BAIT

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)
PREY

RAD17

L000001566, YOR368W
Checkpoint protein; involved in the activation of the DNA damage and meiotic pachytene checkpoints; with Mec3p and Ddc1p, forms a clamp that is loaded onto partial duplex DNA; homolog of human and S. pombe Rad1 and U. maydis Rec1 proteins
GO Process (3)
GO Function (1)
GO Component (2)

Gene Ontology Molecular Function

Gene Ontology Cellular Component

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

DNA bending facilitates the error-free DNA damage tolerance pathway and upholds genome integrity.

Gonzalez-Huici V, Szakal B, Urulangodi M, Psakhye I, Castellucci F, Menolfi D, Rajakumara E, Fumasoni M, Bermejo R, Jentsch S, Branzei D

DNA replication is sensitive to damage in the template. To bypass lesions and complete replication, cells activate recombination-mediated (error-free) and translesion synthesis-mediated (error-prone) DNA damage tolerance pathways. Crucial for error-free DNA damage tolerance is template switching, which depends on the formation and resolution of damage-bypass intermediates consisting of sister chromatid junctions. Here we show that a chromatin architectural pathway involving ... [more]

EMBO J. Feb. 18, 2014; 33(4);327-40 [Pubmed: 24473148]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Additional Notes

  • MMS

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RAD5 RAD17
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.

High-BioGRID
2607074
RAD5 RAD17
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-0.1982BioGRID
396960
RAD17 RAD5
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-0.2575BioGRID
2188077
RAD5 RAD17
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-0.2048BioGRID
2149304
RAD17 RAD5
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-0.1705BioGRID
2434415
RAD5 RAD17
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-12.6BioGRID
2357178
RAD5 RAD17
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
447409
RAD17 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
457568
RAD5 RAD17
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
457582

Curated By

  • BioGRID