BAIT

SSN3

CDK8, GIG2, NUT7, RYE5, SRB10, SSX7, UME5, URR1, cyclin-dependent serine/threonine protein kinase SSN3, L000002795, S000029631, L000002443, S000029520, L000002103, YPL042C
Cyclin-dependent protein kinase; component of RNA polymerase II holoenzyme; involved in phosphorylation of the RNA polymerase II C-terminal domain; involved in glucose repression
Saccharomyces cerevisiae (S288c)
PREY

CTK1

cyclin-dependent serine/threonine protein kinase CTK1, L000000432, YKL139W
Catalytic (alpha) subunit of C-terminal domain kinase I (CTDK-I); phosphorylates both RNA pol II subunit Rpo21p to affect transcription and pre-mRNA 3' end processing, and ribosomal protein Rps2p to increase translational fidelity; required for H3K36 trimethylation but not dimethylation by Set2p; similar to the Drosophila dCDK12 and human CDK12 and probably CDK13
Saccharomyces cerevisiae (S288c)

Synthetic Growth Defect

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

Publication

Functional relationships of Srb10-Srb11 kinase, carboxy-terminal domain kinase CTDK-I, and transcriptional corepressor Ssn6-Tup1.

Kuchin S, Carlson M

The Srb10-Srb11 protein kinase of Saccharomyces cerevisiae is a cyclin-dependent kinase (cdk)-cyclin pair which has been found associated with the carboxy-terminal domain (CTD) of RNA polymerase II holoenzyme forms. Previous genetic findings implicated the Srb10-Srb11 kinase in transcriptional repression. Here we use synthetic promoters and LexA fusion proteins to test the requirement for Srb10-Srb11 in repression by Ssn6-Tup1, a global ... [more]

Mol. Cell. Biol. Mar. 01, 1998; 18(3);1163-71 [Pubmed: 9488431]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: vegetative growth (APO:0000106)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SSN3 CTK1
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-6.135BioGRID
510252

Curated By

  • BioGRID