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

MRE11

NGS1, RAD58, XRS4, MRX complex nuclease subunit, L000004732, L000001149, L000004275, YMR224C
Nuclease subunit of the MRX complex with Rad50p and Xrs2p; complex functions in repair of DNA double-strand breaks and in telomere stability; Mre11p associates with Ser/Thr-rich ORFs in premeiotic phase; nuclease activity required for MRX function; widely conserved; forms nuclear foci upon DNA replication stress
Saccharomyces cerevisiae (S288c)

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.

Publication

The Saccharomyces cerevisiae Mre11-Rad50-Xrs2 complex promotes trinucleotide repeat expansions independently of homologous recombination.

Ye Y, Kirkham-McCarthy L, Lahue RS

Trinucleotide repeats (TNRs) are tandem arrays of three nucleotides that can expand in length to cause at least 17 inherited human diseases. Somatic expansions in patients can occur in differentiated tissues where DNA replication is limited and cannot be a primary source of somatic mutation. Instead, mouse models of TNR diseases have shown that both inherited and somatic expansions can ... [more]

DNA Repair (Amst.) Jul. 01, 2016; 43(0);1-8 [Pubmed: 27173583]

Throughput

  • Low Throughput

Ontology Terms

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

Additional Notes

  • Figure 3
  • MRE11 deletion suppresses increased expansion rate of rad5 mutant

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RAD5 MRE11
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
2607155
MRE11 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-BioGRID
3492786
RAD5 MRE11
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-2.81BioGRID
2356670
MRE11 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
269246
MRE11 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
456988
RAD5 MRE11
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
457070

Curated By

  • BioGRID