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
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
The rapamycin-sensitive phosphoproteome reveals that TOR controls protein kinase A toward some but not all substrates.
Regulation of cell growth requires extensive coordination of several processes including transcription, ribosome biogenesis, translation, nutrient metabolism, and autophagy. In yeast, the protein kinases Target of Rapamycin (TOR) and protein kinase A (PKA) regulate these processes and are thereby the main activators of cell growth in response to nutrients. How TOR, PKA, and their corresponding signaling pathways are coordinated to ... [more]
Throughput
- Low Throughput
Ontology Terms
- phenotype: chemical compound accumulation (APO:0000095)
Additional Notes
- Mpk1 deletion abolishes the hyperaccumulation of glycogen seen in a Tor1 mutant
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 | 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 | |
| TOR1 SLT2 | 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. | High | - | BioGRID | 256653 | |
| 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