The Phosphatase Cdc14 Triggers Mitotic Exit by Reversal of Cdk-Dependent Phosphorylation
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This work shows that the Cdc14 phosphatase triggers mitotic exit by three parallel mechanisms, each of which inhibits Cdk activity, and induces degradation of mitotic cyclins.About:
This article is published in Molecular Cell.The article was published on 1998-12-01 and is currently open access. It has received 780 citations till now. The article focuses on the topics: Mitotic exit & Polo-like kinase.read more
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The cyclin-dependent kinase inhibitor Roughex is involved in mitotic exit in Drosophila
Edan Foley,Frank Sprenger +1 more
TL;DR: Rux inhibits Cdk1-cyclin A kinase activity during metaphase, thereby contributing to exit from mitosis, the first mitotic function ascribed to a CKI in a multicellular organism and indicates the existence of a novel regulatory mechanism for the metaphase to anaphase transition during development.
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The Mitotic Exit Network Mob1p-Dbf2p Kinase Complex Localizes to the Nucleus and Regulates Passenger Protein Localization
TL;DR: Evidence is presented that the MEN protein kinase complex Mob1p-Dbf2p localizes to mitotic nuclei and partially colocalizes with Cdc14p and kinetochore proteins, which implicate MEN in coordinating chromosome segregation and/or spindle integrity with mitotic exit and cytokinesis via regulation of chromosome passenger proteins.
Structure-Templated Predictions of Novel Protein Interactions from Sequence
Information Betel,Kevin E. Breitkreuz,Ruth Isserlin,Danielle Dewar-Darch,Mike Tyers,Christopher W. V. Hogue +5 more
TL;DR: In this paper, a predictive method known as domain-motif interactions from structural topology (D-MIST) was proposed for elucidating the binding profiles of interacting domains.
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The Spo12 protein of Saccharomyces cerevisiae: a regulator of mitotic exit whose cell cycle-dependent degradation is mediated by the anaphase-promoting complex.
TL;DR: Site-directed mutagenesis of highly conserved residues in the Spo12 protein sequence abolishes both its mitotic suppressor activity as well as its meiotic function, the first indication that Spo12 may carry out the same biochemical function in mitosis as it does in meiosis.
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FgCDC14 regulates cytokinesis, morphogenesis, and pathogenesis in Fusarium graminearum
Chaohui Li,Michael Melesse,Shijie Zhang,Shijie Zhang,Chaofeng Hao,Chenfang Wang,Hongchang Zhang,Mark C. Hall,Jin-Rong Xu,Jin-Rong Xu +9 more
TL;DR: Results indicate that Cdc14 phosphatase functions in cell division and septum formation in F. graminearum, likely by counteracting Cdk phosphorylation, and is required for plant infection.
References
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Cyclin-dependent kinases: engines, clocks, and microprocessors.
TL;DR: This work has shown that Cdk activity is governed by a complex network of regulatory subunits and phosphorylation events whose precise effects on Cdk conformation have been revealed by recent crystallographic studies.
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SKP1 connects cell cycle regulators to the ubiquitin proteolysis machinery through a novel motif, the F-box.
TL;DR: Different skp1 mutants arrest cells in either G1 or G2, suggesting a connection between regulation of proteolysis in different stages of the cycle.
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How proteolysis drives the cell cycle
TL;DR: Proteolysis drives cell cycle progression not only by regulating CDK activity, but by directly influencing chromosome and spindle dynamics, and also how proteolysis may directly trigger the transition from metaphase to anaphase.
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F-Box Proteins Are Receptors that Recruit Phosphorylated Substrates to the SCF Ubiquitin-Ligase Complex
TL;DR: The ubiquitination pathway for the Cdk inhibitor Sic1 is reconstituted using recombinant proteins and the constituents of the SCF complex are members of protein families, likely to serve as the prototype for a large class of E3s formed by combinatorial interactions of related family members.
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The Saccharomyces cerevisiae Cell Cycle
TL;DR: The bibliography is intended more as a guide to the literature than as a historically accurate record of the development of the field; the authors apologize to the earlier workers whose contributions thus get less explicit credit than they deserve.