Genetic and biochemical characterization of dTOR, the Drosophila homolog of the target of rapamycin
What this study shows
The authors identified and characterised dTOR, the fruit fly version of TOR. Genetic and biochemical experiments indicated that dTOR affects growth in a cell-autonomous way by changing the activity of the fly S6 kinase, dS6K, and so connects to the insulin signalling pathway. Unlike other insulin pathway components, partial loss of dTOR reduced growth mainly in endoreplicating tissues, which copy their DNA without dividing. The authors read this as evidence that dTOR sits on a parallel pathway that senses amino acids. Boundary: Drosophila genetics and biochemistry; the parallel amino acid pathway is an interpretation from fly phenotypes, not a direct measurement of amino acid sensing.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Drosophila melanogaster dTOR mutants (partial and full loss), genetic interaction with insulin pathway; biochemistry of dS6K) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is. |
| Study type | 5 - Mechanistic / In Vitro |
| Model system | Drosophila melanogaster dTOR mutants (partial and full loss), genetic interaction with insulin pathway; biochemistry of dS6K |
| Journal | Genes & Development |
| Year | 2000 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1101/gad.845700 · PMID 11069885 · Free full text (PMC317036) |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | dTOR loss-of-function alleles |
| Target | dS6K activity; tissue growth |
| Model | Drosophila melanogaster |
| Effect | Loss of dTOR -> reduced dS6K activity and reduced growth, mainly in endoreplicating tissues |
In the Atlas
Related topics
More studies on this topic
- Temporal coding of insulin action through multiplexing of the AKT pathway (2012)
- Hypoinsulinaemia, glucose intolerance and diminished beta-cell size in S6K1-deficient mice (2000)
- Inappropriate activation of the TSC/Rheb/mTOR/S6K cassette induces IRS1/2 depletion, insulin resistance, and cell survival deficiencies (2004)
- Insulin activation of Rheb, a mediator of mTOR/S6K/4E-BP signaling, is inhibited by TSC1 and 2 (2003)
Thank you. Your answer was counted anonymously.