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Molecular and Cellular Biology, June 2008, p. 4173-4187, Vol. 28, No. 12
0270-7306/08/$08.00+0     doi:10.1128/MCB.01620-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

JunB Breakdown in Mid-/Late G2 Is Required for Down-Regulation of Cyclin A2 Levels and Proper Mitosis{triangledown}

Rosa Farràs,1,2* Véronique Baldin,4 Sandra Gallach,2 Claire Acquaviva,3 Guillaume Bossis,1 Isabelle Jariel-Encontre,1 and Marc Piechaczyk1*

Institut de Génétique Moléculaire de Montpellier, CNRS, 1919 route de Mende, 34293 Montpellier Cedex 05, France,1 Centro de Investigación Príncipe Felipe, c/ EP Autopista del Saler, 16 Camino de las Moreras, 46013 Valencia, Spain,2 The Wellcome Trust/CR UK Gurdon Institute, Tennis Court Road, Cambridge CB2 1ON, United Kingdom,3 Centre de Recherche en Biochimie Macromoléculaire, CNRS, 1919 route de Mende, 34293 Montpellier Cedex 05, France4

Received 3 September 2007/ Returned for modification 12 October 2007/ Accepted 15 March 2008

JunB, a member of the AP-1 family of dimeric transcription factors, is best known as a cell proliferation inhibitor, a senescence inducer, and a tumor suppressor, although it also has been attributed a cell division-promoting activity. Its effects on the cell cycle have been studied mostly in G1 and S phases, whereas its role in G2 and M phases still is elusive. Using cell synchronization experiments, we show that JunB levels, which are high in S phase, drop during mid- to late G2 phase due to accelerated phosphorylation-dependent degradation by the proteasome. The forced expression of an ectopic JunB protein in late G2 phase indicates that JunB decay is necessary for the subsequent reduction of cyclin A2 levels in prometaphase, the latter event being essential for proper mitosis. Consistently, abnormal JunB expression in late G2 phase entails a variety of mitotic defects. As these aberrations may cause genetic instability, our findings contrast with the acknowledged tumor suppressor activity of JunB and reveal a mechanism by which the deregulation of JunB might contribute to tumorigenesis.

* Corresponding author. Mailing address: Institut de Génétique Moléculaire de Montpellier (IGMM), CNRS, 1919 route de Mende, 34293 Montpellier Cedex 05, France. Phone: 33-1-67-61-36-68. Fax: 33-1-67-04-02-31. E-mail for Rosa Farràs: rfarras{at}cipf.es. E-mail for Marc Piechaczyk: marc.piechaczyk{at}igmm.cnrs.fr

{triangledown} Published ahead of print on 7 April 2008.

Molecular and Cellular Biology, June 2008, p. 4173-4187, Vol. 28, No. 12
0270-7306/08/$08.00+0     doi:10.1128/MCB.01620-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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