BAIT

ESS1

PIN1, PTF1, peptidylprolyl isomerase ESS1, L000000587, YJR017C
Peptidylprolyl-cis/trans-isomerase (PPIase); specific for phosphorylated serine and threonine residues N-terminal to proline; regulates phosphorylation of the RNAP II large subunit (Rpo21p) C-terminal domain (CTD); associates with phospho-Ser5 form of RNAP II in vivo; regulates phosphorylation of Ser7 within CTD; present along entire coding length of genes; represses initiation of CUTs; required for efficient termination of mRNA transcription and trimethylation of histone H3
Saccharomyces cerevisiae (S288c)
PREY

PTA1

FUN39, RNA-processing protein PTA1, L000001522, YAL043C
Subunit of holo-CPF; holo-CPF is a multiprotein complex and functional homolog of mammalian CPSF, required for the cleavage and polyadenylation of mRNA and snoRNA 3' ends; involved in pre-tRNA processing; binds to the phosphorylated CTD of RNAPII
Saccharomyces cerevisiae (S288c)

Dosage Lethality

A genetic interaction is inferred when over expression or increased dosage of one gene causes lethality in a strain that is mutated or deleted for another gene.

Publication

Functional interaction of the Ess1 prolyl isomerase with components of the RNA polymerase II initiation and termination machineries.

Krishnamurthy S, Ghazy MA, Moore C, Hampsey M

The C-terminal domain (CTD) of the largest subunit of RNA polymerase II (Pol II) is a reiterated heptad sequence (Tyr1-Ser2-Pro3-Thr4-Ser5-Pro6-Ser7) that plays a key role in the transcription cycle, coordinating the exchange of transcription and RNA processing factors. The structure of the CTD is flexible and undergoes conformational changes in response to serine phosphorylation and proline isomerization. Here we report ... [more]

Mol. Cell. Biol. Jun. 01, 2009; 29(11);2925-34 [Pubmed: 19332564]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
PTA1 ESS1
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-0.1521BioGRID
1918969

Curated By

  • BioGRID