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J. Biol. Chem., Vol. 278, Issue 40, 38287-38291, October 3, 2003

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Translation Termination Factor eRF3 Mediates mRNA Decay through the Regulation of Deadenylation^*,

Nao Hosoda , Tetsuo Kobayashi , Naoyuki Uchida , Yuji Funakoshi , Yoshiko Kikuchi , Shinichi Hoshino  ¶ and Toshiaki Katada 

From the Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, and the Department of Biological Sciences, Graduate School of Science, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan

Messenger RNA decay, which is a regulated process intimately linked to translation, begins with the deadenylation of the poly(A) tail at the 3' end. However, the precise mechanism triggering the first step of mRNA decay and its relationship to translation have not been elucidated. Here, we show that the translation termination factor eRF3 mediates mRNA deadenylation and decay in the yeast Saccharomyces cerevisiae. The N-domain of eRF3, which is not necessarily required for translation termination, interacts with the poly(A)-binding protein PABP. When this interaction is blocked by means of deletion or overexpression of the N-domain of eRF3, half-lives of all mRNAs are prolonged. The eRF3 mutant lacking the N-domain is deficient in the poly(A) shortening. Furthermore, the eRF3-mediated mRNA decay requires translation to proceed, especially ribosomal transition through the termination codon. These results indicate that the N-domain of eRF3 mediates mRNA decay by regulating deadenylation in a manner coupled to translation.

Received for publication, July 9, 2003 , and in revised form, August 6, 2003.

^* This work was supported in part by research grants from the "Research for the Future" Program of the Japan Society for the Promotion of Science (JSPS-RFTF 96L00505), the Mitsubishi Foundation, and the Scientific Funds on the Ministry of Education, Culture, Sports, Science, and Technology of Japan. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains Supplemental Fig. S1.

^¶ To whom correspondence should be addressed: Dept. of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, University of Tokyo, Hongo, Tokyo 113-0033, Japan. Tel.: 81-3-5841-4754; Fax: 81-3-5841-4751; E-mail: hoshino{at}mol.f.u-tokyo.ac.jp.

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