BAIT

CLN2

cyclin CLN2, L000000358, YPL256C
G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN2 has a paralog, CLN1, that arose from the whole genome duplication
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
Saccharomyces cerevisiae (S288c)

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.

Publication

Stb1 collaborates with other regulators to modulate the G1-specific transcriptional circuit.

de Bruin RA, Kalashnikova TI, Wittenberg C

G(1)-specific transcription in the budding yeast Saccharomyces cerevisiae depends upon SBF and MBF. Whereas inactivation of SBF-regulated genes during the G(1)/S transition depends upon mitotic B-type cyclins, inactivation of MBF has been reported to involve multiple regulators, Nrm1 and Stb1. Nrm1 is a transcriptional corepressor that inactivates MBF-regulated transcription via negative feedback as cells exit G(1) phase. Cln/cyclin-dependent kinase (CDK)-dependent ... [more]

Mol. Cell. Biol. Nov. 01, 2008; 28(22);6919-28 [Pubmed: 18794370]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: rna accumulation (APO:0000224)

Additional Notes

  • Inactivation of the Clb/CDK specific inhibitor Sic1 in a cln1 cln2 double mutant lowers the increased G1-specific transcript levels observed in the double mutant..

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SIC1 CLN2
Affinity Capture-Western
Affinity Capture-Western

An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and the associated interaction partner identified by Western blot with a specific polyclonal antibody or second epitope tag. This category is also used if an interacting protein is visualized directly by dye stain or radioactivity. Note that this differs from any co-purification experiment involving affinity capture in that the co-purification experiment involves at least one extra purification step to get rid of potential contaminating proteins.

Low-BioGRID
-
SIC1 CLN2
Affinity Capture-Western
Affinity Capture-Western

An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and the associated interaction partner identified by Western blot with a specific polyclonal antibody or second epitope tag. This category is also used if an interacting protein is visualized directly by dye stain or radioactivity. Note that this differs from any co-purification experiment involving affinity capture in that the co-purification experiment involves at least one extra purification step to get rid of potential contaminating proteins.

Low-BioGRID
-
CLN2 SIC1
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
818548
CLN2 SIC1
Synthetic Rescue
Synthetic Rescue

A genetic interaction is inferred when mutations or deletions of one gene rescues the lethality or growth defect of a strain mutated or deleted for another gene.

Low-BioGRID
252996

Curated By

  • BioGRID