SYNERGISTIC ACTION OF DROSOPHILA CYCLIN-A AND CYCLIN-B DURING THE G2-M TRANSITION

SYNERGISTIC ACTION OF DROSOPHILA CYCLIN-A AND CYCLIN-B DURING THE G2-M TRANSITION
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DOI:
10.1002/j.1460-2075.1993.tb05632.x
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发表时间:
1993-01-01
期刊:
影响因子:
11.4
通讯作者:
LEHNER, CF
LEHNER, CF
中科院分区:
生物学1区
文献类型:
--
作者:
KNOBLICH, JA;LEHNER, CF

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在高等真核生物中已经鉴定出多种不同的细胞周期蛋白。在细胞周期蛋白B的情况下,功能分析已经清楚地表明了进入有丝分裂的控制中的重要作用。cyclin A的功能更为复杂。它似乎在S期和M期的控制中起作用。我们在果蝇中的遗传分析结果表明,细胞周期蛋白A具有有丝分裂的功能,它与细胞周期蛋白B在G2-M转换的协同作用。在合子上既不表达细胞周期蛋白A也不表达细胞周期蛋白B的双突变胚胎中,细胞周期进程在母体贡献的细胞周期蛋白A和B储存耗尽之前被阻断。BrdU标记实验表明,细胞周期进程被阻止在G2进入第十五轮有丝分裂之前。来自热诱导转基因的细胞周期蛋白A或B的表达足以克服这种细胞周期阻滞。在缺乏细胞周期蛋白A或B的单突变胚胎中也没有观察到这种阻断。在细胞周期蛋白B缺陷的胚胎中,细胞周期进程在母体贡献明显耗尽后继续,表明细胞周期蛋白B可能不是有丝分裂所必需的。然而,有丝分裂纺锤体明显异常,在这些细胞周期蛋白B缺陷的胚胎中,有丝分裂的进程被延迟。
A variety of different cyclin proteins have been identified in higher eukaryotes. In the case of cyclin B, functional analyses have clearly demonstrated an important role in the control of entry into mitosis. The function of cyclin A is more complex. It appears to function in the control of both S- and M-phase. The results of our genetic analyses in Drosophila demonstrate that cyclin A has a mitotic function and that it acts synergistically with cyclin B during the G2-M transition. In double mutant embryos that express neither cyclin A nor cyclin B zygotically, cell cycle progression is blocked just before the exhaustion of the maternally contributed cyclin A and B stores. BrdU-labeling experiments indicate that cell cycle progression is blocked in G2 before entry into the fifteenth round of mitosis. Expression of either cyclin A or B from heat-inducible transgenes is sufficient to overcome this cell cycle block. This block is also not observed in single mutant embryos deficient for either cyclin A or B. In cyclin B deficient embryos, cell cycle progression continues after the apparent exhaustion of the maternal contribution, suggesting that cyclin B might not be essential for mitosis. However, mitotic spindles are clearly abnormal and progression through mitosis is delayed in these cyclin B deficient embryos.