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

JLP2

YMR132C
Protein of unknown function; contains sequence that closely resembles a J domain (typified by the E. coli DnaJ protein)
GO Process (0)
GO Function (0)
GO Component (1)

Gene Ontology Cellular Component

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

The Yeast Ess1 Prolyl Isomerase Controls Swi6 and Whi5 Nuclear Localization.

Atencio D, Barnes C, Duncan TM, Willis IM, Hanes SD

The Ess1 prolyl isomerase from Saccharomyces cerevisiae and its human ortholog, Pin1, play critical roles in transcription by regulating RNA polymerase II. In human cells, Pin1 also regulates a variety of signaling proteins and Pin1 misexpression is linked to several human diseases. To gain insight into Ess1/Pin1 function, we carried out a synthetic genetic array screen to identify novel targets ... [more]

G3 (Bethesda) Jan. 27, 2014; 0(0); [Pubmed: 24470217]

Quantitative Score

  • 1.0 [Confidence Score]

Throughput

  • High Throughput

Ontology Terms

  • phenotype: vegetative growth (APO:0000106)

Additional Notes

  • SGA analysis with bait strain ess1-H164R

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
JLP2 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-0.2977BioGRID
2062233

Curated By

  • BioGRID