BAIT

EXO1

DHS1, Rad2 family nuclease EXO1, L000000505, L000003929, YOR033C
5'-3' exonuclease and flap-endonuclease; involved in recombination, double-strand break repair, MMS2 error-free branch of the post replication (PRR) pathway and DNA mismatch repair; role in telomere maintenance; member of the Rad2p nuclease family, with conserved N and I nuclease domains; relative distribution to the nucleus increases upon DNA replication stress; EXO1 has a paralog, DIN7, that arose from the whole genome duplication
Saccharomyces cerevisiae (S288c)
PREY

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)

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

A mutation in EXO1 defines separable roles in DNA mismatch repair and post-replication repair.

Tran PT, Fey JP, Erdeniz N, Gellon L, Boiteux S, Liskay RM

Replication forks stall at DNA lesions or as a result of an unfavorable replicative environment. These fork stalling events have been associated with recombination and gross chromosomal rearrangements. Recombination and fork bypass pathways are the mechanisms accountable for restart of stalled forks. An important lesion bypass mechanism is the highly conserved post-replication repair (PRR) pathway that is composed of error-prone ... [more]

DNA Repair (Amst.) Nov. 01, 2007; 6(11);1572-83 [Pubmed: 17602897]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
EXO1 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
269245
EXO1 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
1105091

Curated By

  • BioGRID