Open AccessRapid Deadenylation and Poly(A)-Dependent Translational Repression Mediated by the Caenorhabditis elegans tra-2 3′ Untranslated Region in Xenopus Embryos
Author(s) -
Sunnie R. Thompson,
Elizabeth B. Goodwin,
Marvin Wickens
Publication year - 2000
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.20.6.2129-2137.2000
Subject(s) - biology , xenopus , caenorhabditis elegans , psychological repression , untranslated region , translational regulation , translation (biology) , messenger rna , three prime untranslated region , microbiology and biotechnology , rna interference , caenorhabditis , genetics , rna , gene expression , gene
The 3′ untranslated region (3′UTR) of many eukaryotic mRNAs is essential for their control during early development. Negative translational control elements in 3′UTRs regulate pattern formation, cell fate, and sex determination in a variety of organisms.tra-2 mRNA inCaenorhabditis elegans is required for female development but must be repressed to permit spermatogenesis in hermaphrodites. Translational repression oftra-2 mRNA inC. elegans is mediated by tandemly repeated elements in its 3′UTR; these elements are called TGEs (fortra-2 and GLI element). To examine the mechanism of TGE-mediated repression, we first demonstrate that TGE-mediated translational repression occurs inXenopus embryos and thatXenopus 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 inC. elegans , the poly(A) tail of wild-typetra-2 mRNA is shorter than that of a mutant mRNA lacking the TGEs. To determine whether TGEs regulate poly(A) length directly, synthetictra-2 3′UTRs with and without the TGEs were injected intoXenopus embryos. We find that TGEs accelerate the rate of deadenylation and permit the last 15 adenosines to be removed from the RNA, resulting in the accumulation of fully deadenylated molecules. We conclude that TGE-mediated translational repression involves either interference with poly(A)'s function in translation and/or regulated deadenylation.