BAIT

DUN1

serine/threonine protein kinase DUN1, L000000531, YDL101C
Cell-cycle checkpoint serine-threonine kinase; required for DNA damage-induced transcription of certain target genes, phosphorylation of Rad55p and Sml1p, and transient G2/M arrest after DNA damage; Mec1p and Dun1p function in same pathway to regulate both dNTP pools and telomere length; also regulates postreplicative DNA repair
GO Process (3)
GO Function (1)
GO Component (1)

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)
PREY

RAD5

REV2, SNM2, DNA helicase RAD5, L000001559, YLR032W
DNA helicase/Ubiquitin ligase; involved in error-free branch of DNA damage tolerance (DDT) pathway; proposed to promote replication fork regression during postreplication repair by template switching; stimulates synthesis of free and PCNA-bound polyubiquitin chains by Ubc13p-Mms2p; required for error-prone translesion synthesis; forms nuclear foci upon DNA replication stress; associates with native telomeres, cooperates with homologous recombination in senescent cells
Saccharomyces cerevisiae (S288c)

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.

Publication

A Network of Conserved Synthetic Lethal Interactions for Exploration of Precision Cancer Therapy.

Srivas R, Shen JP, Yang CC, Sun SM, Li J, Gross AM, Jensen J, Licon K, Bojorquez-Gomez A, Klepper K, Huang J, Pekin D, Xu JL, Yeerna H, Sivaganesh V, Kollenstart L, van Attikum H, Aza-Blanc P, Sobol RW, Ideker T

An emerging therapeutic strategy for cancer is to induce selective lethality in a tumor by exploiting interactions between its driving mutations and specific drug targets. Here we use a multi-species approach to develop a resource of synthetic lethal interactions relevant to cancer therapy. First, we screen in yeast ∼169,000 potential interactions among orthologs of human tumor suppressor genes (TSG) and ... [more]

Mol. Cell Aug. 04, 2016; 63(3);514-25 [Pubmed: 27453043]

Quantitative Score

  • -8.63 [Confidence Score]

Throughput

  • High Throughput

Ontology Terms

  • colony size (APO:0000063)

Additional Notes

  • Untreated conditions. SGA was used to score genetic interactions based on the colony size of double versus single mutants. Genetic interactions were considered significant if they had an S score >= 2.0 for positive interactions (epistatic or suppressor interactions) and S score <= -2.5 for negative interactions (synthetic sick/lethal interactions).

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
DUN1 RAD5
Dosage Lethality
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.

Low-BioGRID
153925
RAD5 DUN1
Phenotypic Enhancement
Phenotypic Enhancement

A genetic interaction is inferred when mutation or overexpression of one gene results in enhancement of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.

Low-BioGRID
349814
DUN1 RAD5
Synthetic Growth Defect
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.

High-BioGRID
452897
RAD5 DUN1
Synthetic Growth Defect
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.

High-BioGRID
457063

Curated By

  • BioGRID