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

QRI1

UAP1, UDP-N-acetylglucosamine diphosphorylase, L000002652, YDL103C
UDP-N-acetylglucosamine pyrophosphorylase; catalyzes the formation of UDP-N-acetylglucosamine (UDP-GlcNAc), which is important in cell wall biosynthesis, protein N-glycosylation, and GPI anchor biosynthesis; protein abundance increases in response to DNA replication stress
GO Process (1)
GO Function (1)
GO Component (2)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)

Dosage Lethality

A genetic interaction is inferred when over expression or increased dosage of one gene causes lethality in a strain that is mutated or deleted for another gene.

Publication

Regulation of cell polarity through phosphorylation of Bni4 by Pho85 G1 cyclin-dependent kinases in Saccharomyces cerevisiae.

Zou J, Friesen H, Larson J, Huang D, Cox M, Tatchell K, Andrews B

In the budding yeast Saccharomyces cerevisiae, the G1-specific cyclin-dependent kinases (Cdks) Cln1,2-Cdc28 and Pcl1,2-Pho85 are essential for ensuring that DNA replication and cell division are properly linked to cell polarity and bud morphogenesis. However, the redundancy of Cdks and cyclins means that identification of relevant Cdk substrates remains a significant challenge. We used array-based genetic screens (synthetic genetic array or ... [more]

Mol. Biol. Cell Jul. 01, 2009; 20(14);3239-50 [Pubmed: 19458192]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
CLN2 QRI1
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-0.1919BioGRID
2446071

Curated By

  • BioGRID