BAIT

DBF2

serine/threonine-protein kinase DBF2, L000000487, YGR092W
Ser/Thr kinase involved in transcription and stress response; functions as part of a network of genes in exit from mitosis; localization is cell cycle regulated; activated by Cdc15p during the exit from mitosis; also plays a role in regulating the stability of SWI5 and CLB2 mRNAs; phosphorylates Chs2p to regulate primary septum formation and Hof1p to regulate cytokinesis; DBF2 has a paralog, DBF20, that arose from the whole genome duplication
Kinome Project (Sc)
Saccharomyces cerevisiae (S288c)
PREY

SIC1

SDB25, cyclin-dependent protein serine/threonine kinase inhibiting protein SIC1, L000001886, L000001822, YLR079W
Cyclin-dependent kinase inhibitor (CKI); inhibitor of Cdc28-Clb kinase complexes that controls G1/S phase transition, preventing premature S phase and ensuring genomic integrity; phosphorylated by Clb5/6-Cdk1 and Cln1/2-Cdk1 kinase which regulate timing of Sic1p degradation; phosphorylation targets Sic1p for SCF(CDC4)-dependent turnover; functional homolog of mammalian Kip1
Kinome Project (Sc)
Saccharomyces cerevisiae (S288c)

Dosage Rescue

A genetic interaction is inferred when over expression or increased dosage of one gene rescues the lethality or growth defect of a strain that is mutated or deleted for another gene.

Publication

DNA replication is completed in Saccharomyces cerevisiae cells that lack functional Cdc14, a dual-specificity protein phosphatase.

Fitzpatrick PJ, Toyn JH, Millar JB, Johnston LH

The Cdc14 protein encodes a dual-specificity protein phosphatase which functions in late mitosis, and considerable genetic evidence suggests a role in DNA replication. We find that cdc14 mutants arrested in late mitosis maintain persistent levels of mitotic kinase activity, suggesting that Cdc14 controls inactivation of this kinase. Overexpression of Sicl, a cyclin-dependent protein kinase inhibitor, is able to suppress telophase ... [more]

Mol. Gen. Genet. May. 01, 1998; 258(4);437-41 [Pubmed: 9648751]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: cell cycle progression in telophase (APO:0000265)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
DBF2 SIC1
Dosage Rescue
Dosage Rescue

A genetic interaction is inferred when over expression or increased dosage of one gene rescues the lethality or growth defect of a strain that is mutated or deleted for another gene.

Low-BioGRID
155424
DBF2 SIC1
Dosage Rescue
Dosage Rescue

A genetic interaction is inferred when over expression or increased dosage of one gene rescues the lethality or growth defect of a strain that is mutated or deleted for another gene.

Low-BioGRID
155418
SIC1 DBF2
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-0.1311BioGRID
397366
SIC1 DBF2
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-9.82BioGRID
2358716
SIC1 DBF2
Synthetic Lethality
Synthetic Lethality

A genetic interaction is inferred when mutations or deletions in separate genes, each of which alone causes a minimal phenotype, result in lethality when combined in the same cell under a given condition.

High-BioGRID
456735
SIC1 DBF2
Synthetic Lethality
Synthetic Lethality

A genetic interaction is inferred when mutations or deletions in separate genes, each of which alone causes a minimal phenotype, result in lethality when combined in the same cell under a given condition.

Low-BioGRID
158811

Curated By

  • BioGRID