BAIT

RAD27

ERC11, FEN1, RTH1, multifunctional nuclease RAD27, L000002742, L000000565, YKL113C
5' to 3' exonuclease, 5' flap endonuclease; required for Okazaki fragment processing and maturation, for long-patch base-excision repair and large loop repair (LLR), ribonucleotide excision repair; member of the S. pombe RAD2/FEN1 family; relocalizes to the cytosol in response to hypoxia
Saccharomyces cerevisiae (S288c)
PREY

MRC1

YCL060C, chromatin-modulating protein MRC1, YCL061C
S-phase checkpoint protein required for DNA replication; couples DNA helicase and DNA polymerase; interacts with and stabilizes Pol2p at stalled replication forks during stress, where it forms a pausing complex with Tof1p and is phosphorylated by Mec1p; with Hog1p defines a novel S-phase checkpoint that permits eukaryotic cells to prevent conflicts between DNA replication and transcription; protects uncapped telomeres; degradation via Dia2p help cells resume cell cycle
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

Tel1/ATM prevents degradation of replication forks that reverse after topoisomerase poisoning.

Menin L, Ursich S, Trovesi C, Zellweger R, Lopes M, Longhese MP, Clerici M

In both yeast and mammals, the topoisomerase poison camptothecin (CPT) induces fork reversal, which has been proposed to stabilize replication forks, thus providing time for the repair of CPT-induced lesions and supporting replication restart. We show that Tel1, the Saccharomyces cerevisiae orthologue of human ATM kinase, stabilizes CPT-induced reversed forks by counteracting their nucleolytic degradation by the MRX complex. Tel1-lacking ... [more]

EMBO Rep. May. 08, 2018; (); [Pubmed: 29739811]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: vegetative growth (APO:0000106)
  • phenotype: resistance to chemicals (APO:0000087)

Additional Notes

  • MRC1 deletion increased the CPT hypersensitivity of rad27, sae2, and tdp1/rad1 double mutant cells

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RAD27 MRC1
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-9.913BioGRID
214303
MRC1 RAD27
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-0.1484BioGRID
360507
RAD27 MRC1
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-0.1484BioGRID
394074
RAD27 MRC1
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-0.2389BioGRID
2143613
MRC1 RAD27
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-0.1647BioGRID
2086375
RAD27 MRC1
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-10.1042BioGRID
322331
MRC1 RAD27
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
430789
RAD27 MRC1
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
341805
MRC1 RAD27
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
452998
RAD27 MRC1
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
453326
MRC1 RAD27
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
451425
RAD27 MRC1
Synthetic Lethality
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.

Low-BioGRID
166756

Curated By

  • BioGRID