Radford Helois E, Meijer Hedda A, de Moor Cornelia H
School of Pharmacy, Centre for Biomolecular Sciences, University of Nottingham, University Park, Nottingham, UK.
Biochim Biophys Acta. 2008 Apr;1779(4):217-29. doi: 10.1016/j.bbagrm.2008.02.002. Epub 2008 Feb 14.
Elongation of the poly(A) tails of specific mRNAs in the cytoplasm is a crucial regulatory step in oogenesis and early development of many animal species. The best studied example is the regulation of translation by cytoplasmic polyadenylation elements (CPEs) in the 3' untranslated region of mRNAs involved in Xenopus oocyte maturation. In this review we discuss the mechanism of translational control by the CPE binding protein (CPEB) in Xenopus oocytes as follows: 1. The cytoplasmic polyadenylation machinery such as CPEB, the subunits of cleavage and polyadenylation specificity factor (CPSF), symplekin, Gld-2 and poly(A) polymerase (PAP). 2. The signal transduction that leads to the activation of CPE-mediated polyadenylation during oocyte maturation, including the potential roles of kinases such as MAPK, Aurora A, CamKII, cdk1/Ringo and cdk1/cyclin B. 3. The role of deadenylation and translational repression, including the potential involvement of PARN, CCR4/NOT, maskin, pumilio, Xp54 (Ddx6, Rck), other P-body components and isoforms of the cap binding initiation factor eIF4E. Finally we discuss some of the remaining questions regarding the mechanisms of translational regulation by cytoplasmic polyadenylation and give our view on where our knowledge is likely to be expanded in the near future.
特定mRNA在细胞质中的多聚腺苷酸尾延长是许多动物物种卵子发生和早期发育中的关键调控步骤。研究得最透彻的例子是非洲爪蟾卵母细胞成熟过程中,mRNA 3'非翻译区的细胞质多聚腺苷酸化元件(CPE)对翻译的调控。在本综述中,我们将如下讨论非洲爪蟾卵母细胞中CPE结合蛋白(CPEB)的翻译控制机制:1. 细胞质多聚腺苷酸化机制,如CPEB、切割和多聚腺苷酸化特异性因子(CPSF)的亚基、共生蛋白、Gld-2和多聚腺苷酸聚合酶(PAP)。2. 卵母细胞成熟过程中导致CPE介导的多聚腺苷酸化激活的信号转导,包括丝裂原活化蛋白激酶(MAPK)、极光激酶A、钙/钙调蛋白依赖性蛋白激酶II(CamKII)、细胞周期蛋白依赖性激酶1/林戈(cdk1/Ringo)和细胞周期蛋白依赖性激酶1/细胞周期蛋白B(cdk1/cyclin B)等激酶的潜在作用。3. 去腺苷酸化和翻译抑制的作用,包括多聚腺苷酸核糖核酸酶(PARN)、CCR4/NOT、maskin、pumilio、Xp54(Ddx6、Rck)、其他P小体成分以及帽结合起始因子eIF4E的亚型的潜在参与。最后,我们讨论了关于细胞质多聚腺苷酸化翻译调控机制的一些遗留问题,并对近期知识可能扩展的方向发表了看法。