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Published online 2 May 2005. doi:10.1083/jcb.200411013
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 169, Number 3, 405-413
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Article

Mnt–Max to Myc–Max complex switching regulates cell cycle entry



William Walker1, Zi-Qiang Zhou1,2, Sara Ota1, Anthony Wynshaw-Boris3,4, and Peter J. Hurlin1,2

1 Shriners Hospitals for Children, Oregon Health and Sciences University, Portland, OR 97201
2 Department of Cell and Developmental Biology, Oregon Health and Sciences University, Portland, OR 97201
3 Department of Pediatrics, University of California, San Diego, School of Medicine, La Jolla, San Diego, CA 92093
4 Department of Medicine, University of California, San Diego, School of Medicine, La Jolla, San Diego, CA 92093

Correspondence to Peter J. Hurlin: pjh{at}shcc.org

The c-Myc oncoprotein is strongly induced during the G0 to S-phase transition and is an important regulator of cell cycle entry. In contrast to c-Myc, the putative Myc antagonist Mnt is maintained at a constant level during cell cycle entry. Mnt and Myc require interaction with Max for specific DNA binding at E-box sites, but have opposing transcriptional activities. Here, we show that c-Myc induction during cell cycle entry leads to a transient decrease in Mnt–Max complexes and a transient switch in the ratio of Mnt–Max to c-Myc–Max on shared target genes. Mnt overexpression suppressed cell cycle entry and cell proliferation, suggesting that the ratio of Mnt–Max to c-Myc–Max is critical for cell cycle entry. Furthermore, simultaneous Cre-Lox mediated deletion of Mnt and c-Myc in mouse embryo fibroblasts rescued the cell cycle entry and proliferative block caused by c-Myc ablation alone. These results demonstrate that Mnt-Myc antagonism plays a fundamental role in regulating cell cycle entry and proliferation.

Abbreviations used in this paper: ChIP, chromatin immunoprecipitation; MEF, mouse embryo fibroblast.


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