MRC1
Gene Ontology Biological Process
- DNA repair [IGI, IMP]
- DNA replication [IMP]
- DNA replication checkpoint [IGI, IMP, IPI]
- chromatin silencing at silent mating-type cassette [IGI, IMP]
- chromatin silencing at telomere [IGI, IMP]
- intra-S DNA damage checkpoint [IMP]
- maintenance of DNA repeat elements [IMP]
- mitotic sister chromatid cohesion [IGI, IMP]
- regulation of nuclear cell cycle DNA replication [IMP]
- replication fork protection [IGI, IMP, IPI]
- telomere maintenance [IMP]
Gene Ontology Cellular Component
RAD6
Gene Ontology Biological Process
- DNA-templated transcription, termination [IMP]
- ER-associated ubiquitin-dependent protein catabolic process [IGI]
- chromatin silencing at telomere [IMP]
- double-strand break repair via homologous recombination [IGI]
- error-free postreplication DNA repair [IGI]
- error-free translesion synthesis [IGI]
- error-prone translesion synthesis [IGI]
- histone monoubiquitination [IMP]
- meiotic DNA double-strand break formation [IMP]
- mitotic G1 DNA damage checkpoint [IMP]
- protein monoubiquitination [IMP]
- protein polyubiquitination [IMP]
- protein ubiquitination involved in ubiquitin-dependent protein catabolic process [IMP]
- regulation of dipeptide transport [IMP]
- telomere maintenance via recombination [IGI]
- transcription from RNA polymerase II promoter [IPI]
- ubiquitin-dependent protein catabolic process via the N-end rule pathway [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
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.
Publication
Post-replication repair suppresses duplication-mediated genome instability.
RAD6 is known to suppress duplication-mediated gross chromosomal rearrangements (GCRs) but not single-copy sequence mediated GCRs. Here, we found that the RAD6- and RAD18-dependent post-replication repair (PRR) and the RAD5-, MMS2-, UBC13-dependent error-free PRR branch acted in concert with the replication stress checkpoint to suppress duplication-mediated GCRs formed by homologous recombination (HR). The Rad5 helicase activity, but not its RING ... [more]
Throughput
- Low Throughput
Ontology Terms
- phenotype: chromosome/plasmid maintenance (APO:0000143)
Additional Notes
- double mutants show a synergistic increase in the rate of GCRs
Related interactions
| Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
|---|---|---|---|---|---|---|
| MRC1 RAD6 | 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 | 453002 | |
| RAD6 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 | 457385 |
Curated By
- BioGRID