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Originally published In Press as doi:10.1074/jbc.M201667200 on March 13, 2002

J. Biol. Chem., Vol. 277, Issue 21, 18334-18339, May 24, 2002
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Normal Assembly of 60 S Ribosomal Subunits Is Required for the Signaling in Response to a Secretory Defect in Saccharomyces cerevisiae*

Keita MiyoshiDagger §, Rota Tsujii§, Hideji Yoshida, Yasushi Maki, Akira Wada, Yasushi Matsui||, Akio Toh-e||, and Keiko MizutaDagger §**

From the Dagger  Department of Biological Sciences, Graduate School of Biosphere Sciences and § Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, Kagamiyama, Higashi-Hiroshima 739-8528, Japan,  Department of Physics, Osaka Medical College, Takatsuki, Osaka 569-0084, Japan, and the || Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan

A secretory defect leads to transcriptional repression of both ribosomal protein and rRNA genes in yeast. To elucidate the mechanism of the signaling, we previously isolated rrs mutants that were unable to respond to a secretory defect, and we cloned RRS1 encoding a nuclear protein that was required for ribosome biogenesis (Tsuno, A., Miyoshi, K., Tsujii, R., Miyakawa, T., and Mizuta, K. (2000) Mol. Cell. Biol. 20, 2066-2074). We identified duplicated genes encoding ribosomal protein L11, RPL11B as a wild-type allele complementing the rrs2 mutation, and RPL11A in two-hybrid screening using RRS1 as bait. Rpl11p was copurified with Rrs1p in immunoprecipitation analysis. Ultracentrifugation analysis revealed that Rrs1p associated fairly tightly with 60 S preribosomal subunits. These results suggest that signaling in response to a secretory defect requires the normal assembly of 60 S ribosomal subunits including Rrs1p and Rpl11p.


* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

** To whom correspondence should be addressed: Dept. of Biological Sciences, Graduate School of Biosphere Sciences, Hiroshima University, Kagamiyama 1-4-4, Higashi-Hiroshima 739-8528, Japan. Tel.: 81-824-24-7926; Fax: 81-824-24-7926; E-mail: kmizuta@hiroshima-u.ac.jp.


Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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