TOR1
S. cerevisiae
phosphatidylinositol kinase-related protein kinase TOR1
What the model saw
Gene: TOR1 Organism: Saccharomyces cerevisiae Known functions: phosphatidylinositol kinase-related protein kinase TOR1. kinase activity. protein binding. protein kinase activity. protein serine kinase activity. protein serine/threonine kinase activity. protein-containing complex binding.
View unredacted entry
phosphatidylinositol kinase-related protein kinase TOR1. kinase activity. protein binding. protein kinase activity. protein serine kinase activity. protein serine/threonine kinase activity. protein-containing complex binding.
Solver output
TOR1 encodes the catalytic subunit of TORC1 (Target of Rapamycin Complex 1) in S. cerevisiae, a central nutrient-sensing serine/threonine kinase. In nutrient-replete conditions, active TOR1/TORC1 phosphorylates and inhibits downstream effectors such as Atg13 (suppressing autophagy) and promotes ribosome biogenesis and protein synthesis via Sch9 and S6K-like substrates. This anabolic signaling program, when constitutively active, accelerates aging. Loss-of-function mutations in TOR1 (tor1Δ) are well-established to extend chronological and replicative lifespan in yeast, phenocopying caloric restriction. The normal (active) function of TOR1 therefore opposes longevity by suppressing autophagy, promoting growth signaling, and overriding the pro-longevity effects of nutrient limitation.
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 identified TOR1 as anti_longevity with high confidence (0.93). The mechanistic reasoning is excellent and accurate: TOR1 encodes the catalytic subunit of TORC1, which when active suppresses autophagy, promotes anabolic signaling, and opposes longevity. The model correctly notes that tor1Δ loss-of-function extends both chronological and replicative lifespan in yeast, phenocopying caloric restriction. The key pathways identified (TORC1 nutrient sensing, autophagy suppression via Atg13, ribosome biogenesis via Sch9) are all well-established and accurate. This is a textbook example of an anti-longevity gene in yeast aging research.
Raw API responses
solver
{
"reasoning": "TOR1 encodes the catalytic subunit of TORC1 (Target of Rapamycin Complex 1) in S. cerevisiae, a central nutrient-sensing serine/threonine kinase. In nutrient-replete conditions, active TOR1/TORC1 phosphorylates and inhibits downstream effectors such as Atg13 (suppressing autophagy) and promotes ribosome biogenesis and protein synthesis via Sch9 and S6K-like substrates. This anabolic signaling program, when constitutively active, accelerates aging. Loss-of-function mutations in TOR1 (tor1Δ) are well-established to extend chronological and replicative lifespan in yeast, phenocopying caloric restriction. The normal (active) function of TOR1 therefore opposes longevity by suppressing autophagy, promoting growth signaling, and overriding the pro-longevity effects of nutrient limitation.",
"confidence": 0.93,
"key_pathways": [
"TORC1 nutrient sensing pathway",
"Autophagy suppression via Atg13 phosphorylation",
"Ribosome biogenesis and protein synthesis via Sch9"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly identified TOR1 as anti_longevity with high confidence (0.93). The mechanistic reasoning is excellent and accurate: TOR1 encodes the catalytic subunit of TORC1, which when active suppresses autophagy, promotes anabolic signaling, and opposes longevity. The model correctly notes that tor1Δ loss-of-function extends both chronological and replicative lifespan in yeast, phenocopying caloric restriction. The key pathways identified (TORC1 nutrient sensing, autophagy suppression via Atg13, ribosome biogenesis via Sch9) are all well-established and accurate. This is a textbook example of an anti-longevity gene in yeast aging research.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}