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J. Biol. Chem., Vol. 280, Issue 38, 32640-32648, September 23, 2005

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Regulation of Cdc2p and Cdc13p Is Required for Cell Cycle Arrest Induced by Defective RNA Splicing in Fission Yeast^*

From the Department of Biochemistry and Cell Biology, Graduate School of Medicine, Nagoya City University, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan

Screening of cdc mutants of fission yeast for those whose cell cycle arrest is independent of the DNA damage checkpoint identified the RNA splicing-deficient cdc28 mutant. A search for mutants of cdc28 cells that enter mitosis with unspliced RNA resulted in the identification of an orb5 point mutant. The orb5⁺ gene, which encodes a catalytic subunit of casein kinase II, was found to be required for cell cycle arrest in other mutants with defective RNA metabolism but not for operation of the DNA replication or DNA damage checkpoints. Loss of function of wee1⁺ or rad24⁺ also suppressed the arrest of several splicing mutants. Overexpression of the major B-type cyclin Cdc13p induced cdc28 cells to enter mitosis. The abundance of Cdc13p was reduced, and the phosphorylation of Cdc2p on tyrosine 15 was maintained in splicing-defective cells. These results suggest that regulation of Cdc13p and Cdc2p is required for G₂ arrest in splicing mutants.

Received for publication, April 29, 2005 , and in revised form, June 27, 2005.

^* This work was supported in part by a grant-in-aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan (to H. M.). 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.

¹ Research Fellow of the Japan Society for the Promotion of Science.

² To whom correspondence should be addressed. Tel.: 81-52-853-8145; Fax: 81-52-842-3955; E-mail: hmura{at}med.nagoya-cu.ac.jp.

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