mTor
D. melanogaster
mechanistic Target of rapamycin
What the model saw
Gene: mTor Organism: Drosophila melanogaster Known functions: mechanistic Target of rapamycin. mechanistic target of rapamycin. chromatin DNA binding. kinase activity. protein binding. protein kinase activity. protein serine kinase activity. protein serine/threonine kinase activity. protein-containing complex binding.
View unredacted entry
mechanistic Target of rapamycin. mechanistic target of rapamycin. chromatin DNA binding. kinase activity. protein binding. protein kinase activity. protein serine kinase activity. protein serine/threonine kinase activity. protein-containing complex binding.
Solver output
mTOR (mechanistic Target of Rapamycin) is the catalytic serine/threonine kinase subunit of the TORC1 and TORC2 complexes, which serve as master regulators of nutrient sensing and anabolic metabolism. In its normal active state, mTOR phosphorylates downstream effectors such as S6K and 4E-BP1 to promote protein synthesis and cell growth while suppressing autophagy. Chronic activation of mTOR signaling accelerates aging by inhibiting autophagy-mediated proteostasis, suppressing stress resistance pathways, and promoting cellular hypertrophy. Genetic or pharmacological inhibition of mTOR (e.g., via rapamycin or loss-of-function mutations) consistently extends lifespan in Drosophila and other model organisms, demonstrating that the normal pro-growth function of mTOR is anti-longevity. This places mTOR squarely within the deregulated nutrient-sensing hallmark of aging, as it integrates amino acid and energy availability signals to drive anabolic programs that shorten lifespan when chronically active.
GenAge curators classify each gene's normal function as promoting (Pro-Longevity) or opposing (Anti-Longevity) longevity, based on synthesis across studies. Loss-of-function effects can vary from this depending on the manipulation.
Advisor judgment
The model correctly predicted mTor as anti_longevity in Drosophila melanogaster with high confidence (0.95). The mechanistic reasoning is thorough and accurate: mTOR as a serine/threonine kinase that promotes anabolic metabolism, inhibits autophagy, and whose inhibition (via rapamycin or loss-of-function) extends lifespan. The classification under "deregulated nutrient sensing" is appropriate. Key pathways identified (TOR/S6K/4E-BP1, autophagy suppression, insulin/IGF-1 crosstalk) are all well-established and correct.
Raw API responses
solver
{
"reasoning": "mTOR (mechanistic Target of Rapamycin) is the catalytic serine/threonine kinase subunit of the TORC1 and TORC2 complexes, which serve as master regulators of nutrient sensing and anabolic metabolism. In its normal active state, mTOR phosphorylates downstream effectors such as S6K and 4E-BP1 to promote protein synthesis and cell growth while suppressing autophagy. Chronic activation of mTOR signaling accelerates aging by inhibiting autophagy-mediated proteostasis, suppressing stress resistance pathways, and promoting cellular hypertrophy. Genetic or pharmacological inhibition of mTOR (e.g., via rapamycin or loss-of-function mutations) consistently extends lifespan in Drosophila and other model organisms, demonstrating that the normal pro-growth function of mTOR is anti-longevity. This places mTOR squarely within the deregulated nutrient-sensing hallmark of aging, as it integrates amino acid and energy availability signals to drive anabolic programs that shorten lifespan when chronically active.",
"confidence": 0.95,
"key_pathways": [
"TOR/S6K/4E-BP1 nutrient sensing",
"Autophagy suppression via TORC1",
"Insulin/IGF-1 signaling crosstalk"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted mTor as anti_longevity in Drosophila melanogaster with high confidence (0.95). The mechanistic reasoning is thorough and accurate: mTOR as a serine/threonine kinase that promotes anabolic metabolism, inhibits autophagy, and whose inhibition (via rapamycin or loss-of-function) extends lifespan. The classification under \"deregulated nutrient sensing\" is appropriate. Key pathways identified (TOR/S6K/4E-BP1, autophagy suppression, insulin/IGF-1 crosstalk) are all well-established and correct.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}