BAIT

RAD53

LSD1, MEC2, SPK1, serine/threonine/tyrosine protein kinase RAD53, L000001573, YPL153C
DNA damage response protein kinase; required for cell-cycle arrest in response to DNA damage; activated by trans autophosphorylation when interacting with hyperphosphorylated Rad9p; also interacts with ARS1 and plays a role in initiation of DNA replication; activates the downstream kinase Dun1p; differentially senses mtDNA depletion and mitochondrial ROS; required for regulation of copper genes in response to DNA-damaging agents; relocalizes to cytosol in response to hyoxia
Saccharomyces cerevisiae (S288c)
PREY

RRM3

RTT104, S000007420, YHR031C
DNA helicase involved in rDNA replication and Ty1 transposition; binds to and suppresses DNA damage at G4 motifs in vivo; relieves replication fork pauses at telomeric regions; structurally and functionally related to Pif1p
Saccharomyces cerevisiae (S288c)

Synthetic Rescue

A genetic interaction is inferred when mutations or deletions of one gene rescues the lethality or growth defect of a strain mutated or deleted for another gene.

Publication

Rad53-Mediated Regulation of Rrm3 and Pif1 DNA Helicases Contributes to Prevention of Aberrant Fork Transitions under Replication Stress.

Rossi SE, Ajazi A, Carotenuto W, Foiani M, Giannattasio M

Replication stress activates the Mec1(ATR) and Rad53 kinases. Rad53 phosphorylates nuclear pores to counteract gene gating, thus preventing aberrant transitions at forks approaching transcribed genes. Here, we show that Rrm3 and Pif1, DNA helicases assisting fork progression across pausing sites, are detrimental in rad53 mutants experiencing replication stress. Rrm3 and Pif1 ablations rescue cell lethality, chromosome fragmentation, replisome-fork dissociation, fork ... [more]

Cell Rep Oct. 06, 2015; 13(1);80-92 [Pubmed: 26411679]

Throughput

  • Low Throughput

Ontology Terms

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

Additional Notes

  • Figure 4
  • RRM3 deletion partially rescues HU-sensitivity of sml1 rad53 double mutant
  • genetic complex

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RAD53 RRM3
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-0.179BioGRID
1892461
RAD53 RRM3
Phenotypic Suppression
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.

Low-BioGRID
258511
RAD53 RRM3
Phenotypic Suppression
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.

Low-BioGRID
2344831
RAD53 RRM3
Positive Genetic
Positive Genetic

Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a less severe fitness defect than expected under a given condition. This term is reserved for high or low throughput studies with scores.

High0.2515BioGRID
1892460
RRM3 RAD53
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
437106
RAD53 RRM3
Synthetic Rescue
Synthetic Rescue

A genetic interaction is inferred when mutations or deletions of one gene rescues the lethality or growth defect of a strain mutated or deleted for another gene.

Low-BioGRID
2340212

Curated By

  • BioGRID