BAIT

RAD52

recombinase RAD52, L000001572, YML032C
Protein that stimulates strand exchange; stimulates strand exchange by facilitating Rad51p binding to single-stranded DNA; anneals complementary single-stranded DNA; involved in the repair of double-strand breaks in DNA during vegetative growth and meiosis and UV induced sister chromatid recombination
Saccharomyces cerevisiae (S288c)
PREY

TEL1

DNA-binding protein kinase TEL1, L000002281, YBL088C
Protein kinase primarily involved in telomere length regulation; contributes to cell cycle checkpoint control in response to DNA damage; acts with Red1p and Mec1p to promote interhomolog recombination by phosphorylation of Hop1; functionally redundant with Mec1p; regulates P-body formation induced by replication stress; homolog of human ataxia-telangiectasia mutated (ATM) gene, the gene responsible for ataxia telangiectasia (AT) (OMIM 607585)
Kinome Project (Sc)
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

Tel1/ATM prevents degradation of replication forks that reverse after topoisomerase poisoning.

Menin L, Ursich S, Trovesi C, Zellweger R, Lopes M, Longhese MP, Clerici M

In both yeast and mammals, the topoisomerase poison camptothecin (CPT) induces fork reversal, which has been proposed to stabilize replication forks, thus providing time for the repair of CPT-induced lesions and supporting replication restart. We show that Tel1, the Saccharomyces cerevisiae orthologue of human ATM kinase, stabilizes CPT-induced reversed forks by counteracting their nucleolytic degradation by the MRX complex. Tel1-lacking ... [more]

EMBO Rep. May. 08, 2018; (); [Pubmed: 29739811]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: resistance to chemicals (APO:0000087)
  • phenotype: vegetative growth (APO:0000106)

Additional Notes

  • Tel1 deletion increased CPT (CHEBI:27656) hypersensitivity in the single mutant cells

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RAD52 TEL1
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-3.3995BioGRID
221123
TEL1 RAD52
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
2542700
RAD52 TEL1
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
937504
RAD52 TEL1
Phenotypic Suppression
Phenotypic Suppression

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

Low-BioGRID
1174300
TEL1 RAD52
Phenotypic Suppression
Phenotypic Suppression

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

Low-BioGRID
2598589

Curated By

  • BioGRID