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
UPS Project
Saccharomyces cerevisiae (S288c)
PREY

MMS2

E2 ubiquitin-conjugating protein MMS2, L000004015, YGL087C
Ubiquitin-conjugating enzyme variant; involved in error-free postreplication repair; forms a heteromeric complex with Ubc13p, an active ubiquitin-conjugating enzyme; cooperates with chromatin-associated RING finger proteins, Rad18p and Rad5p; protein abundance increases in response to DNA replication stress
UPS Project
GO Process (4)
GO Function (1)
GO Component (3)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

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

The Rad5 Helicase and RING Domains Contribute to Genome Stability through their Independent Catalytic Activities.

Toth R, Balogh D, Pinter L, Jaksa G, Szeplaki B, Graf A, Gyorfy Z, Enyedi MZ, Kiss E, Haracska L, Unk I

Genomic stability is compromised by DNA damage that obstructs replication. Rad5 plays a prominent role in DNA damage bypass processes that evolved to ensure the continuation of stalled replication. Like its human orthologs, the HLTF and SHPRH tumor suppressors, yeast Rad5 has a RING domain that supports ubiquitin ligase activity promoting PCNA polyubiquitylation and a helicase domain that in the ... [more]

J Mol Biol Mar. 15, 2022; 434(5);167437 [Pubmed: 34990655]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: vegetative growth (APO:0000106)
  • phenotype: uv resistance (APO:0000085)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RAD5 MMS2
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
156605
MMS2 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.

Low-BioGRID
438207
RAD5 MMS2
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
2354681
RAD5 MMS2
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
518922
MMS2 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.

Low-BioGRID
940821
RAD5 MMS2
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
1519032

Curated By

  • BioGRID