TOR1
Gene Ontology Biological Process
- TOR signaling [IC, IMP]
- cellular response to DNA damage stimulus [IMP]
- fungal-type cell wall organization [IMP]
- meiotic nuclear division [IMP]
- mitochondria-nucleus signaling pathway [IMP]
- negative regulation of autophagy [IGI]
- regulation of cell cycle [IMP]
- regulation of cell growth [IMP]
- regulation of sphingolipid biosynthetic process [IMP]
- ribosome biogenesis [IMP]
- transcription of nuclear large rRNA transcript from RNA polymerase I promoter [IMP]
- translational initiation [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
SLT2
Gene Ontology Biological Process
- UFP-specific transcription factor mRNA processing involved in endoplasmic reticulum unfolded protein response [IMP]
- barrier septum assembly [IGI]
- endoplasmic reticulum unfolded protein response [IDA, IMP]
- fungal-type cell wall biogenesis [IGI]
- peroxisome degradation [IMP]
- protein phosphorylation [IDA, IMP]
- regulation of cell size [IMP]
- regulation of fungal-type cell wall organization [IGI, IMP]
- regulation of transcription factor import into nucleus [IMP]
- response to acidic pH [IMP]
- signal transduction [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
Probing the membrane environment of the TOR kinases reveals functional interactions between TORC1, actin, and membrane trafficking in Saccharomyces cerevisiae.
The TOR kinases are regulators of growth in eukaryotic cells that assemble into two distinct protein complexes, TORC1 and TORC2, where TORC1 is inhibited by the antibiotic rapamycin. Present models favor a view wherein TORC1 regulates cell mass accumulation, and TORC2 regulates spatial aspects of growth, including organization of the actin cytoskeleton. Here, we demonstrate that in yeast both TORC1 ... [more]
Throughput
- High Throughput
Ontology Terms
- phenotype: inviable (APO:0000112)
Related interactions
| Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
|---|---|---|---|---|---|---|
| TOR1 SLT2 | Co-fractionation Co-fractionation Interaction inferred from the presence of two or more protein subunits in a partially purified protein preparation. If co-fractionation is demonstrated between 3 or more proteins, then add them as a complex. | High | - | BioGRID | - | |
| TOR1 SLT2 | Dosage Rescue Dosage Rescue A genetic interaction is inferred when over expression or increased dosage of one gene rescues the lethality or growth defect of a strain that is mutated or deleted for another gene. | Low | - | BioGRID | 426521 | |
| TOR1 SLT2 | 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 | 514222 | |
| TOR1 SLT2 | 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 | 429505 | |
| SLT2 TOR1 | Synthetic Lethality 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. | Low | - | BioGRID | 158294 |
Curated By
- BioGRID