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Originally published In Press as doi:10.1074/jbc.M106460200 on September 14, 2001

J. Biol. Chem., Vol. 276, Issue 46, 42971-42977, November 16, 2001
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Involvement of the Interaction between p21 and Proliferating Cell Nuclear Antigen for the Maintenance of G2/M Arrest after DNA Damage*

Tomoaki AndoDagger §, Takumi KawabeDagger , Hirotaka Ohara§, Bernard Ducommun, Makoto Itoh§, and Takashi OkamotoDagger ||

From the Dagger  Department of Molecular Genetics and § First Department of Internal Medicine, Nagoya City University Medical School, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi 467-8601, Japan and  Laboratoire de Biologie Cellulaire et Moléculaire du Contrôle de la Prolifération Cellulaire, UMR CNRS 5088, Université Paul Sabatier, 118 Route de Narbonne, 31062 Toulouse Cedex, France

Although a major effect of p21, a cyclin-dependent kinase inhibitor, is considered to be exerted during G1 phase of the cell cycle, p21 gene knock-out studies suggested its involvement in G2/M checkpoint as well. Here we demonstrate evidence that p21 is required for the cell cycle arrest at G2 upon DNA damage. We found that expression of wild-type p21 (p21WT), not mutant p21 (p21PCNA-) lacking the interaction with proliferating cell nuclear antigen (PCNA), caused G2 cell cycle arrest in p53-deficient DLD1 colon cancer cell line after the DNA damage by treatment with cis-diamminedichloroplatinum (II). We also found that p21WT was associated with Cdc2/cyclin B1 together with PCNA. Furthermore, coimmunoprecipitation experiments revealed that PCNA interacted with Cdc25C at the G2/M transition, and this interaction was abolished when p21WT was expressed presumably due to the competition between p21WT and Cdc25C in the binding to PCNA. These findings suggest that p21 plays a regulatory role in the maintenance of cell cycle arrest at G2 by blocking the interaction of Cdc25C with PCNA.

* This work was supported in part by grants-in-aid from the Ministry of Health, Labor, and Welfare, the Ministry of Education, Culture, Sports, Science, and Technology of Japan, and the Japanese Health Sciences Foundation.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 Molecular Genetics, Nagoya City University Medical School, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi 467-8601, Japan. Tel.: 81-52-853-8204; Fax: 81-52-859-1235; E-mail: tokamoto@med.nagoya-cu.ac.jp.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.


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