RAD53
Gene Ontology Biological Process
Gene Ontology Molecular Function
MRE11
Gene Ontology Biological Process
- DNA double-strand break processing involved in repair via synthesis-dependent strand annealing [IMP]
- DNA repair [IMP]
- ascospore formation [IMP]
- base-excision repair [IMP]
- double-strand break repair via break-induced replication [IGI, IMP]
- double-strand break repair via nonhomologous end joining [IMP]
- meiotic DNA double-strand break formation [TAS]
- meiotic DNA double-strand break processing [TAS]
- mitochondrial double-strand break repair via homologous recombination [IMP]
- reciprocal meiotic recombination [IMP]
- regulation of transcription during meiosis [IMP]
Gene Ontology Molecular Function- 3'-5' exonuclease activity [IDA]
- G-quadruplex DNA binding [IDA]
- adenylate kinase activity [IDA]
- double-stranded telomeric DNA binding [IDA]
- endodeoxyribonuclease activity [IDA]
- endonuclease activity [IDA]
- protein complex scaffold [IGI, IMP]
- single-stranded telomeric DNA binding [IDA]
- telomeric DNA binding [IDA]
- 3'-5' exonuclease activity [IDA]
- G-quadruplex DNA binding [IDA]
- adenylate kinase activity [IDA]
- double-stranded telomeric DNA binding [IDA]
- endodeoxyribonuclease activity [IDA]
- endonuclease activity [IDA]
- protein complex scaffold [IGI, IMP]
- single-stranded telomeric DNA binding [IDA]
- telomeric DNA binding [IDA]
Gene Ontology Cellular Component
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
Sae2 Function at DNA Double-Strand Breaks Is Bypassed by Dampening Tel1 or Rad53 Activity.
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]
Throughput
- Low Throughput
Ontology Terms
- phenotype: resistance to chemicals (APO:0000087)
Additional Notes
- deletion of mre11 inhibits the suppression of DNA damage sensitivity by Rad53-H88Y and Tel1-N2021D variants in sae2 mutant cells
Related interactions
Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
---|---|---|---|---|---|---|
RAD53 MRE11 | 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 | 454858 |
Curated By
- BioGRID