This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Farràs, R.
Right arrow Articles by Piechaczyk, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Farràs, R.
Right arrow Articles by Piechaczyk, M.

 Previous Article  |  Next Article 

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.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»