GPR1
S. cerevisiae
Gpr1p
What the model saw
Gene: GPR1 Organism: Saccharomyces cerevisiae Known functions: Gpr1p. D-glucose binding. G protein-coupled receptor activity.
View unredacted entry
Gpr1p. D-glucose binding. G protein-coupled receptor activity.
Solver output
GPR1 encodes a G protein-coupled receptor in S. cerevisiae that directly binds D-glucose and activates the Gpa2/PKA (cAMP-PKA) signaling pathway in response to glucose availability. Activation of this pathway suppresses stress resistance, promotes growth, and inhibits autophagy and quiescence programs that are associated with extended lifespan. In yeast, high glucose/PKA signaling is a well-established pro-aging axis; deletion of GPR1 reduces PKA activity and extends chronological and replicative lifespan. Thus, the normal function of GPR1—sensing glucose and stimulating PKA—actively opposes longevity by driving nutrient-sensing pathways analogous to the TOR/insulin-IGF-1 axis in higher eukaryotes.
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 GPR1 as anti_longevity with high confidence (0.75). The mechanistic reasoning is accurate and detailed: GPR1 encodes a glucose-sensing GPCR that activates the Gpa2/cAMP-PKA pathway, which suppresses stress resistance and longevity programs. The model correctly identifies that deletion of GPR1 extends lifespan by reducing PKA activity, and appropriately draws the analogy to the TOR/insulin-IGF-1 axis. The mechanism class "deregulated_nutrient_sensing" is appropriate. Overall, this is an excellent prediction with correct answer and correct mechanistic reasoning.
Raw API responses
solver
{
"reasoning": "GPR1 encodes a G protein-coupled receptor in S. cerevisiae that directly binds D-glucose and activates the Gpa2/PKA (cAMP-PKA) signaling pathway in response to glucose availability. Activation of this pathway suppresses stress resistance, promotes growth, and inhibits autophagy and quiescence programs that are associated with extended lifespan. In yeast, high glucose/PKA signaling is a well-established pro-aging axis; deletion of GPR1 reduces PKA activity and extends chronological and replicative lifespan. Thus, the normal function of GPR1—sensing glucose and stimulating PKA—actively opposes longevity by driving nutrient-sensing pathways analogous to the TOR/insulin-IGF-1 axis in higher eukaryotes.",
"confidence": 0.75,
"key_pathways": [
"cAMP-PKA signaling",
"glucose sensing / Gpa2 activation",
"nutrient-dependent growth regulation"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted GPR1 as anti_longevity with high confidence (0.75). The mechanistic reasoning is accurate and detailed: GPR1 encodes a glucose-sensing GPCR that activates the Gpa2/cAMP-PKA pathway, which suppresses stress resistance and longevity programs. The model correctly identifies that deletion of GPR1 extends lifespan by reducing PKA activity, and appropriately draws the analogy to the TOR/insulin-IGF-1 axis. The mechanism class \"deregulated_nutrient_sensing\" is appropriate. Overall, this is an excellent prediction with correct answer and correct mechanistic reasoning.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}