BAIT

SGV1

BUR1, cyclin-dependent serine/threonine protein kinase SGV1, L000001878, YPR161C
Cyclin (Bur2p)-dependent protein kinase; part of the BUR kinase complex which functions in transcriptional regulation; phosphorylates the carboxy-terminal domain (CTD) of Rpo21p and the C-terminal repeat domain of Spt5p; recruits Spt6p to the CTD at the onset of transcription; regulated by Cak1p; similar to metazoan CDK9 proteins
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 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

Phosphorylation of the RNA polymerase II carboxy-terminal domain by the Bur1 cyclin-dependent kinase.

Murray S, Udupa R, Yao S, Hartzog G, Prelich G

BUR1, which was previously identified by a selection for mutations that have general effects on transcription in Saccharomyces cerevisiae, encodes a cyclin-dependent kinase that is essential for viability, but none of its substrates have been identified to date. Using an unbiased biochemical approach, we have identified the carboxy-terminal domain (CTD) of Rpb1, the largest subunit of RNA polymerase II, as ... [more]

Mol. Cell. Biol. Jul. 01, 2001; 21(13);4089-96 [Pubmed: 11390638]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SGV1 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-0.1937BioGRID
2024836
CTK1 SGV1
Phenotypic Enhancement
Phenotypic Enhancement

A genetic interaction is inferred when mutation or overexpression of one gene results in enhancement of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.

Low-BioGRID
2343422
SGV1 CTK1
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
157685

Curated By

  • BioGRID