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)

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

Uncoupling Sae2 Functions in Downregulation of Tel1 and Rad53 Signaling Activities.

Colombo CV, Menin L, Ranieri R, Bonetti D, Clerici M, Longhese MP

The Mre11-Rad50-Xrs2 (MRX) complex acts together with the Sae2 protein to initiate resection of DNA double-strand breaks (DSBs) and to regulate a checkpoint response that couples cell cycle progression with DSB repair. Sae2 supports resistance to DNA damage and downregulates the signaling activities of MRX, Tel1, and Rad53 checkpoint proteins at the sites of damage. How these functions are connected ... [more]

Genetics Dec. 01, 2018; 211(2);515-530 [Pubmed: 30538107]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: resistance to chemicals (APO:0000087)

Additional Notes

  • The sae2-ms allele failed to suppress the HU hypersensitivity of tel1/mec1, rad9/mec1 and rad53/mec1 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
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
SAE2 RAD53
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
2204382

Curated By

  • BioGRID