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M109362200v1
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Papers In Press, published online ahead of print November 13, 2001
J. Biol. Chem, 10.1074/jbc.M109362200
Submitted on September 27, 2001
Revised on October 24, 2001
Accepted on November 12, 2001

c-jun ARE targets mRNA deadenylation by an EDEN-BP (Embryo deadenylation element binding protein) dependent pathway

Luc Paillard, Vincent Legagneux, Dominique Maniey, and H. Beverley Osborne

CNRS UMR 6061, Rennes 35043

Corresponding Author: Luc.Paillard{at}univ-rennes1.fr

In mammalian cells, certain mRNAs encoding cytokines or proto-oncogenes are especially unstable, due to the presence of a particular sequence element in their 3' untranslated region named ARE (A/U Rich Element). AREs cause this instability by provoking the rapid shortening of the poly(A) tail of the mRNA. The deadenylation of mRNAs mediated by AREs containing repeats of the AUUUA motif (class I/II AREs) is conserved in Xenopus embryos. Here, we first extend these observations by showing that c-jun ARE, a representative of class III (non AUUUA) AREs, also provokes the deadenylation of a reporter RNA in Xenopus embryos. Next, by immunodepletion and immunoneutralization experiments, we show that, in Xenopus, the rapid deadenylation of RNAs that contain the c-jun ARE, but not an AUUUA ARE, requires EDEN-BP. This RNA binding protein was previously shown to provoke the rapid deadenylation of certain Xenopus maternal RNAs. Finally, we show that CUG-BP, the human homologue of EDEN-BP, specifically binds to c-jun ARE. Together, these results identify CUG-BP as a plausible deadenylation factor responsible for the post-transcriptional control of c-jun proto-oncogene mRNA in mammalian cells.


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