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

IKI3

ELP1, KTI7, TOT1, Elongator subunit IKI3, L000003563, YLR384C
Subunit of Elongator complex; Elongator is required for modification of wobble nucleosides in tRNA; maintains structural integrity of Elongator; homolog of human IKAP, mutations in which cause familial dysautonomia (FD)
GO Process (2)
GO Function (1)
GO Component (3)

Gene Ontology Molecular Function

Gene Ontology Cellular Component

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

Involvement of yeast carboxy-terminal domain kinase I (CTDK-I) in transcription elongation in vivo.

Jona G, Wittschieben BO, Svejstrup JQ, Gileadi O

Yeast cells lacking transcription elongation factor genes such as PPR2 (TFIIS) and ELP (Elongator) are viable and show deleterious phenotypes only when transcription is rendered less effective by RNA polymerase mutations or by decreasing nucleotide pools. Here we demonstrate that deletion of the CTK1 gene, encoding the kinase subunit of RNA polymerase II carboxy-terminal domain kinase I (CTDK-I), is synthetically ... [more]

Gene Apr. 04, 2001; 267(1);31-6 [Pubmed: 11311553]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
CTK1 IKI3
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-10.5634BioGRID
308220

Curated By

  • BioGRID