BAIT

ELG1

RTT110, S000007438, YOR144C
Subunit of an alternative replication factor C complex; important for DNA replication and genome integrity; suppresses spontaneous DNA damage; involved in homologous recombination-mediated repair and telomere homeostasis; required for PCNA (Pol30p) unloading during DNA replication
Saccharomyces cerevisiae (S288c)
PREY

RAD59

L000003987, YDL059C
Protein involved DNA double-strand break repair; repairs breaks in DNA during vegetative growth via recombination and single-strand annealing; anneals complementary single-stranded DNA; forms nuclear foci upon DNA replication stress; required for loading of Rad52p to DSBs; paralog of Rad52p
GO Process (4)
GO Function (1)
GO Component (2)
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

Access to PCNA by Srs2 and Elg1 Controls the Choice between Alternative Repair Pathways in Saccharomyces cerevisiae.

Arbel M, Bronstein A, Sau S, Liefshitz B, Kupiec M

During DNA replication, stalling can occur when the replicative DNA polymerases encounter lesions or hard-to replicate regions. Under these circumstances, the processivity factor PCNA gets ubiquitylated at lysine 164, inducing the DNA damage tolerance (DDT) mechanisms that can bypass lesions encountered during DNA replication. PCNA can also be SUMOylated at the same residue or at lysine 127. Surprisingly, pol30-K164R mutants ... [more]

mBio May. 05, 2020; 11(3); [Pubmed: 32371600]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: resistance to chemicals (APO:0000087)

Additional Notes

  • Deletion of RAD59 partly abolished the suppression of pol30-K164R by either RAD52 or ELG1 OE

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
ELG1 RAD59
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-0.2263BioGRID
2427320

Curated By

  • BioGRID