Tay J, Hodgman R, Richter J D
Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.
Dev Biol. 2000 May 1;221(1):1-9. doi: 10.1006/dbio.2000.9669.
In maturing mouse oocytes, protein synthesis is required for meiotic maturation subsequent to germinal vesicle breakdown (GVBD). While the number of different proteins that must be synthesized for this progression to occur is unknown, at least one of them appears to be cyclin B1, the regulatory subunit of M-phase-promoting factor. Here, we investigate the mechanism of cyclin B1 mRNA translational control during mouse oocyte maturation. We show that the U-rich cytoplasmic polyadenylation element (CPE), a cis element in the 3' UTR of cyclin B1 mRNA, mediates translational repression in GV-stage oocytes. The CPE is also necessary for cytoplasmic polyadenylation, which stimulates translation during oocyte maturation. The injection of oocytes with a cyclin B1 antisense RNA, which probably precludes the binding of a factor to the CPE, delays cytoplasmic polyadenylation as well as the transition from GVBD to metaphase II. CPEB, which interacts with the cyclin B1 CPE and is present throughout meiotic maturation, becomes phosphorylated at metaphase I. These data indicate that CPEB is involved in both the repression and the stimulation of cyclin B1 mRNA and suggest that the phosphorylation of this protein could be involved in regulating its activity.
在成熟的小鼠卵母细胞中,生发泡破裂(GVBD)后减数分裂成熟需要蛋白质合成。虽然尚不清楚为实现这一进程必须合成的不同蛋白质的数量,但其中至少有一种似乎是细胞周期蛋白B1,即M期促进因子的调节亚基。在此,我们研究小鼠卵母细胞成熟过程中细胞周期蛋白B1 mRNA翻译控制的机制。我们发现,富含尿苷的细胞质聚腺苷酸化元件(CPE),即细胞周期蛋白B1 mRNA 3'非翻译区(UTR)中的一个顺式元件,在GV期卵母细胞中介导翻译抑制。CPE对于细胞质聚腺苷酸化也是必需的,而细胞质聚腺苷酸化在卵母细胞成熟过程中刺激翻译。向卵母细胞注射细胞周期蛋白B1反义RNA(这可能会阻止一种因子与CPE结合)会延迟细胞质聚腺苷酸化以及从GVBD到中期II的转变。CPEB与细胞周期蛋白B1 CPE相互作用且在整个减数分裂成熟过程中都存在,它在中期I时发生磷酸化。这些数据表明CPEB参与了细胞周期蛋白B1 mRNA的抑制和刺激过程,并提示该蛋白的磷酸化可能参与调节其活性。