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
PEP5
Gene Ontology Biological Process
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
Efficient Tor signaling requires a functional class C Vps protein complex in Saccharomyces cerevisiae.
The Tor kinases regulate responses to nutrients and control cell growth. Unlike most organisms that only contain one Tor protein, Saccharomyces cerevisiae expresses two, Tor1 and Tor2, which are thought to share all of the rapamycin-sensitive functions attributable to Tor signaling. Here we conducted a genetic screen that defined the global TOR1 synthetic fitness or lethal interaction gene network. This ... [more]
Throughput
- Low Throughput
Ontology Terms
- phenotype: inviable (APO:0000112)
Related interactions
Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
---|---|---|---|---|---|---|
PEP5 TOR1 | 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 | 948334 |
Curated By
- BioGRID