ASF1
Gene Ontology Biological Process
- DNA replication-dependent nucleosome assembly [IDA]
- DNA replication-independent nucleosome assembly [IDA]
- chromatin silencing at silent mating-type cassette [IGI]
- chromatin silencing at telomere [IGI]
- histone H2B ubiquitination [IMP]
- histone acetylation [IMP]
- histone exchange [IMP]
- nucleosome disassembly [IMP]
- positive regulation of histone acetylation [IDA, IGI, IMP, IPI]
- positive regulation of transcription elongation from RNA polymerase II promoter [IDA]
- regulation of transcription from RNA polymerase II promoter in response to stress [IMP]
Gene Ontology Molecular Function
RAD52
Gene Ontology Biological Process
- DNA amplification [IMP]
- DNA recombinase assembly [IDA]
- DNA strand renaturation [IDA]
- double-strand break repair via break-induced replication [IMP]
- double-strand break repair via homologous recombination [IMP]
- double-strand break repair via single-strand annealing [IGI]
- meiotic joint molecule formation [IGI, IMP]
- postreplication repair [IMP]
- telomere maintenance via recombination [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Synthetic Lethality
A genetic interaction is inferred when mutations or deletions in separate genes, each of which alone causes a minimal phenotype, result in lethality when combined in the same cell under a given condition.
Publication
Histone H3K56 acetylation, CAF1, and Rtt106 coordinate nucleosome assembly and stability of advancing replication forks.
Chromatin assembly mutants accumulate recombinogenic DNA damage and are sensitive to genotoxic agents. Here we have analyzed why impairment of the H3K56 acetylation-dependent CAF1 and Rtt106 chromatin assembly pathways, which have redundant roles in H3/H4 deposition during DNA replication, leads to genetic instability. We show that the absence of H3K56 acetylation or the simultaneous knock out of CAF1 and Rtt106 ... [more]
Throughput
- Low Throughput
Ontology Terms
- phenotype: inviable (APO:0000112)
Related interactions
| Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
|---|---|---|---|---|---|---|
| RAD52 ASF1 | Phenotypic Enhancement 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. | Low | - | BioGRID | 156625 | |
| ASF1 RAD52 | 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 | 556674 | |
| ASF1 RAD52 | 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 | 3553309 | |
| ASF1 RAD52 | 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 | 452799 | |
| RAD52 ASF1 | 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 | 457180 | |
| ASF1 RAD52 | 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 | 163409 |
Curated By
- BioGRID