Ballantyne S, Daniel D L, Wickens M
Department of Biochemistry, University of Wisconsin, Madison 53706, USA.
Mol Biol Cell. 1997 Aug;8(8):1633-48. doi: 10.1091/mbc.8.8.1633.
During oocyte maturation and early development, mRNAs receive poly(A) in the cytoplasm at distinct times relative to one another and to the cell cycle. These cytoplasmic polyadenylation reactions do not occur during oogenesis, but begin during oocyte maturation and continue throughout early development. In this report, we focus on the link between cytoplasmic polyadenylation and control of the cell cycle during meiotic maturation. Activation of maturation promoting factor, a complex of CDK1 and cyclin, is required for maturation and dependent on c-mos protein kinase. We demonstrate here that two classes of polyadenylation exist during oocyte maturation, defined by their dependence of c-mos and CDK1 protein kinases. Polyadenylation of the first class of mRNAs (class I) is independent of c-mos and CDK1 kinase activities, whereas polyadenylation of the second class (class II) requires both of these activities. Class I polyadenylation, through its effects on c-mos mRNA, is required for class II polyadenylation. cis-acting elements responsible for this distinction reside in the 3'-untranslated region, upstream of the polyadenylation signal AAUAAA. Cytoplasmic polyadenylation elements (CPEs) are sufficient to specify class I polyadenylation, and subtle changes in the CPE can substantially, though not entirely, shift an RNA from class I to class II. Activation of class I polyadenylation events is independent of hyperphosphorylation of CPE-binding protein or poly(A) polymerase, and requires cellular protein synthesis. The two classes of polyadenylation and of mRNA define a dependent pathway, in which polyadenylation of certain mRNAs requires the prior polyadenylation of another. We propose that this provides one method of regulating the temporal order of polyadenylation events, and links polyadenylation to the control of the meiotic cell cycle.
在卵母细胞成熟和早期发育过程中，信使核糖核酸（mRNAs）在相对于彼此以及细胞周期的不同时间在细胞质中接受多聚腺苷酸化（poly(A)）。这些细胞质多聚腺苷酸化反应在卵子发生过程中不发生，而是在卵母细胞成熟期间开始，并在整个早期发育过程中持续。在本报告中，我们聚焦于减数分裂成熟过程中细胞质多聚腺苷酸化与细胞周期调控之间的联系。成熟促进因子（一种由细胞周期蛋白依赖性激酶1（CDK1）和细胞周期蛋白组成的复合物）的激活是成熟所必需的，并且依赖于c-mos蛋白激酶。我们在此证明，卵母细胞成熟过程中存在两类多聚腺苷酸化，根据它们对c-mos和CDK1蛋白激酶的依赖性来定义。第一类信使核糖核酸（I类）的多聚腺苷酸化独立于c-mos和CDK1激酶活性，而第二类（II类）的多聚腺苷酸化则需要这两种活性。I类多聚腺苷酸化通过其对c-mos信使核糖核酸的作用，是II类多聚腺苷酸化所必需的。负责这种区分的顺式作用元件位于多聚腺苷酸化信号AAUAAA上游的3'非翻译区。细胞质多聚腺苷酸化元件（CPEs）足以指定I类多聚腺苷酸化，并且CPE中的细微变化虽然不能完全但能显著地将一种核糖核酸从I类转变为II类。I类多聚腺苷酸化事件的激活独立于CPE结合蛋白或多聚（A）聚合酶的过度磷酸化，并且需要细胞蛋白质合成。这两类多聚腺苷酸化和信使核糖核酸定义了一条依赖途径，其中某些信使核糖核酸的多聚腺苷酸化需要另一种信使核糖核酸先进行多聚腺苷酸化。我们提出，这提供了一种调节多聚腺苷酸化事件时间顺序的方法，并将多聚腺苷酸化与减数分裂细胞周期的调控联系起来。
