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

RAD9

chromatin-binding protein RAD9, L000001562, YDR217C
DNA damage-dependent checkpoint protein; required for cell-cycle arrest in G1/S, intra-S, and G2/M, plays a role in postreplication repair (PRR) pathway; transmits checkpoint signal by activating Rad53p and Chk1p; hyperphosphorylated by Mec1p and Tel1p; multiple cyclin dependent kinase consensus sites and the C-terminal BRCT domain contribute to DNA damage checkpoint activation; Rad9p Chk1 Activating Domain (CAD) is phosphorylated at multiple sites by Cdc28p/Clb2p
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

The Main Role of Srs2 in DNA Repair Depends on Its Helicase Activity, Rather than on Its Interactions with PCNA or Rad51.

Bronstein A, Gershon L, Grinberg G, Alonso-Perez E, Kupiec M

Homologous recombination (HR) is a mechanism that repairs a variety of DNA lesions. Under certain circumstances, however, HR can generate intermediates that can interfere with other cellular processes such as DNA transcription or replication. Cells have therefore developed pathways that abolish undesirable HR intermediates. The Saccharomyces cerevisiae yeast Srs2 helicase has a major role in one of these pathways. Srs2 ... [more]

MBio Jul. 17, 2018; 9(4); [Pubmed: 30018112]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SRS2 RAD9
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-0.145BioGRID
390691
RAD9 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-0.145BioGRID
368354
SRS2 RAD9
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-0.1628BioGRID
2438247
SRS2 RAD9
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
252578
RAD9 SRS2
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
532149
RAD9 SRS2
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
479491

Curated By

  • BioGRID