Rapid deadenylation and poly(A)-dependent translational repression mediated by the Caenorhabditis elegans tra-2 3 ' untranslated region in Xenopus embryos

Citation
Sr. Thompson et al., Rapid deadenylation and poly(A)-dependent translational repression mediated by the Caenorhabditis elegans tra-2 3 ' untranslated region in Xenopus embryos, MOL CELL B, 20(6), 2000, pp. 2129-2137
Citations number
64
Categorie Soggetti
Molecular Biology & Genetics
Journal title
MOLECULAR AND CELLULAR BIOLOGY
ISSN journal
02707306 → ACNP
Volume
20
Issue
6
Year of publication
2000
Pages
2129 - 2137
Database
ISI
SICI code
0270-7306(200003)20:6<2129:RDAPTR>2.0.ZU;2-R
Abstract
The 3' untranslated region (3'UTR) of many eukaryotic mRNAs is essential fo r their control during early development. Negative translational control el ements in 3'UTRs regulate pattern formation, cell fate, and sex determinati on in a variety of organisms. tra-2 mRNA in Caenorhabditis elegans is requi red for female development but must be repressed to permit spermatogenesis in hermaphrodites. Translational repression of tra-2 mRNA in C. elegans is mediated by tandemly repeated elements in its 3'UTR; these elements are cal led TGEs (for tra-2 and GLI element). To examine the mechanism of TGE-media ted repression, we first demonstrate that TGE-mediated translational repres sion occurs in Xenopus embryos and that Xenopus egg extracts contain a TGE- specific binding factor. Translational repression by the TGEs requires that the mRNA possess a poly(A) tail. We show that in C. elegans, the poly(A) t ail of wild-type tra-2 mRNA is shorter than that of a mutant mRNA lacking t he TGEs. To determine whether TGEs regulate poly(A) length directly, synthe tic tra-2 3'UTRs with and without the TGEs were injected into Xenopus embry os. We find that TGEs accelerate the rate of deadenylation and permit the l ast 15 adenosines to be removed from the RNA, resulting in the accumulation of fully deadenylated molecules. We conclude that TGE-mediated translation al repression involves either interference with poly(A)'s function in trans lation and/or regulated deadenylation.