FB2026_02 , released June 18, 2026
FB2026_02 , released June 18, 2026
Gene: Dmel\mTor
Open Close
General Information
Symbol
Dmel\mTor
Species
D. melanogaster
Name
mechanistic Target of rapamycin
Annotation Symbol
CG5092
Feature Type
FlyBase ID
FBgn0021796
Gene Model Status
Stock Availability
Gene Summary
Promotes cell and tissue growth, maintains tissue homeostatis and controls responses to environmental stress and aging (PubMed:11069885, PubMed:11069888, PubMed:19211682, PubMed:19225150). Regulates growth during animal development by coupling growth factor signaling to nutrient availability (PubMed:11069888). Central regulators of autophagy (PubMed:18604198, PubMed:19225150). May be involved in atg1 phosphorylation (PubMed:19225150). May also be involved, directly or indirectly, in the control of neuronal function (PubMed:15454083). Phosphorylates S6K/p70S6K, in vitro (PubMed:11069888). May regulate the activity of S6K (PubMed:11069885). Overexpression inhibits growth and reduces cell size (PubMed:14505573). Affects the timing of neuronal cell differentiation (PubMed:15454083). Hyperactivation of the signaling leads to accelerated differentiation, whereas inhibition of the signaling retards differentiation (PubMed:15454083). Thus, in addition to controlling growth of the cell in which it resides, it can also influence growth of distant cells and organs during development via a humoral mechanism (PubMed:14505573). As part of the TORC1 complex regulates energy homeostasis and promotes certain aspects of larval growth by negatively regulating REPTOR (PubMed:25920570). REPTOR functions downstream of TORC1 to regulate the expression of stress response genes in response to TORC1 inhibition resulting from nutrient deprivation (PubMed:25920570). When TORC1 activity is high it phosphorylates REPTOR which inhibits its recruitment into the nucleus and antagonizes their function (PubMed:25920570). This function is essential under normal feeding conditions to promote TORC1-dependent growth during larval development and, in adults and larvae to prevent the REPTOR-dependent expression of nutrient stress response genes (PubMed:25920570). In short, during development, it primarily controls growth, whereas in the adult, where there is relatively little growth, it controls aging and other aspects of nutrient-related physiology (PubMed:11069885, PubMed:11069888, PubMed:19211682, PubMed:19225150). Rag GTPases act as activators of TORC1 in response to amino acid signals (PubMed:18604198). (UniProt, Q9VK45)
Contribute a Gene Snapshot for this gene.
Also Known As

