Gabrielli B G, Roy L M, Maller J L
Department of Pharmacology, University of Colorado School of Medicine, Denver 80262.
Science. 1993 Mar 19;259(5102):1766-9. doi: 10.1126/science.8456304.
The unfertilized eggs of vertebrates are arrested in metaphase of meiosis II because of the activity of cytostatic factor (CSF). Xenopus CSF is thought to contain the product of the Mos proto-oncogene, but other proteins synthesized during meiosis II are also required for arrest induced by CSF. In Xenopus oocytes, ablation of synthesis of cyclin-dependent kinase 2 (Cdk2) during meiosis resulted in absence of the metaphase II block, even though the Mosxe protein kinase was fully active at metaphase. Introduction of purified Cdk2 restored metaphase II arrest, and increasing the amount of Cdk2 during meiosis I (when Mosxe is present) led to metaphase arrest at meiosis I. These data indicate that metaphase arrest is a result of cooperation between a proto-oncogene kinase and a cyclin-dependent kinase and illustrate the interaction of a cell growth regulator with a cell cycle control element.
由于细胞静止因子(CSF)的活性,脊椎动物的未受精卵停滞在减数分裂II中期。非洲爪蟾CSF被认为包含Mos原癌基因的产物,但减数分裂II期间合成的其他蛋白质对于CSF诱导的停滞也是必需的。在非洲爪蟾卵母细胞中,减数分裂期间细胞周期蛋白依赖性激酶2(Cdk2)合成的缺失导致了减数分裂II中期阻滞的缺失,尽管Mosxe蛋白激酶在中期完全活跃。引入纯化的Cdk2可恢复减数分裂II中期阻滞,并且在减数分裂I期间(当Mosxe存在时)增加Cdk2的量会导致减数分裂I中期阻滞。这些数据表明中期阻滞是原癌基因激酶和细胞周期蛋白依赖性激酶之间合作的结果,并说明了细胞生长调节剂与细胞周期控制元件之间的相互作用。