BAIT

CDC14

OAF3, phosphoprotein phosphatase CDC14, L000000254, YFR028C
Protein phosphatase required for mitotic exit; required for rDNA segregation, cytokinesis, meiosis I spindle disassembly, and environmental stress response; maintained in nucleolus by Cdc55p in early meiosis until liberated by the FEAR and Mitotic Exit Network in anaphase, enabling it to effect a decrease in CDK/B-cyclin activity and mitotic exit; sequestered in metaphase II, then released again upon entry into anaphase II
Kinome Project (Sc)
Saccharomyces cerevisiae (S288c)
PREY

SWI5

DNA-binding transcription factor SWI5, L000002253, YDR146C
Transcription factor that recruits Mediator and Swi/Snf complexes; activates transcription of genes expressed at the M/G1 phase boundary and in G1 phase; required for expression of the HO gene controlling mating type switching; localization to nucleus occurs during G1 and appears to be regulated by phosphorylation by Cdc28p kinase; SWI5 has a paralog, ACE2, that arose from the whole genome duplication
Saccharomyces cerevisiae (S288c)

Biochemical Activity (Dephosphorylation)

An interaction is inferred from the biochemical effect of one protein upon another, for example, GTP-GDP exchange activity or phosphorylation of a substrate by a kinase. The bait protein executes the activity on the substrate hit protein. A Modification value is recorded for interactions of this type with the possible values Phosphorylation, Ubiquitination, Sumoylation, Dephosphorylation, Methylation, Prenylation, Acetylation, Deubiquitination, Proteolytic Processing, Glucosylation, Nedd(Rub1)ylation, Deacetylation, No Modification, Demethylation.

Publication

The phosphatase Cdc14 triggers mitotic exit by reversal of Cdk-dependent phosphorylation.

Visintin R, Craig K, Hwang ES, Prinz S, Tyers M, Amon A

Exit from mitosis requires the inactivation of mitotic cyclin-dependent kinases (CDKs) by an unknown mechanism. We show that the Cdc14 phosphatase triggers mitotic exit by three parallel mechanisms, each of which inhibits Cdk activity. Cdc14 dephosphorylates Sic1, a Cdk inhibitor, and Swi5, a transcription factor for SIC1, and induces degradation of mitotic cyclins, likely by dephosphorylating the activator of mitotic ... [more]

Mol. Cell Dec. 01, 1998; 2(6);709-18 [Pubmed: 9885559]

Throughput

  • Low Throughput

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
CDC14 SWI5
Negative Genetic
Negative Genetic

Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores.

High-0.3759BioGRID
378106
SWI5 CDC14
Negative Genetic
Negative Genetic

Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores.

High-0.4298BioGRID
2034609
CDC14 SWI5
Negative Genetic
Negative Genetic

Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores.

High-0.4821BioGRID
1980146
CDC14 SWI5
Phenotypic Suppression
Phenotypic Suppression

A genetic interaction is inferred when mutation or over expression of one gene results in suppression of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.

Low-BioGRID
657488

Curated By

  • BioGRID