Tor, dTOR, target of rapamycin, TORC1, target-of-rapamycin

Key Links
Genomic Location
Cytogenetic map
Sequence location
Recombination map
2-47
RefSeq locus
NT_033779 REGION:13004480..13013197
Sequence
Genomic Maps
Other Genome Views
The following external sites may use different assemblies or annotations than FlyBase.
Function
Gene Ontology (GO) Annotations (39 terms)
Molecular Function (6 terms)
Terms Based on Experimental Evidence (3 terms)
CV Term
Evidence
References
inferred from direct assay
inferred from physical interaction with UniProtKB:Q9W328
inferred from direct assay
Terms Based on Predictions or Assertions (3 terms)
CV Term
Evidence
References
inferred from electronic annotation with InterPro:IPR018936
inferred from sequence model
inferred from sequence or structural similarity with UniProtKB:P42345
inferred from electronic annotation with InterPro:IPR026683
inferred from biological aspect of ancestor with PANTHER:PTN000124197
Biological Process (30 terms)
Terms Based on Experimental Evidence (29 terms)
CV Term
Evidence
References
inferred from mutant phenotype
inferred from direct assay
inferred from mutant phenotype
inferred from mutant phenotype
inferred from direct assay
inferred from mutant phenotype
involved_in gonad development
inferred from mutant phenotype
inferred from direct assay
inferred from mutant phenotype
inferred from mutant phenotype
involved_in macroautophagy
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:gig; FB:FBgn0005198
inferred from mutant phenotype
inferred from mutant phenotype
inferred from direct assay
inferred from mutant phenotype
inferred from mutant phenotype
involved_in TORC1 signaling
inferred from mutant phenotype
inferred from mutant phenotype
Terms Based on Predictions or Assertions (3 terms)
CV Term
Evidence
References
inferred from biological aspect of ancestor with PANTHER:PTN000124327
involved_in TORC1 signaling
inferred from biological aspect of ancestor with PANTHER:PTN000124328
involved_in TORC2 signaling
inferred from biological aspect of ancestor with PANTHER:PTN000124328
Cellular Component (3 terms)
Terms Based on Experimental Evidence (3 terms)
CV Term
Evidence
References
located_in cytoplasm
inferred from high throughput direct assay
inferred from mutant phenotype
inferred from direct assay
Terms Based on Predictions or Assertions (2 terms)
CV Term
Evidence
References
inferred from sequence or structural similarity with UniProtKB:P42345
inferred from biological aspect of ancestor with PANTHER:PTN001673232
inferred from biological aspect of ancestor with PANTHER:PTN001673232
inferred from sequence or structural similarity with UniProtKB:P42345
Protein Family (UniProt)
Belongs to the PI3/PI4-kinase family. (Q9VK45)
Summaries
Gene Group (FlyBase)
ATYPICAL PROTEIN KINASES -
Atypical kinases are protein kinases or putative protein kinases that do not share clear sequence similarity with conventional eukaryotic protein kinases, but they or their orthologs have been shown experimentally to have protein kinase activity. Atypical kinases are defined in FBrf0201870.
TORC1 COMPLEX -
TOR complex 1 (TORC1) is a target of rapamycin (Tor) kinase-containing complex that mediates the response to a variety of stimuli including stress, insulin-like peptides and amino acids. TORC1 regulates processes such as translation, cell growth and autophagy. It can be inhibited by rapamycin. (Adapted from FBrf0238220).
TORC2 COMPLEX -
TOR complex 2 (TORC2) is a target of rapamycin (Tor) kinase-containing complex that phosphorylates several AGC family kinases, including Akt1 (PKB). mTORC2 regulates a variety of cellular processes such as insulin signaling and actin reorganization. It is insensitive to rapamycin. (Adapted from FBrf0238220).
Pathway (FlyBase)
POSITIVE REGULATORS OF INSULIN-LIKE RECEPTOR SIGNALING PATHWAY -
Positive regulators of the Insulin-like Receptor signaling pathway enhance Insulin-like receptor (InR) activation or the activity of intracellular effectors. (Adapted from FBrf0232297, FBrf0230017 and FBrf0229989).
INSULIN-LIKE RECEPTOR SIGNALING PATHWAY CORE COMPONENTS -
The Insulin-like Receptor (IR) signaling pathway in Drosophila is initiated by the binding of an insulin-like peptides to the Insulin-like receptor (InR). (Adapted from FBrf0232297, FBrf0230017 and FBrf0229989.)
PVR SIGNALING PATHWAY CORE COMPONENTS -
PDGF/VEGF (Platelet-Derived Growth Factor/Vascular Endothelial Growth Factor)-receptor related (Pvr) encodes a receptor tyrosine kinase activated by the binding of PDGF- and VEGF-related factors (Pvf1,Pvf2 or Pvf3). Pvr has been shown to activate the canonical Ras/Raf/MAP kinase (ERK) cascade, the PI3K kinase pathway, TORC1 (FBrf0222697), Rho family small GTPases (FBrf0221764, FBrf0180198) and the JNK cascade (FBrf0180198), in a context-dependent manner. (Adapted from FBrf0222697 and FBrf0221727).
Protein Function (UniProtKB)
Promotes cell and tissue growth, maintains tissue homeostatis and controls responses to environmental stress and aging (PubMed:11069885, PubMed:11069888, PubMed:19211682, PubMed:19225150). Regulates growth during animal development by coupling growth factor signaling to nutrient availability (PubMed:11069888). Central regulators of autophagy (PubMed:18604198, PubMed:19225150). May be involved in atg1 phosphorylation (PubMed:19225150). May also be involved, directly or indirectly, in the control of neuronal function (PubMed:15454083). Phosphorylates S6K/p70S6K, in vitro (PubMed:11069888). May regulate the activity of S6K (PubMed:11069885). Overexpression inhibits growth and reduces cell size (PubMed:14505573). Affects the timing of neuronal cell differentiation (PubMed:15454083). Hyperactivation of the signaling leads to accelerated differentiation, whereas inhibition of the signaling retards differentiation (PubMed:15454083). Thus, in addition to controlling growth of the cell in which it resides, it can also influence growth of distant cells and organs during development via a humoral mechanism (PubMed:14505573). As part of the TORC1 complex regulates energy homeostasis and promotes certain aspects of larval growth by negatively regulating REPTOR (PubMed:25920570). REPTOR functions downstream of TORC1 to regulate the expression of stress response genes in response to TORC1 inhibition resulting from nutrient deprivation (PubMed:25920570). When TORC1 activity is high it phosphorylates REPTOR which inhibits its recruitment into the nucleus and antagonizes their function (PubMed:25920570). This function is essential under normal feeding conditions to promote TORC1-dependent growth during larval development and, in adults and larvae to prevent the REPTOR-dependent expression of nutrient stress response genes (PubMed:25920570). In short, during development, it primarily controls growth, whereas in the adult, where there is relatively little growth, it controls aging and other aspects of nutrient-related physiology (PubMed:11069885, PubMed:11069888, PubMed:19211682, PubMed:19225150). Rag GTPases act as activators of TORC1 in response to amino acid signals (PubMed:18604198).
(UniProt, Q9VK45)
Summary (Interactive Fly)

Phosphatidylinositol 3-kinase - involved in perception of nutrient status - pivotal member of the TOR pathway involved in regulation of growth and cell proliferation

Gene Model and Products
Number of Transcripts
2
Number of Unique Polypeptides
2

Please see the JBrowse view of Dmel\mTor for information on other features

To submit a correction to a gene model please use the Contact FlyBase form

Protein Domains (via Pfam)
Isoform displayed:
Pfam protein domains
InterPro name
classification
start
end
Protein Domains (via SMART)
Isoform displayed:
SMART protein domains
InterPro name
classification
start
end
Structure
Protein 3D structure   (Predicted by AlphaFold)   (AlphaFold entry Q9VK45)

If you don't see a structure in the viewer, refresh your browser.
Model Confidence:
  • Very high (pLDDT > 90)
  • Confident (90 > pLDDT > 70)
  • Low (70 > pLDDT > 50)
  • Very low (pLDDT < 50)

AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.

