期蛋白B显示表达的时间延迟。
Ionizing radiation induces a G2 delay in eukaryotic cells. Since mitotic cyclins are required to trigger the transition from G2 into and through mitosis, we chose to investigate their expression after irradiation in HeLa cells. In normally cycling HeLa cells, both cyclin A and B mRNA and protein levels rise dramatically in G2/M and rapidly fall coincident with the completion of mitosis. The rise of cyclin A mRNA at the S/G2 boundary slightly precedes that of cyclin B mRNA. Although the peaks of expression of each of these molecules overlap, cyclin A mRNA and protein diminish before cyclin B. After irradiation in S, cyclin A mRNA and protein levels rose with the same kinetics as in the controls, but ultimately exceeded the levels seen in the control population. Cyclin A mRNA and protein levels remained high throughout the G2 delay induced by irradiation. In contrast, cyclin B mRNA and protein levels did not rise as the irradiated cells entered G2/M. Only later, before the irradiated cells exited from G2/M, did levels of cyclin B reach the levels seen in the unirradiated controls. The decreased amount of cyclin B mRNA and protein was inversely proportional to the dose of radiation. These data indicate that irradiation that results in a G2 delay appears to block cells at a point after production of cyclin A but before cyclin B can be fully expressed and that cells do not exit from the delay until cyclin B is again expressed. Thus, cyclin A and cyclin B expression respond differentially to radiation, with cyclin A rising at the same time as the control and to even higher levels than that seen in the controls, whereas cyclin B shows a temporal delay in expression.