Progression through the cell cycle: an overview.
Tissues in adults can be maintained at constant mass or they can increase or decrease in size because of imbalances of synthetic and degradative processes acting at the cellular and molecular levels. Some size changes are caused by physiologic conditions to which the tissue must adjust. Alternatively, the balance may be distorted in favor of net tissue increase in pathologic situations such as cancer. Strict regulatory mechanisms are required to keep proliferation responsive to the organism's needs; these mechanisms may be defective in disease. Net tissue proliferation requires repeated rounds of cell duplication in excess of that necessary to counterbalance cell death. Duplication of a cell requires a net doubling of its every molecule and structure. The myriad of molecular events required for cell proliferation such as DNA duplication and its partitioning at mitosis are tightly regulated in normal cells. One may conceive of two classes of molecules: those required for "housekeeping," which constitute the cell's structural and functional machinery, and those such as growth factors, their receptors, and second messengers involved in signal transduction responsible for regulating the activities of the housekeeping molecules. These molecular events and the cascade of processes that control them can be organized within the sequence of the cell cycle. In this brief overview, we illustrate these issues with a few examples taken from very recent discoveries of novel proteins that appear to have major regulatory roles. Most of these results have been obtained with mammalian fibroblasts, but some have originated with discoveries made using two very different yeasts.(ABSTRACT TRUNCATED AT 250 WORDS)
Fridovich-Keil
J L
JL
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA.
Hansen
L J
LJ
Keyomarsi
K
K
Pardee
A B
AB
D000818:Animals; D016203:CDC2 Protein Kinase / Q000502:physiology*; D002453:Cell Cycle / Q000502:physiology*; D002455:Cell Division / Q000502:physiology; D002471:Cell Transformation, Neoplastic; D006801:Humans; D009369:Neoplasms / Q000209:etiology*; D016160:Retinoblastoma Protein / Q000502:physiology*; D016159:Tumor Suppressor Protein p53 / Q000502:physiology*
D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53; D016203:CDC2 Protein Kinase