Experimentally Determined Structures
Crossreferences
Comments on Gene Model

Low-frequency RNA-Seq exon junction(s) not annotated.

Gene model reviewed during 5.48

Transcript Data
Annotated Transcripts
Name
FlyBase ID
RefSeq ID
Length (nt)
Assoc. CDS (aa)
FBtr0080422
7984
2470
FBtr0336615
7987
2471
Additional Transcript Data and Comments
Reported size (kB)
Comments
External Data
Crossreferences
Polypeptide Data
Annotated Polypeptides
Name
FlyBase ID
Predicted MW (kDa)
Length (aa)
Theoretical pI
UniProt
RefSeq ID
GenBank
FBpp0080003
281.0
2470
6.91
FBpp0307598
281.2
2471
6.91
Polypeptides with Identical Sequences

None of the polypeptides share 100% sequence identity.

Additional Polypeptide Data and Comments
Reported size (kDa)
Comments
External Data
Subunit Structure (UniProtKB)

May be part of a minimal complex, TORC1, consisting of mTor, raptor and lst8. May be part of a minimal complex, TORC2, consisting of mTor, rictor and lst8 (By similarity). Self-associates; assembles into homomultimeric complexes. Component of a multiprotein complex.

(UniProt, Q9VK45)
Linkouts
Sequences Consistent with the Gene Model
Mapped Features

Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\mTor using the Feature Mapper tool.

External Data
Crossreferences
Eukaryotic Promoter Database - A collection of databases of experimentally validated promoters for selected model organisms.
Linkouts
Expression Data
Testis-specificity index

The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).

-0.85

Transcript Expression
Additional Descriptive Data
Marker for
 
Subcellular Localization
CV Term
Polypeptide Expression
mass spectroscopy
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data
Marker for
 
Subcellular Localization
CV Term
Evidence
References
located_in cytoplasm
inferred from high throughput direct assay
inferred from mutant phenotype
inferred from direct assay
Expression Deduced from Reporters
High-Throughput Expression Data
Associated Tools

JBrowse - Visual display of RNA-Seq signals

View Dmel\mTor in JBrowse
RNA-Seq by Region - Search RNA-Seq expression levels by exon or genomic region
Reference
See Gelbart and Emmert, 2013 for analysis details and data files for all genes.
Developmental Proteome: Life Cycle
Developmental Proteome: Embryogenesis
External Data and Images
Linkouts
DRscDB - A single-cell RNA-seq resource for data mining and data comparison across species
EMBL-EBI Single Cell Expression Atlas - Single cell expression across species
FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
FlyAtlas2 - A Drosophila melanogaster expression atlas with RNA-Seq, miRNA-Seq and sex-specific data
Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
Flygut - An atlas of the Drosophila adult midgut
Images
Alleles, Insertions, Transgenic Constructs, and Aberrations
Classical and Insertion Alleles ( 29 )
For All Classical and Insertion Alleles Show
 
