PREY

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)

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.

Publication

Mammalian Cdk5 is a functional homologue of the budding yeast Pho85 cyclin-dependent protein kinase.

Huang D, Patrick G, Moffat J, Tsai LH, Andrews B

Mammalian Cdk5 is a member of the cyclin-dependent kinase family that is activated by a neuron-specific regulator, p35, to regulate neuronal migration and neurite outgrowth. p35/Cdk5 kinase colocalizes with and regulates the activity of the Pak1 kinase in neuronal growth cones and likely impacts on actin cytoskeletal dynamics through Pak1. Here, we describe a functional homologue of Cdk5 in budding ... [more]

Proc. Natl. Acad. Sci. U.S.A. Dec. 07, 1999; 96(25);14445-50 [Pubmed: 10588725]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Additional Notes

  • pho85 cln1 cln2 triple mutant inviable

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
PHO85 CLN2
Dosage Lethality
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.

High-BioGRID
350219

Curated By

  • BioGRID