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A more recent version of this article appeared on September 23, 2005
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M504746200v1
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Papers In Press, published online ahead of print July 27, 2005
J. Biol. Chem, 10.1074/jbc.M504746200
Submitted on April 29, 2005
Revised on June 27, 2005
Accepted on July 27, 2005

Regulation of Cdc2p and Cdc13p is required for cell cycle arrest induced by defective RNA splicing in fission yeast

Midori Shimada, Chisato Namikawa-Yamada, Makoto Nakanishi, and Hiroshi Murakami

Department of Biochemistry and Cell Biology, Nagoya City University, Graduate School of Medicine, Nagoya, Aichi 467-8601

Corresponding Author: hmura{at}med.nagoya-cu.ac.jp

Screening of cdc mutants of fission yeast for those whose cell cycle arrest is independent of the DNA damage checkpoint identified 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.


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