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

MGS1

ssDNA-dependent ATPase MGS1, YNL218W
Protein with DNA-dependent ATPase and ssDNA annealing activities; involved in maintenance of genome; interacts functionally with DNA polymerase delta; homolog of human Werner helicase interacting protein (WHIP); forms nuclear foci upon DNA replication stress
UPS Project
GO Process (3)
GO Function (2)
GO Component (2)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)

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.

Publication

Post-replication repair suppresses duplication-mediated genome instability.

Putnam CD, Hayes TK, Kolodner RD

RAD6 is known to suppress duplication-mediated gross chromosomal rearrangements (GCRs) but not single-copy sequence mediated GCRs. Here, we found that the RAD6- and RAD18-dependent post-replication repair (PRR) and the RAD5-, MMS2-, UBC13-dependent error-free PRR branch acted in concert with the replication stress checkpoint to suppress duplication-mediated GCRs formed by homologous recombination (HR). The Rad5 helicase activity, but not its RING ... [more]

PLoS Genet. May. 01, 2010; 6(5);e1000933 [Pubmed: 20463880]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: chromosome/plasmid maintenance (APO:0000143)

Additional Notes

  • double mutants show increased rates of duplication-mediated GCRs

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
MGS1 RAD5
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
262012
MGS1 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
262019
MGS1 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
204245
RAD5 MGS1
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
457068

Curated By

  • BioGRID