BAIT

ESP1

L000000584, YGR098C
Separase, a caspase-like cysteine protease; promotes sister chromatid separation by mediating dissociation of the cohesin Scc1p from chromatin; inhibits protein phosphatase 2A-Cdc55p to promote mitotic exit; inhibited by Pds1p; relative distribution to the nucleus increases upon DNA replication stress
Saccharomyces cerevisiae (S288c)
PREY

DED1

SPP81, DEAD-box ATP-dependent RNA helicase DED1, L000000500, YOR204W
ATP-dependent DEAD (Asp-Glu-Ala-Asp)-box RNA helicase; required for translation initiation of all yeast mRNAs; binds to mRNA cap-associated factors, and binding stimulates Ded1p RNA-dependent ATPase activity; mutation in human homolog DBY is associated with male infertility; human homolog DDX3X complements ded1 null mutation; DED1 has a paralog, DBP1, that arose from the whole genome duplication
GO Process (2)
GO Function (3)
GO Component (2)

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)

Affinity Capture-MS

An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and the associated interaction partner is identified by mass spectrometric methods.

Publication

A role for the budding yeast separase, Esp1, in Ty1 element retrotransposition.

Ho KL, Ma L, Cheung S, Manhas S, Fang N, Wang K, Young B, Loewen C, Mayor T, Measday V

Separase/Esp1 is a protease required at the onset of anaphase to cleave cohesin and thereby enable sister chromatid separation. Esp1 also promotes release of the Cdc14 phosphatase from the nucleolus to enable mitotic exit. To uncover other potential roles for separase, we performed two complementary genome-wide genetic interaction screens with a strain carrying the budding yeast esp1-1 separase mutation. We ... [more]

PLoS Genet. Mar. 01, 2015; 11(3);e1005109 [Pubmed: 25822502]

Throughput

  • High Throughput

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
ESP1 DED1
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-0.2253BioGRID
1934718

Curated By

  • BioGRID