mRNA去腺苷酸化机制:翻译终止因子eRF3与mRNA去腺苷酸酶之间分子相互作用的证据

Mechanism of mRNA deadenylation: evidence for a molecular interplay between translation termination factor eRF3 and mRNA deadenylases.

作者信息

Funakoshi Yuji, Doi Yusuke, Hosoda Nao, Uchida Naoyuki, Osawa Masanori, Shimada Ichio, Tsujimoto Masafumi, Suzuki Tsutomu, Katada Toshiaki, Hoshino Shin-ichi

机构信息

Department of Biological Chemistry, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya 467-8603, Japan.

出版信息

Genes Dev. 2007 Dec 1;21(23):3135-48. doi: 10.1101/gad.1597707.

Abstract

In eukaryotes, shortening of the 3'-poly(A) tail is the rate-limiting step in the degradation of most mRNAs, and two major mRNA deadenylase complexes--Caf1-Ccr4 and Pan2-Pan3--play central roles in this process, referred to as deadenylation. However, the molecular mechanism triggering deadenylation remains elusive. Previously, we demonstrated that eukaryotic releasing factor eRF3 mediates deadenylation and decay of mRNA in a manner coupled to translation termination. Here, we report the mechanism of mRNA deadenylation. The eRF3-mediated deadenylation is catalyzed by both Caf1-Ccr4 and Pan2-Pan3. Interestingly, translation termination complexes eRF1-eRF3, Pan2-Pan3, and Caf1-Ccr4 competitively interact with polyadenylate-binding protein PABPC1. In each complex, eRF3, Pan3, and Tob, respectively, mediate PABPC1 binding, and a combination of a PAM2 motif and a PABC domain is commonly utilized for their contacts. A translation-dependent exchange of eRF1-eRF3 for the deadenylase occurs on PABPC1. Consequently, PABPC1 binding leads to the activation of Pan2-Pan3 and Caf1-Ccr4. From these results, we suggest a mechanism of mRNA deadenylation by Pan2-Pan3 and Caf1-Ccr4 in cooperation with eRF3 and PABPC1.

摘要

在真核生物中,3'-多聚腺苷酸尾的缩短是大多数mRNA降解的限速步骤,两种主要的mRNA去腺苷酸化酶复合物——Caf1-Ccr4和Pan2-Pan3——在这个被称为去腺苷酸化的过程中发挥核心作用。然而,触发去腺苷酸化的分子机制仍然不清楚。此前,我们证明了真核释放因子eRF3以与翻译终止偶联的方式介导mRNA的去腺苷酸化和降解。在这里,我们报道了mRNA去腺苷酸化的机制。eRF3介导的去腺苷酸化由Caf1-Ccr4和Pan2-Pan3共同催化。有趣的是,翻译终止复合物eRF1-eRF3、Pan2-Pan3和Caf1-Ccr4与聚腺苷酸结合蛋白PABPC1竞争性相互作用。在每个复合物中,分别由eRF3、Pan3和Tob介导与PABPC1的结合,并且PAM2基序和PABC结构域的组合通常用于它们之间的接触。eRF1-eRF3与去腺苷酸化酶之间依赖翻译的交换发生在PABPC1上。因此,PABPC1的结合导致Pan2-Pan3和Caf1-Ccr4的激活。基于这些结果,我们提出了一种Pan2-Pan3和Caf1-Ccr4与eRF3和PABPC1协同作用进行mRNA去腺苷酸化的机制。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索