title: Cell cycle exit upon myogenic differentiation.
abstract: Myogenic precursor cells withdraw irreversibly from the cell cycle as they differentiate into mature myotubes. Cell cycle exit occurs early during the differentiation program and is required for normal expression of the contractile phenotype. Differentiated myocytes also display a decreased propensity to undergo apoptotic cell death. The upregulation of the cyclin-dependent kinase inhibitor p21 and the dephosphorylation of retinoblastoma protein (pRb) appear to be critical regulatory events for the establishment of both the postmitotic and apoptosis-resistant states. The coordinated regulation of cell proliferation and death provides the developing embryo with a mechanism for controlling muscle mass and thereby the size of individual motor units.
authors.affiliation: Division of Cardiovascular Research, St Elizabeth's Medical Center, Tufts University School of Medicine, Boston, Massachusetts, USA. kwalsh@opal.tufts.edu
authors.forename: K
authors.initials: K
authors.lastname: Walsh
authors.forename: H
authors.initials: H
authors.lastname: Perlman
mesh_terms: D000818:Animals; D017209:Apoptosis; D002453:Cell Cycle / Q000502:physiology*; D002454:Cell Differentiation / Q000502:physiology*; D050759:Cyclin-Dependent Kinase Inhibitor p21; D018844:Cyclin-Dependent Kinases / Q000378:metabolism; D016213:Cyclins / Q000502:physiology; D004627:Embryonic Induction; D008938:Mitosis; D009119:Muscle Contraction; D018482:Muscle, Skeletal / Q000166:cytology / Q000196:embryology*; D016160:Retinoblastoma Protein / Q000096:biosynthesis
chemical_list: D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D016160:Retinoblastoma Protein; D018844:Cyclin-Dependent Kinases