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

SPT6

CRE2, SSN20, chromatin-remodeling histone chaperone SPT6, L000002032, YGR116W
Nucleosome remodeling protein; functions in various aspects of transcription, chromatin maintenance, and RNA processing; required for the maintenance of chromatin structure during transcription in order to inhibit transcription from promoters within the coding region; required for H3K36 trimethylation but not dimethylation by Set2p
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
SPT6 SGV1
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-0.2403BioGRID
1934931

Curated By

  • BioGRID