BAIT

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)
PREY

MEC1

ESR1, RAD31, SAD3, protein kinase MEC1, L000000586, S000029404, S000007656, YBR136W
Genome integrity checkpoint protein and PI kinase superfamily member; Mec1p and Dun1p function in same pathway to regulate dNTP pools and telomere length; signal transducer required for cell cycle arrest and transcriptional responses to damaged or unreplicated DNA; facilitates replication fork progression and regulates P-body formation under replication stress; promotes interhomolog recombination by phosphorylating Hop1p; associates with shortened, dysfunctional telomeres
Kinome Project (Sc)
Saccharomyces cerevisiae (S288c)

Synthetic Rescue

A genetic interaction is inferred when mutations or deletions of one gene rescues the lethality or growth defect of a strain mutated or deleted for another gene.

Publication

Recovery from checkpoint-mediated arrest after repair of a double-strand break requires Srs2 helicase.

Vaze MB, Pellicioli A, Lee SE, Ira G, Liberi G, Arbel-Eden A, Foiani M, Haber JE

In Saccharomyces strains in which homologous recombination is delayed sufficiently to activate the DNA damage checkpoint, Rad53p checkpoint kinase activity appears 1 hr after DSB induction and disappears soon after completion of repair. Cells lacking Srs2p helicase fail to recover even though they apparently complete DNA repair; Rad53p kinase remains activated. srs2Delta cells also fail to adapt when DSB repair ... [more]

Mol. Cell Aug. 01, 2002; 10(2);373-85 [Pubmed: 12191482]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: cell cycle progression through the g2/m phase transition (APO:0000257)

Additional Notes

  • Mec1/Sml1 double mutants suppress the recovery defect of Srs2 mutants from check-point mediated cell cycle arrest
  • genetic complex

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
MEC1 SRS2
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
531097
MEC1 SRS2
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-BioGRID
3750248
MEC1 SRS2
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-BioGRID
-
SRS2 MEC1
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
480371
MEC1 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
196096

Curated By

  • BioGRID