Journal
MOLECULAR BIOLOGY OF THE CELL
Volume 14, Issue 3, Pages 823-835Publisher
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E02-10-0649
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Funding
- NIGMS NIH HHS [R01 GM041690, GM-41690] Funding Source: Medline
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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 G, phase (four- to fivefold) and a more limited lengthening of G(2) 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.
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