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
Kinome Project (Sc)
Saccharomyces cerevisiae (S288c)
PREY

RPB2

RPB150, RPO22, SIT2, SOH2, DNA-directed RNA polymerase II core subunit RPB2, B150, L000001588, L000001676, YOR151C
RNA polymerase II second largest subunit B150; part of central core; similar to bacterial beta subunit
GO Process (1)
GO Function (3)
GO Component (3)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

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

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: vegetative growth (APO:0000106)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SGV1 RPB2
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-0.2002BioGRID
1957074

Curated By

  • BioGRID