Other relevant insertions
Transgenic Constructs ( 25 )
For All Alleles Carried on Transgenic Constructs Show
Transgenic constructs containing/affecting coding region of mTor
Transgenic constructs containing regulatory region of mTor
Aberrations (Deficiencies and Duplications) ( 2 )
Variants
Variant Molecular Consequences
Alleles Representing Disease-Implicated Variants
Phenotypes
For more details about a specific phenotype click on the relevant allele symbol.
Lethality
Allele
Sterility
Allele
Other Phenotypes
Allele
Phenotype manifest in
Allele
anterior fascicle & synapse, with Scer\GAL4elav-C155
dorsal mesothoracic disc & nucleolus
larval salivary gland & nucleus (with mTor2L1)
larval salivary gland & nucleus (with mTork17004)
Orthologs
Human Orthologs (via DIOPT v9.1)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
Homo sapiens (Human) (19)
14 of 14
Yes
Yes
1  
3 of 14
No
No
2  
3 of 14
No
Yes
3 of 14
No
No
2 of 14
No
No
2 of 14
No
No
1 of 14
No
No
1  
1 of 14
No
Yes
1 of 14
No
No
2  
1 of 14
No
No
2  
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
2  
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
Model Organism Orthologs (via DIOPT v9.1)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
Rattus norvegicus (Norway rat) (12)
14 of 14
Yes
Yes
3 of 14
No
No
2 of 14
No
No
2 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
Mus musculus (laboratory mouse) (16)
13 of 14
Yes
Yes
3 of 14
No
No
3 of 14
No
Yes
3 of 14
No
No
2 of 14
No
No
2 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
Xenopus tropicalis (Western clawed frog) (10)
7 of 13
Yes
Yes
2 of 13
No
No
2 of 13
No
No
2 of 13
No
No
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
Danio rerio (Zebrafish) (18)
13 of 14
Yes
Yes
3 of 14
No
Yes
3 of 14
No
No
2 of 14
No
No
2 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
Caenorhabditis elegans (Nematode, roundworm) (8)
11 of 14
Yes
Yes
2 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
Anopheles gambiae (African malaria mosquito) (11)
12 of 12
Yes
Yes
Arabidopsis thaliana (thale-cress) (10)
13 of 13
Yes
Yes
2 of 13
No
No
2 of 13
No
No
2 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
Saccharomyces cerevisiae (Brewer's yeast) (8)
12 of 13
Yes
Yes
11 of 13
No
Yes
2 of 13
No
No
2 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
Schizosaccharomyces pombe (Fission yeast) (9)
12 of 12
Yes
Yes
10 of 12
No
Yes
2 of 12
No
No
2 of 12
No
No
2 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
Escherichia coli (enterobacterium) (0)
Other Organism Orthologs (via OrthoDB)
Data provided directly from OrthoDB:mTor. Refer to their site for version information.
Paralogs
Paralogs (via DIOPT v9.1)
Drosophila melanogaster (Fruit fly) (10)
5 of 13
4 of 13
4 of 13
3 of 13
2 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
Human Disease Associations
FlyBase Human Disease Model Reports
    Disease Ontology (DO) Annotations
    Models Based on Experimental Evidence ( 0 )
    Allele
    Disease
    Evidence
    References
    Potential Models Based on Orthology ( 1 )
    Human Ortholog
    Disease
    Evidence
    References
    Modifiers Based on Experimental Evidence ( 8 )
    Allele
    Disease
    Interaction
    References
    Disease Associations of Human Orthologs (via DIOPT v9.1 and OMIM)
    Note that ortholog calls supported by only 1 or 2 algorithms (DIOPT score < 3) are not shown.
    Functional Complementation Data
    Functional complementation data is computed by FlyBase using a combination of the orthology data obtained from DIOPT and OrthoDB and the allele-level genetic interaction data curated from the literature.
    Interactions
    Summary of Physical Interactions
    Interaction Browsers

    Please see the Physical Interaction reports below for full details
    protein-protein
    Physical Interaction
    Assay
    References
    Summary of Genetic Interactions
    Interaction Browsers

    Please look at the allele data for full details of the genetic interactions
    Starting gene(s)
    Interaction type
    Interacting gene(s)
    Reference
    Starting gene(s)
    Interaction type
    Interacting gene(s)
    Reference
    External Data
    Subunit Structure (UniProtKB)
    May be part of a minimal complex, TORC1, consisting of mTor, raptor and lst8. May be part of a minimal complex, TORC2, consisting of mTor, rictor and lst8 (By similarity). Self-associates; assembles into homomultimeric complexes. Component of a multiprotein complex.
    (UniProt, Q9VK45 )
    Linkouts
    BioGRID - A database of protein and genetic interactions.
    DroID - A comprehensive database of gene and protein interactions.
    MIST (genetic) - An integrated Molecular Interaction Database
    MIST (protein-protein) - An integrated Molecular Interaction Database
    Pathways
    Class of Gene
    Genomic Location and Detailed Mapping Data
    Chromosome (arm)
    2L
    Recombination map
    2-47
    Cytogenetic map
    Sequence location
    FlyBase Computed Cytological Location
    Cytogenetic map
    Evidence for location
    34A4-34A4
    Limits computationally determined from genome sequence between P{lacW}l(2)k07015k07015&P{PZ}l(2)rK639rK639 and P{lacW}l(2)k11328k11328&P{lacW}l(2)k10105k10105
    Experimentally Determined Cytological Location
    Cytogenetic map
    Notes
    References
    34A3-34A4
    (determined by in situ hybridisation)
    Experimentally Determined Recombination Data
    Location
    Left of (cM)
    Right of (cM)
    Notes
    Stocks and Reagents
    Stocks (26)
    Genomic Clones (12)
     

    Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete

    cDNA Clones (6)
     

    Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see JBrowse for alignment of the cDNAs and ESTs to the gene model.

    cDNA clones, fully sequenced
    BDGP DGC clones
    Other clones
      Drosophila Genomics Resource Center cDNA clones

      For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.

      cDNA Clones, End Sequenced (ESTs)
      BDGP DGC clones
      Other clones
      RNAi and Array Information
      Linkouts
      DRSC - Results frm RNAi screens
      Antibody Information
      Laboratory Generated Antibodies
       

      polyclonal

      Commercially Available Antibodies
       
      Cell Line Information
      Publicly Available Cell Lines
       
        Other Stable Cell Lines
         
        Other Comments

        Tor is specifically required for developmental axon regrowth but not initial axon outgrowth.

        dsRNA made from templates generated with primers directed against this gene results in a reduced mean cell diameter and a corresponding decrease in S6k phosphorylation. Silencing Tor generates a cell-expression profile similar to that of rapamycin-treated cells.

        dsRNA made from templates generated with primers directed against this gene used to treat S2 cells.

        dsRNA made from templates generated with primers directed against this gene decreases the level of phosphorylation of both Akt1 and S6k in S2 cells.

