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A more recent version of this article appeared on March 1, 2003
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Submitted on October 11, 2002
Accepted on November 6, 2002
1 Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, Rhode Island 02912
* Corresponding author. E-mail address: john_sedivy{at}brown.edu.
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 (2-3-fold) retardation of proliferation. The rates of RNA and protein synthesis are reduced by approximately the same factor while cell size remains unaffected. We have performed a detailed kinetic cell cycle analysis of c-myc-/- cells using several labeling and synchronization methods. The great 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 (4 to 5-fold) and a more limited lengthening of G2 phase (2-fold), while 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.
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