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FBP1

S. cerevisiae

fructose 1,6-bisphosphate 1-phosphatase

What the model saw

Gene: FBP1
Organism: Saccharomyces cerevisiae
Known functions: fructose 1,6-bisphosphate 1-phosphatase. fructose 1,6-bisphosphate 1-phosphatase activity. phosphatase activity. phosphoric ester hydrolase activity.
View unredacted entry
fructose 1,6-bisphosphate 1-phosphatase. fructose 1,6-bisphosphate 1-phosphatase activity. phosphatase activity. phosphoric ester hydrolase activity.

Solver output

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

FBP1 encodes fructose-1,6-bisphosphatase, the key gluconeogenic enzyme that hydrolyzes fructose-1,6-bisphosphate to fructose-6-phosphate, opposing glycolysis. In S. cerevisiae, FBP1 expression is strongly repressed by glucose and induced during caloric restriction or growth on non-fermentable carbon sources. Active gluconeogenesis via FBP1 is a hallmark of low-nutrient/low-glucose signaling states, which are associated with reduced PKA and TOR pathway activity — both of which are pro-longevity when downregulated. By promoting gluconeogenic flux and being upregulated under caloric restriction conditions, FBP1 activity is functionally coupled to the nutrient-sensing axis that extends lifespan. Loss of FBP1 would impair the metabolic shift away from fermentation, effectively mimicking a high-glucose/high-nutrient state that shortens lifespan.

Key pathways
gluconeogenesis / fructose-1,6-bisphosphatase activityTOR/PKA nutrient sensing pathwaycaloric restriction metabolic reprogramming
Longevity influence
Anti-longevity
Lifespan effect
Decrease

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
Incorrect
Mechanism
Incorrect
Reasoning quality
2/5
Failure mode
Confident wrong
Notes

The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is plausible-sounding but ultimately incorrect. While FBP1 is indeed upregulated under caloric restriction conditions, the model incorrectly infers that this makes it pro-longevity. In reality, FBP1 is anti-longevity in yeast. The model's logic — that FBP1 upregulation under CR conditions means it promotes longevity — is a correlation/causation error. The model was fairly confident (0.72) in its wrong answer. The mechanistic reasoning about gluconeogenesis and nutrient sensing is partially correct in describing FBP1's biochemical role, but the conclusion about its longevity effect is wrong.

Raw API responses

solver

{
  "reasoning": "FBP1 encodes fructose-1,6-bisphosphatase, the key gluconeogenic enzyme that hydrolyzes fructose-1,6-bisphosphate to fructose-6-phosphate, opposing glycolysis. In S. cerevisiae, FBP1 expression is strongly repressed by glucose and induced during caloric restriction or growth on non-fermentable carbon sources. Active gluconeogenesis via FBP1 is a hallmark of low-nutrient/low-glucose signaling states, which are associated with reduced PKA and TOR pathway activity — both of which are pro-longevity when downregulated. By promoting gluconeogenic flux and being upregulated under caloric restriction conditions, FBP1 activity is functionally coupled to the nutrient-sensing axis that extends lifespan. Loss of FBP1 would impair the metabolic shift away from fermentation, effectively mimicking a high-glucose/high-nutrient state that shortens lifespan.",
  "confidence": 0.72,
  "key_pathways": [
    "gluconeogenesis / fructose-1,6-bisphosphatase activity",
    "TOR/PKA nutrient sensing pathway",
    "caloric restriction metabolic reprogramming"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is plausible-sounding but ultimately incorrect. While FBP1 is indeed upregulated under caloric restriction conditions, the model incorrectly infers that this makes it pro-longevity. In reality, FBP1 is anti-longevity in yeast. The model's logic — that FBP1 upregulation under CR conditions means it promotes longevity — is a correlation/causation error. The model was fairly confident (0.72) in its wrong answer. The mechanistic reasoning about gluconeogenesis and nutrient sensing is partially correct in describing FBP1's biochemical role, but the conclusion about its longevity effect is wrong.",
  "failure_mode": "confident_wrong",
  "answer_correct": false,
  "mechanism_correct": false,
  "reasoning_quality": 2,
  "ground_truth_questionable": false
}