BAIT

SAE2

COM1, ssDNA endodeoxyribonuclease SAE2, L000002892, YGL175C
Endonuclease required for telomere elongation; also required for telomeric 5' C-rich strand resection; involved in processing hairpin DNA structures with MRX complex; involved in double-strand break repair; required for normal resistance to DNA-damaging agents; exists in form of inactive oligomers that are transiently released into smaller active units by a series of phosphorylations; DNA damage triggers removal of Sae2p ensuring that active Sae2p is present only transiently
Saccharomyces cerevisiae (S288c)
PREY

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
Kinome Project (Sc)
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

Sae2 Function at DNA Double-Strand Breaks Is Bypassed by Dampening Tel1 or Rad53 Activity.

Gobbini E, Villa M, Gnugnoli M, Menin L, Clerici M, Longhese MP

The MRX complex together with Sae2 initiates resection of DNA double-strand breaks (DSBs) to generate single-stranded DNA (ssDNA) that triggers homologous recombination. The absence of Sae2 not only impairs DSB resection, but also causes prolonged MRX binding at the DSBs that leads to persistent Tel1- and Rad53-dependent DNA damage checkpoint activation and cell cycle arrest. Whether this enhanced checkpoint signaling ... [more]

PLoS Genet. Nov. 01, 2015; 11(11);e1005685 [Pubmed: 26584331]

Throughput

  • Low Throughput

Ontology Terms

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

Additional Notes

  • The Rad53-H88Y and Tel1-N2021D variants suppress the DNA damage hypersensitivity of sae2 mutant cells

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SAE2 RAD53
Affinity Capture-MS
Affinity Capture-MS

An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and the associated interaction partner is identified by mass spectrometric methods.

High-BioGRID
-
RAD53 SAE2
Dosage Growth Defect
Dosage Growth Defect

A genetic interaction is inferred when over expression or increased dosage of one gene causes a growth defect in a strain that is mutated or deleted for another gene.

Low-BioGRID
519355
SAE2 RAD53
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
2543630
RAD53 SAE2
Protein-peptide
Protein-peptide

An interaction is detected between a protein and a peptide derived from an interaction partner. This includes phage display experiments.

High-BioGRID
-
SAE2 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.

High-BioGRID
1173459
RAD53 SAE2
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
3575294

Curated By

  • BioGRID