BAIT

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)
PREY

SUB1

TSP1, L000003936, YMR039C
Transcriptional coactivator; facilitates elongation through factors that modify RNAP II; role in peroxide resistance involving Rad2p; role in nonhomologous end-joining (NHEJ) of ds breaks in plasmid DNA, but not chromosomal DNA; role in the hyperosmotic stress response through polymerase recruitment at RNAP II and RNAP III genes; protein abundance increases in response to DNA replication stress
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

Sub1 globally regulates RNA polymerase II C-terminal domain phosphorylation.

Garcia A, Rosonina E, Manley JL, Calvo O

The transcriptional coactivator Sub1 has been implicated in several aspects of mRNA metabolism in yeast, such as activation of transcription, termination, and 3'-end formation. Here, we present evidence that Sub1 plays a significant role in controlling phosphorylation of the RNA polymerase II large subunit C-terminal domain (CTD). We show that SUB1 genetically interacts with the genes encoding all four known ... [more]

Mol. Cell. Biol. Nov. 01, 2010; 30(21);5180-93 [Pubmed: 20823273]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
CTK1 SUB1
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-0.1481BioGRID
2144028

Curated By

  • BioGRID