Regulation of CDC14: pathways and checkpoints of mitotic exit.
Progression of the mitotic cell cycle is driven by fluctuations of the cyclin-dependent kinase (Cdk) activities. Entry into mitosis is promoted by the elevated activity of Cdk1 associated with B-type cyclins. Conversely, exit from mitosis requires the inactivation of Cdk1 and the dephosphorylation of at least a subset of Cdk1 substrates. The Cdc14 family of phosphatases antagonizes the action of Cdk1, and is thus a major player in controlling the mitotic exit. We review recent discoveries in several model systems that have shed light on the function of Cdc14 and propose a general framework within which Cdc14 plays conserved roles in regulating the exit from mitosis and cytokinesis.
Bembenek
Joshua
J
Department of Pharmacology, UT Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9041, USA.
Yu
Hongtao
H
D002453:Cell Cycle / Q000235:genetics / Q000502:physiology*; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism* / Q000502:physiology; D006801:Humans; D017027:Protein Tyrosine Phosphatases / Q000235:genetics / Q000378:metabolism* / Q000502:physiology; D029701:Saccharomyces cerevisiae Proteins / Q000235:genetics / Q000378:metabolism* / Q000502:physiology; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology*
C074860:CDC14 protein, S cerevisiae; D018797:Cell Cycle Proteins; D029701:Saccharomyces cerevisiae Proteins; D017027:Protein Tyrosine Phosphatases