This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Coisy-Quivy, M. Articles by Dantonel, J.-C. Search for Related Content PubMed PubMed Citation Articles by Coisy-Quivy, M. Articles by Dantonel, J.-C.

Role for Brm in Cell Growth Control

¹ Institut de Génétique Moléculaire, Centre National de la Recherche Scientifique, Montpellier, France and ² Institut Pasteur, Paris, France

Requests for reprints: Jean-Christophe Dantonel, Institut de Génétique Moléculaire, Centre National de la Recherche Scientifique, UMR 5535, 1919 route de Mende, 34293 Montpellier cedex 5, France. Phone: 33-4-67-61-36-53; E-mail: dantonel{at}igmm.cnrs.fr.

Recently, we have shown implication of Brm, the catalytic subunit of the SWI/SNF chromatin remodeling complex, in repression of cyclin A expression in quiescent cells. Here, we have examined the fate of cells lacking Brm throughout the cycle. We find that despite elevated levels of cyclins A and E, these cells can respond to serum starvation, however, without reaching a canonical G₀ phase as they continue to express high levels of c-Myc and have an abnormally large average size. The response to serum starvation can be correlated with increased levels of Rb proteins p130 and p107 as well as increased association of p27 with the cyclin-dependent kinases, possibly compensating for the higher levels of G₁ cyclins by reducing their associated kinase activity. After serum stimulation, reentry into the cycle occurs normally, but the S phase is delayed and shorter. In addition, the M phase has an increased duration, and we observed frequent faulty chromosome segregation events in anaphase. Altogether, our data suggest that cells can partially overcome the absence of Brm by activating several compensatory mechanisms to control the cell cycle. However, they remain profoundly affected, unable to enter a canonical quiescent state, presenting a shorter S phase, and finally unable to perform correct chromosome segregation. (Cancer Res 2006; 66(10): 5069-76)

This article has been cited by other articles:

				Y. Xu, J. Zhang, and X. Chen The Activity of p53 Is Differentially Regulated by Brm- and Brg1-containing SWI/SNF Chromatin Remodeling Complexes J. Biol. Chem., December 28, 2007; 282(52): 37429 - 37435. [Abstract] [Full Text] [PDF]