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Originally published as MBC in Press, 10.1091/mbc.E02-10-0649 on December 7, 2002
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Vol. 14, Issue 3, 823-835, March 2003

Loss of Protooncogene c-Myc Function Impedes G1 Phase Progression Both before and after the Restriction Point

Christoph Schorl, and John M. Sedivy*

Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, Rhode Island 02912

c-myc is an important protooncogene whose misregulation is believed to causally affect the development of numerous human cancers. c-myc null rat fibroblasts are viable but display a severe (two- to threefold) retardation of proliferation. The rates of RNA and protein synthesis are reduced by approximately the same factor, whereas cell size remains unaffected. We have performed a detailed kinetic cell cycle analysis of c-myc-/- cells by using several labeling and synchronization methods. The majority of cells (>90%) in asynchronous, exponential phase c-myc-/- cultures cycle continuously with uniformly elongated cell cycles. Cell cycle elongation is due to a major lengthening of G1 phase (four- to fivefold) and a more limited lengthening of G2 phase (twofold), whereas S phase duration is largely unaffected. Progression from mitosis to the G1 restriction point and the subsequent progression from the restriction point into S phase are both drastically delayed. These results are best explained by a model in which c-Myc directly affects cell growth (accumulation of mass) and cell proliferation (the cell cycle machinery) by independent pathways.

* Corresponding author. E-mail address: john_sedivy{at}brown.edu.

Molecular Biology of the Cell
Vol. 14, 823-835, March 2003
Copyright © 2003 by The American Society for Cell Biology


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