        Allelic series: TorR248stop = TorQ528stop = TorV2148D > TorG2256D = Tor2L1 > TorR97C = TorE161K = TorA948V = TorW1251R based on the stage of lethality.

        Identified in an RNAi screen for host factors that alter infection of SL2 cells by L.monocytogenes.

        When dsRNA constructs are made and transiently transfected into S2 cells in RNAi experiments, an increase in the proportion of G1 phase cells, a decrease in cell size and a decrease in cytokinetic index is seen.

        Signaling through Tor and its upstream regulators Pi3K92E/Pi3K21B and Rheb is necessary and sufficient to suppress starvation-induced autophagy in the fat body. Tor suppresses autophagy independently of S6k.

        Loss of Tor activity causes induction of autophagy in normally fed animals.

        dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.

        Relationship to Other Genes
        Source for database merge of

        Source for merge of: Tor CG5092

        Additional comments
        Nomenclature History
        Source for database identify of

        Source for identity of: l(2)k17004 Tor

        Source for identity of: mTor Tor

        Nomenclature comments

        Changed gene symbol 'Tor' to 'mTor' to reflect the symbol used for the vertebrate ortholog and to eliminate the case-insensitive duplication with the 'tor' (torso) gene symbol.

        Etymology
        Synonyms and Secondary IDs (35)
        Reported As
        Symbol Synonym
        MTOR
        TOR
        (Ding et al., 2026, Ahrentløv et al., 2025, Scopelliti et al., 2025, Wang et al., 2025, Yadav et al., 2025, Zhang et al., 2025, Delescluse et al., 2024, Jeong, 2024, Lee and Min, 2024, Luo et al., 2024, Matsuka et al., 2024, Nagata and Igaki, 2024, Tan et al., 2024, Zhu et al., 2024, Kang et al., 2023, Sanal et al., 2023, Bahuguna et al., 2022, Koehler et al., 2022, Mushtaq et al., 2022, Neophytou and Pitsouli, 2022, Noguchi et al., 2022, Wu et al., 2022, Bailey et al., 2021, Cai et al., 2021, Heier et al., 2021, Joy et al., 2021, Kannangara et al., 2021, Kim et al., 2021, Lam Wong and Verheyen, 2021, Lehmann, 2021, Léopold, 2021, McDonald et al., 2021, Meschi and Delanoue, 2021, Moraes and Montagne, 2021, Morin-Poulard et al., 2021, Osman and Pek, 2021, Parra-Peralbo et al., 2021, Sood et al., 2021, Tiwari and Mandal, 2021, Voo et al., 2021, Ahmad et al., 2020, Bakshi and Joshi, 2020, Blatt et al., 2020, Ding et al., 2020, Gohel et al., 2020, Grenier and Leulier, 2020, Kanda and Igaki, 2020, Koyama et al., 2020, Lee et al., 2020, Li et al., 2020, Luo et al., 2020, Malita and Rewitz, 2020, Nakajima et al., 2020, Shin et al., 2020, Strilbytska et al., 2020, Tafesh-Edwards and Eleftherianos, 2020, Texada et al., 2020, Toprak et al., 2020, Wolterhoff et al., 2020, Zeng et al., 2020, Basar et al., 2019, Bayliak et al., 2019, Borreguero-Muñoz et al., 2019, Chaplot et al., 2019, Hansen et al., 2019, Kim and Choi, 2019, Zheng et al., 2019, Gáliková and Klepsatel, 2018, Kang et al., 2018, Kounatidis and Chtarbanova, 2018, Lee et al., 2018, Lehmann, 2018, Tang et al., 2018, Filer et al., 2017, Haller et al., 2017, Hoedjes et al., 2017, Kamalesh et al., 2017, Kim et al., 2017, Liu et al., 2017, Murillo-Maldonado and Riesgo-Escovar, 2017, Romero-Pozuelo et al., 2017, Strilbytska et al., 2017, Tue et al., 2017, Xiang et al., 2017, Alfa and Kim, 2016, Cannon and Bodmer, 2016, Kuleesha et al., 2016, Li et al., 2016, Marmor-Kollet and Schuldiner, 2016, Niwa and Niwa, 2016, Purice et al., 2016, Rabinovich et al., 2016, Tsokanos et al., 2016, Yaniv and Schuldiner, 2016, Burn et al., 2015, Diop and Bodmer, 2015, Diop et al., 2015, Homem et al., 2015, Ma et al., 2015, Mitchell et al., 2015, Nässel et al., 2015, Obata and Miura, 2015, Schmitt et al., 2015, Tiebe et al., 2015, Wang et al., 2015, Barrio et al., 2014, Frank, 2014, Ghosh et al., 2014, Mulakkal et al., 2014, Nagy et al., 2014, Owusu-Ansah and Perrimon, 2014, Varma et al., 2014, Xu and Cherry, 2014, Callier and Nijhout, 2013, Esslinger et al., 2013, Gems and Partridge, 2013, Laslo et al., 2013, Lee and Brey, 2013, Luo et al., 2013, Mukherjee and Duttaroy, 2013, Nowak et al., 2013, Rajan and Perrimon, 2013, Rallis et al., 2013, Tixier