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

OLE1

MDM2, stearoyl-CoA 9-desaturase, L000001052, L000001297, YGL055W
Delta(9) fatty acid desaturase; required for monounsaturated fatty acid synthesis and for normal distribution of mitochondria
GO Process (1)
GO Function (2)
GO Component (2)
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

Prolyl isomerase Pin1 acts as a switch to control the degree of substrate ubiquitylation.

Siepe D, Jentsch S

Pin1, a conserved eukaryotic peptidyl-prolyl cis/trans isomerase, has important roles in cellular regulation. Because of its activity to switch the conformation of peptidyl-proline bonds in polypeptide chains, Pin1 operates as a binary switch, often in fate-determining pathways. Pin1 activity is usually controlled by substrate phosphorylation, but how Pin1 switches protein fates has been unclear. Here we show that Pin1 controls ... [more]

Nat. Cell Biol. Aug. 01, 2009; 11(8);967-72 [Pubmed: 19597489]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: vegetative growth (APO:0000106)

Additional Notes

  • inviability of ess1 mutant was rescued by overexpression of OLE1

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
OLE1 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-0.1451BioGRID
1932516

Curated By

  • BioGRID