BAIT

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)
PREY

SRS2

HPR5, DNA helicase SRS2, RADH1, RADH, L000000809, L000001578, YJL092W
DNA helicase and DNA-dependent ATPase; involved in DNA repair and checkpoint recovery, needed for proper timing of commitment to meiotic recombination and transition from Meiosis I to II; blocks trinucleotide repeat expansion; affects genome stability; disassembles Rad51p nucleoprotein filaments during meiotic recombination; functional homolog of human RTEL1
Saccharomyces cerevisiae (S288c)

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.

Publication

Srs2 overexpression reveals a helicase-independent role at replication forks that requires diverse cell functions.

Leon Ortiz AM, Reid RJ, Dittmar JC, Rothstein R, Nicolas A

Srs2 is a 3'-5' DNA helicase that regulates many aspects of DNA metabolism in Saccharomyces cerevisiae. It is best known for its ability to counteract homologous recombination by dismantling Rad51 filaments, but is also involved in checkpoint activation, adaptation and recovery, and in resolution of late recombination intermediates. To further address its biological roles and uncover new genetic interactions, we ... [more]

Unknown Mar. 31, 2011; 0(0); [Pubmed: 21459050]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Additional Notes

  • Dosage lethality was observed when SRS2 was overexpressed in a mec1 tel1 double mutant.
  • The deletion of MEC1 was combined with deletion of SML1 to suppress lethality.
  • genetic complex

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SRS2 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-0.1601BioGRID
2438227
TEL1 SRS2
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.

Low-BioGRID
939350

Curated By

  • BioGRID