et al., 2013, Tran et al., 2013, Wong et al., 2013, Yamanaka et al., 2013, Eleftherianos and Castillo, 2012, Ferguson et al., 2012, Grewal, 2012, Kayashima et al., 2012, Marshall et al., 2012, Rincon-Limas et al., 2012, Yaniv et al., 2012, Boyd et al., 2011, Glatter et al., 2011, Lindquist et al., 2011, Oldham, 2011, Parker, 2011, Partridge et al., 2011, Rajan and Perrimon, 2011, Birse et al., 2010, Bjedov et al., 2010, Bryk et al., 2010, Chang and Neufeld, 2010, Iijima-Ando and Iijima, 2010, Lee et al., 2010, Li et al., 2010, Liu and Lu, 2010, Ribeiro and Dickson, 2010, Vargas et al., 2010, Chang and Neufeld, 2009, Kourtis and Tavernarakis, 2009, Dutta and Baehrecke, 2008, Kaplan et al., 2008, Layalle et al., 2008, Lee et al., 2008, Leopold and Layalle, 2008, McNeill et al., 2008, Oldham et al., 2008, Teleman et al., 2008, Ballard and Wharton, 2007, Berry and Baehrecke, 2007, Grewal et al., 2007, Hall et al., 2007, Hoshizaki and Gibbs, 2007, Lee et al., 2007, Ocorr et al., 2007, Wessells et al., 2007, Edgar, 2006, Goraksha and Neufeld, 2006, Guertin et al., 2006, Hennig et al., 2006, Khurana et al., 2006, Min et al., 2006, Mosimann et al., 2006, Ruvinsky, 2006, Takacs-Vellai, 2006, Wu and Brown, 2006, Yang et al., 2006, Bodmer, 2005, Cygnar et al., 2005, Goberdhan et al., 2005, Grewal et al., 2005, Scott et al., 2005, Shingleton, 2005, Teleman et al., 2005, Hay and Sonenberg, 2004, Pan et al., 2004, Scott et al., 2004, Scott et al., 2004, Stocker et al., 2004, Tatar et al., 2004, Tu and Tatar, 2004, Bergmann and Lane, 2003, Nijhout, 2003, Saucedo et al., 2003, Saucedo et al., 2003, Scott and Neufeld, 2003, Stocker et al., 2003, Oldham et al., 2001)
        Tor
        (GenetiVision Corporation, 2026-, Toprak, 2026, Dong et al., 2025, Lee et al., 2025, Park et al., 2025, Qin et al., 2025, Tahan Zadeh et al., 2025, Tyszka et al., 2025, Ma et al., 2024, Mikropoulou et al., 2024, Wang et al., 2024, Zhang et al., 2024, Zirin et al., 2024, Cachoux et al., 2023, Gui et al., 2023, Huang et al., 2023, Kanaoka et al., 2023, Nagai et al., 2023, Roy et al., 2023, Alves et al., 2022, Dalton et al., 2022, Damulewicz et al., 2022, Dong et al., 2022, Huang et al., 2022, Ji et al., 2022, Kakanj et al., 2022, Kamiyama and Niwa, 2022, Li et al., 2022, Liu et al., 2022, Molina et al., 2022, National Institute of Genetics Fly Stocks, 2022-, Palozzi et al., 2022, Suzuta et al., 2022, Tahanzadeh et al., 2022, Weina et al., 2022, Yu et al., 2022, Azuma et al., 2021, Bilder et al., 2021, Bonfini et al., 2021, Buhlman et al., 2021, Fabian et al., 2021, Fan et al., 2021, Jacomin et al., 2021, Johnson and Leatherman, 2021, Kim and O'Connor, 2021, Kim et al., 2021, Lee et al., 2021, Liguori et al., 2021, Nishida et al., 2021, Ohhara et al., 2021, Ostalé et al., 2021, Semaniuk et al., 2021, Zhou et al., 2021, Bosch et al., 2020, Colombani and Andersen, 2020, Cui et al., 2020, Funk et al., 2020, Ishibashi et al., 2020, Jacomin et al., 2020, Jeon et al., 2020, Khan et al., 2020, Luo et al., 2020, Ma et al., 2020, Murakawa et al., 2020, Nakamura et al., 2020, Perez-Gomez et al., 2020, Rambur et al., 2020, Redhai et al., 2020, Sanaki et al., 2020, Sênos Demarco et al., 2020, Wang et al., 2020, Zhao et al., 2020, Bhattacharjee et al., 2019, Birnbaum et al., 2019, Blice-Baum et al., 2019, Bouska et al., 2019, Brown et al., 2019, Chen et al., 2019, Drummond-Barbosa, 2019, Evangelakou et al., 2019, Hegazi et al., 2019, Huang et al., 2019, Johnson and Toettcher, 2019, Kim et al., 2019, Kumar Chaudhary and Rizvi, 2019, Li et al., 2019, Li et al., 2019, Lin et al., 2019, Loeffler, 2019, Meltzer et al., 2019, Mirth et al., 2019, Ramanathan et al., 2019, Sênos Demarco et al., 2019, Singh et al., 2019, Su, 2019, Tang et al., 2019, Tettamanti and Casartelli, 2019, Texada et al., 2019, Westfall et al., 2019, Xi et al., 2019, Yoshinari et al., 2019, Cara et al., 2018, Gene Disruption Project members, 2018-, Ignesti et al., 2018, Kang et al., 2018, Kuo et al., 2018, Lee et al., 2018, Leow et al., 2018, Tamirisa et al., 2018, Tsai et al., 2018, Velentzas et al., 2018, Galluzzi et al., 2017, Lee et al., 2017, Lin et al., 2017, Perry et al., 2017, Song et al., 2017, Wen et al., 2017, Xu et al., 