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SNF3

S. cerevisiae

glucose sensor

What the model saw

Gene: SNF3
Organism: Saccharomyces cerevisiae
Known functions: glucose sensor. D-glucose binding. carbohydrate:proton symporter activity. transmembrane transporter activity.
View unredacted entry
glucose sensor. D-glucose binding. carbohydrate:proton symporter activity. transmembrane transporter activity.

Solver output

Predicted influence
Anti-longevity
Confidence
72%
Mechanism
Deregulated nutrient sensing
Reasoning

SNF3 encodes a high-affinity glucose sensor in S. cerevisiae that detects extracellular glucose and transduces a signal to activate glucose-responsive transcriptional programs, including repression of gluconeogenesis and respiratory metabolism. By promoting robust glucose signaling, SNF3 activates the Ras/PKA and TORC1 nutrient-sensing axes, which are well-established pro-aging pathways in yeast. High glucose sensing through SNF3 suppresses stress-response programs (e.g., Msn2/Msn4 targets) and mitochondrial respiration, both of which are associated with shortened chronological and replicative lifespan. Caloric restriction and reduced glucose signaling—effectively the opposite of SNF3 activation—are among the most robust lifespan-extending interventions in yeast, placing SNF3's normal function squarely in the anti-longevity category.

Key pathways
Glucose/Ras-PKA nutrient sensingTORC1 signalingGlucose repression of stress response (Msn2/Msn4)
Longevity influence
Anti-longevity
Lifespan effect
Increase

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

Answer
Correct
Mechanism
Correct
Reasoning quality
4/5
Failure mode
Correct
Notes

The model correctly predicted anti_longevity for SNF3. The mechanistic reasoning is sound and well-grounded: SNF3 is a high-affinity glucose sensor that promotes glucose signaling, which activates pro-aging pathways (Ras/PKA, TORC1) and suppresses stress-response programs. The connection to caloric restriction as a lifespan-extending intervention (the opposite of SNF3 activation) is appropriate. The reasoning is slightly speculative in directly linking SNF3 to TORC1 (SNF3 primarily signals through the Rgt1/Rgt2 pathway for glucose induction of HXT genes, not directly through Ras/PKA or TORC1), but the overall logic that glucose sensing promotes aging is correct and consistent with the literature. Confidence of 0.72 is reasonable.

Raw API responses

solver

{
  "reasoning": "SNF3 encodes a high-affinity glucose sensor in S. cerevisiae that detects extracellular glucose and transduces a signal to activate glucose-responsive transcriptional programs, including repression of gluconeogenesis and respiratory metabolism. By promoting robust glucose signaling, SNF3 activates the Ras/PKA and TORC1 nutrient-sensing axes, which are well-established pro-aging pathways in yeast. High glucose sensing through SNF3 suppresses stress-response programs (e.g., Msn2/Msn4 targets) and mitochondrial respiration, both of which are associated with shortened chronological and replicative lifespan. Caloric restriction and reduced glucose signaling—effectively the opposite of SNF3 activation—are among the most robust lifespan-extending interventions in yeast, placing SNF3's normal function squarely in the anti-longevity category.",
  "confidence": 0.72,
  "key_pathways": [
    "Glucose/Ras-PKA nutrient sensing",
    "TORC1 signaling",
    "Glucose repression of stress response (Msn2/Msn4)"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for SNF3. The mechanistic reasoning is sound and well-grounded: SNF3 is a high-affinity glucose sensor that promotes glucose signaling, which activates pro-aging pathways (Ras/PKA, TORC1) and suppresses stress-response programs. The connection to caloric restriction as a lifespan-extending intervention (the opposite of SNF3 activation) is appropriate. The reasoning is slightly speculative in directly linking SNF3 to TORC1 (SNF3 primarily signals through the Rgt1/Rgt2 pathway for glucose induction of HXT genes, not directly through Ras/PKA or TORC1), but the overall logic that glucose sensing promotes aging is correct and consistent with the literature. Confidence of 0.72 is reasonable.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}