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Molecular and Cellular Biology, April 2003, p. 2451-2462, Vol. 23, No. 7
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.7.2451-2462.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Involvement of Poly(ADP-Ribose) Polymerase 1 and Poly(ADP-Ribosyl)ation in Regulation of Centrosome Function

Masayuki Kanai,1 Wei-Min Tong,2 Eiji Sugihara,1 Zhao-Qi Wang,2 Kenji Fukasawa,3 and Masanao Miwa1*

Department of Biochemistry and Molecular Oncology, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan,1 International Agency of Research on Cancer, Lyon 69372, France,2 Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati College of Medicine, Cincinnati, Ohio, 45267-05213

Received 7 June 2002/ Returned for modification 23 July 2002/ Accepted 7 January 2003

The regulatory mechanism of centrosome function is crucial to the accurate transmission of chromosomes to the daughter cells in mitosis. Recent findings on the posttranslational modifications of many centrosomal proteins led us to speculate that these modifications might be involved in centrosome behavior. Poly(ADP-ribose) polymerase 1 (PARP-1) catalyzes poly(ADP-ribosyl)ation to various proteins. We show here that PARP-1 localizes to centrosomes and catalyzes poly(ADP-ribosyl)ation of centrosomal proteins. Moreover, centrosome hyperamplification is frequently observed with PARP inhibitor, as well as in PARP-1-null cells. Thus, it is possible that chromosomal instability known in PARP-1-null cells can be attributed to the centrosomal dysfunction. P53 tumor suppressor protein has been also shown to be localized at centrosomes and to be involved in the regulation of centrosome duplication and monitoring of the chromosomal stability. We found that centrosomal p53 is poly(ADP-ribosyl)ated in vivo and centrosomal PARP-1 directly catalyzes poly(ADP-ribosyl)ation of p53 in vitro. These results indicate that PARP-1 and PARP-1-mediated poly(ADP-ribosyl)ation of centrosomal proteins are involved in the regulation of centrosome function.

* Corresponding author. Mailing address: Department of Biochemistry and Molecular Oncology, Institute of Basic Medical Sciences, University of Tsukuba, 1-1-1, Tennoudai, Tsukuba, Ibaraki 305-8575, Japan. Phone: 81-298-53-3272. Fax: 81-298-53-3271. E-mail: m-miwa{at}md.tsukuba.ac.jp.

Molecular and Cellular Biology, April 2003, p. 2451-2462, Vol. 23, No. 7
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.7.2451-2462.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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