2017, Xu et al., 2017, Yan et al., 2017, Di Cara and King-Jones, 2016, Kučerová et al., 2016, Liu et al., 2016, Penney et al., 2016, Puah and Wasser, 2016, Sarov et al., 2016, Wei et al., 2016, Aradska et al., 2015, Diop et al., 2015, Francis and Ghabrial, 2015, Frankel et al., 2015, Gilboa, 2015, Lin et al., 2015, Mensah et al., 2015, Okada et al., 2015, Onyenwoke et al., 2015, Parker and Struhl, 2015, Stratoulias and Heino, 2015, Wu et al., 2015, Xu et al., 2015, Adamson et al., 2014, Deivasigamani et al., 2014, Gómez-Lamarca et al., 2014, Hasygar and Hietakangas, 2014, Moy et al., 2014, Pathak et al., 2014, Sato-Miyata et al., 2014, Sopko et al., 2014, Wei et al., 2014, Brianti et al., 2013, Lanet et al., 2013, Luo et al., 2013, O'Farrell et al., 2013, Soh et al., 2013, Tang et al., 2013, Tixier et al., 2013, Tixier et al., 2013, Vilmos et al., 2013, Adamson and Lajeunesse, 2012, Alvarez-Ponce et al., 2012, Avet-Rochex et al., 2012, Chakrabarti et al., 2012, Dar et al., 2012, Dimitroff et al., 2012, Garcia et al., 2012, Penney et al., 2012, Pritchett and McCall, 2012, Tokusumi et al., 2012, Zhang et al., 2012, Zitserman et al., 2012, Djiane et al., 2011, Friedman et al., 2011, Lindquist et al., 2011, Read, 2011, Resnik-Docampo and de Celis, 2011, Sousa-Nunes et al., 2011, Tang et al., 2011, Turner et al., 2011, Willecke et al., 2011, Ballard et al., 2010, Blanco et al., 2010, Bülow et al., 2010, Cully et al., 2010, Fernández-Ayala et al., 2010, Haberman et al., 2010, Hsieh et al., 2010, Johnson et al., 2010, Kim et al., 2010, Kühnlein, 2010, LaFever et al., 2010, Nisoli et al., 2010, Robinson et al., 2010, Sun et al., 2010, Sun et al., 2010, Zeng et al., 2010, Zhang et al., 2010, Zheng and Sehgal, 2010, Alvarez-Ponce et al., 2009, Chittaranjan et al., 2009, Koike-Kumagai et al., 2009, Kuronen et al., 2009, Nuzhdin et al., 2009, Patch et al., 2009, Sims et al., 2009, Wang and Huang, 2009, Harvey et al., 2008, Holloway et al., 2008, Hou et al., 2008, Juhász et al., 2008, Rehmann et al., 2008, Song et al., 2008, Derré et al., 2007, Frei et al., 2007, Grewal et al., 2007, Juhász et al., 2007, Kim and Yoo, 2007, Knox et al., 2007, Martin et al., 2007, Miranda-Saavedra and Barton, 2007, Parisi et al., 2007, Scott et al., 2007, Scott et al., 2007, Chen et al., 2006, Friedman and Perrimon, 2006, Hariharan, 2006, Patel and Tamanoi, 2006, Walker et al., 2006, Bateman and McNeill, 2005, Mandal et al., 2005, Teleman et al., 2005, Terashima and Bownes, 2005)
        dTOR
        (Liu et al., 2026, Nan et al., 2025, Serebrovska et al., 2025, Dai et al., 2023, Demir and Kacew, 2023, Frappaolo and Giansanti, 2023, Dabrowska et al., 2022, Koranteng et al., 2022, Nayak and Mishra, 2022, Santalla et al., 2022, Singh and Agrawal, 2022, Wang et al., 2022, Sciambra and Chtarbanova, 2021, Wen et al., 2021, Gou et al., 2020, Koliada et al., 2020, Moretti et al., 2020, Lushchak et al., 2019, Westfall et al., 2019, Staats et al., 2018, Westfall et al., 2018, Bolukbasi et al., 2017, Brookheart and Duncan, 2016, David-Morrison et al., 2016, Erdogan et al., 2016, Sanchez et al., 2016, Wu and Storey, 2016, Chen et al., 2015, Kohlmaier et al., 2015, Merkling and van Rij, 2013, Mockett and Nobles, 2013, Shim et al., 2013, Wu et al., 2013, Eleftherianos and Castillo, 2012, Taillebourg et al., 2012, Kamakura, 2011, Nishimura et al., 2011, Partridge et al., 2011, Dekanty et al., 2010, Karbowniczek et al., 2010, Thomson and Johnson, 2010, Zirin and Perrimon, 2010, Wang and Huang, 2009, Wessells et al., 2009, Mattila et al., 2008, Findlay et al., 2007, Lasko and Sonenberg, 2007, Lee et al., 2007, Wu et al., 2007, Guertin et al., 2006, Inoki and Guan, 2006, Luong et al., 2006, Wullschleger, 2006, Yang et al., 2006, Dekanty et al., 2005, Goraksha and Neufeld, 2005, Sarbassov et al., 2005, Buch et al., 2004, Jorgensen and Tyers, 2004, Kapahi et al., 2004, Kapahi et al., 2004, Oldham et al., 2004, Ruhf et al., 2004, Sarbassov et al., 2004, Sarbassov et al., 2004, Bradley and Leevers, 2003, Hennig et al., 2003, Jacinto and Hall, 2003, Lee and Orr-Weaver, 2003, Manning and Cantley, 2003, Miron et al., 2003, Oldham and Hafen, 2003, Hennig and Neufeld, 2002, Hennig and Neufeld, 2002, Kozma and Thomas, 2002, Marygold and Leevers, 2002, Montagne et al., 2002, Radimerski et al., 2002, Radimerski et al., 2002, Cho et al., 2001, Gingras et al., 2001, Potter and Xu, 2001, Prober and Edgar, 2001, Radimerski et al., 2001, Rhode et al., 2001, Oldham et al., 2000, Oldham et al., 2000, Zhang et al., 2000)
