BAIT

KIN28

TFIIH complex serine/threonine-protein kinase subunit KIN28, L000000905, YDL108W
Serine/threonine protein kinase, subunit of transcription factor TFIIH; involved in transcription initiation at RNA polymerase II promoters; phosphorylates Ser5 residue of the PolII C-terminal domain (CTD) at gene promoters; relocalizes to the cytosol in response to hypoxia
Saccharomyces cerevisiae (S288c)
PREY

PDE2

SRA5, 3',5'-cyclic-nucleotide phosphodiesterase PDE2, L000002046, YOR360C
High-affinity cyclic AMP phosphodiesterase; component of the cAMP-dependent protein kinase signaling system, protects the cell from extracellular cAMP, contains readthrough motif surrounding termination codon
GO Process (1)
GO Function (1)
GO Component (2)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)

Dosage Rescue

A genetic interaction is inferred when over expression or increased dosage of one gene rescues the lethality or growth defect of a strain that is mutated or deleted for another gene.

Publication

The C-terminal domain of the largest subunit of RNA polymerase II is required for stationary phase entry and functionally interacts with the Ras/PKA signaling pathway.

Howard SC, Budovskaya YV, Chang YW, Herman PK

The Saccharomyces cerevisiae Ras proteins control cell growth by regulating the activity of the cAMP-dependent protein kinase (PKA). In this study, a genetic approach was used to identify cellular processes that were regulated by Ras/PKA signaling activity. Interestingly, we found that mutations affecting the C-terminal domain (CTD), of Rpb1p, the largest subunit of RNA polymerase II, were very sensitive to ... [more]

J. Biol. Chem. May. 31, 2002; 277(22);19488-97 [Pubmed: 12032176]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: heat sensitivity (APO:0000147)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
PDE2 KIN28
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-0.1833BioGRID
2071452

Curated By

  • BioGRID