BAIT

CDC73

L000002792, YLR418C
Component of the Paf1p complex; binds to and modulates the activity of RNA polymerases I and II; required for expression of certain genes, modification of some histones, and telomere maintenance; involved in transcription elongation as demonstrated by the G-less-based run-on (GLRO) assay; protein abundance increases in response to DNA replication stress; human homologue, parafibromin, is a tumour suppressor linked to breast, renal and gastric cancers
Saccharomyces cerevisiae (S288c)
PREY

YPD1

L000003285, YDL235C
Osmotic stress-responsive phosphorelay intermediate sensor protein; phosphorylated by the plasma membrane sensor Sln1p in response to osmotic stress and then in turn phosphorylates the response regulators Ssk1p in the cytosol and Skn7p in the nucleus
GO Process (1)
GO Function (2)
GO Component (2)
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

Saccharomyces cerevisiae Genetics Predicts Candidate Therapeutic Genetic Interactions at the Mammalian Replication Fork.

van Pel DM, Stirling PC, Minaker SW, Sipahimalani P, Hieter P

The concept of synthetic lethality has gained popularity as a rational guide for predicting chemotherapeutic targets based on negative genetic interactions between tumor-specific somatic mutations and a second-site target gene. One hallmark of most cancers that can be exploited by chemotherapies is chromosome instability (CIN). Because chromosome replication, maintenance, and segregation represent conserved and cell-essential processes, they can be modeled ... [more]

G3 (Bethesda) Feb. 01, 2013; 3(2);273-82 [Pubmed: 23390603]

Quantitative Score

  • 0.00350372 [SGA Score]

Throughput

  • High Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Additional Notes

  • SGA analysis for synthetic lethal interactions between mutations whose human orthologs are found to be mutated in cancers, and the deletion mutant collection, where the interaction probability P < 0.05

Curated By

  • BioGRID