        mtor
        Name Synonyms
        Mechanistic Target of rapamycin
        Target-of-Rapamycin
        Target-of-rapamycin
        mechanistic Target of rapamycin
        target of rapamycin complex 1
        target of rapamycin kinase
        Secondary FlyBase IDs
        • FBgn0032466
        Datasets (1)
        Study focus (1)
        Experimental Role
        Project
        Project Type
        Title
        • bait_protein
        Interaction map generated by purification of insulin pathway factors, with identification of copurifying proteins by mass spectrometry.
        Study result (0)
        Result
        Result Type
        Title
        External Crossreferences and Linkouts ( 79 )
        Sequence Crossreferences
        NCBI Gene - Gene integrates information from a wide range of species. A record may include nomenclature, Reference Sequences (RefSeqs), maps, pathways, variations, phenotypes, and links to genome-, phenotype-, and locus-specific resources worldwide.
        GenBank Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
        GenBank Protein - A collection of sequences from several sources, including translations from annotated coding regions in GenBank, RefSeq and TPA, as well as records from SwissProt, PIR, PRF, and PDB.
        RefSeq - A comprehensive, integrated, non-redundant, well-annotated set of reference sequences including genomic, transcript, and protein.
        UniProt/GCRP - The gene-centric reference proteome (GCRP) provides a 1:1 mapping between genes and UniProt accessions in which a single 'canonical' isoform represents the product(s) of each protein-coding gene.
        UniProt/Swiss-Prot - Manually annotated and reviewed records of protein sequence and functional information
        UniProt/TrEMBL - Automatically annotated and unreviewed records of protein sequence and functional information
        Other crossreferences
        AlphaFold DB - AlphaFold provides open access to protein structure predictions for the human proteome and other key proteins of interest, to accelerate scientific research.
        DRscDB - A single-cell RNA-seq resource for data mining and data comparison across species
        EMBL-EBI Single Cell Expression Atlas - Single cell expression across species
        FlyAtlas2 - A Drosophila melanogaster expression atlas with RNA-Seq, miRNA-Seq and sex-specific data
        FlyMine - An integrated database for Drosophila genomics
        KEGG Genes - Molecular building blocks of life in the genomic space.
        MARRVEL_MODEL - MARRVEL (model organism gene)
        Linkouts
        BioGRID - A database of protein and genetic interactions.
        Drosophila Genomics Resource Center - Drosophila Genomics Resource Center (DGRC) cDNA clones
        DroID - A comprehensive database of gene and protein interactions.
        DRSC - Results frm RNAi screens
        Eukaryotic Promoter Database - A collection of databases of experimentally validated promoters for selected model organisms.
        FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
        FlyCyc Genes - Genes from a BioCyc PGDB for Dmel
        Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
        Flygut - An atlas of the Drosophila adult midgut
        FlyMet - A comprehensive tissue-specific metabolomics resource for Drosophila.
        iBeetle-Base - RNAi phenotypes in the red flour beetle (Tribolium castaneum)
        Interactive Fly - A cyberspace guide to Drosophila development and metazoan evolution
        KEGG Pathways - A collection of manually drawn pathway maps representing knowledge of molecular interaction, reaction and relation networks.
        MIST (genetic) - An integrated Molecular Interaction Database
        MIST (protein-protein) - An integrated Molecular Interaction Database
        SignaLink - A signaling pathway resource with multi-layered regulatory networks.
        References (822)