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fdgt-1

C. elegans

Facilitated glucose transporter protein 1

What the model saw

Gene: fdgt-1
Organism: Caenorhabditis elegans
Known functions: Facilitated glucose transporter protein 1. hexose transmembrane transporter activity. transmembrane transporter activity.
View unredacted entry
Facilitated glucose transporter protein 1. hexose transmembrane transporter activity. transmembrane transporter activity.

Solver output

Predicted influence
Anti-longevity
Confidence
68%
Mechanism
Deregulated nutrient sensing
Reasoning

fdgt-1 encodes a facilitated glucose transporter (GLUT homolog) that mediates hexose uptake across membranes. Increased glucose import elevates intracellular glucose availability, which activates insulin/IGF-1 signaling (IIS) through elevated glucose metabolism and downstream DAF-2 pathway activation, suppressing the pro-longevity transcription factor DAF-16/FOXO. In C. elegans, dietary glucose supplementation is well-established to shorten lifespan via IIS hyperactivation and suppression of DAF-16 nuclear localization. Enhanced glucose transport also promotes glycolysis over mitochondrial respiration, reducing NAD+ levels and dampening sirtuin (SIR-2.1) activity, further opposing longevity. Thus, the normal pro-transport function of fdgt-1 is expected to be anti-longevity by fueling nutrient-sensing pathways that oppose stress resistance and lifespan extension.

Key pathways
insulin/IGF-1 signaling (DAF-2/DAF-16 axis)glucose metabolism and glycolysisNAD+/sirtuin signaling (SIR-2.1)
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 fdgt-1. The mechanistic reasoning is sound and well-grounded: glucose transporters increase intracellular glucose, which activates IIS/DAF-2 pathway and suppresses DAF-16/FOXO, a well-established mechanism for lifespan shortening in C. elegans. The model also correctly notes the NAD+/sirtuin angle. The reasoning is biologically plausible and consistent with published literature on glucose and aging in C. elegans. Confidence of 0.68 is appropriately calibrated given the indirect nature of the inference (the gene's function is inferred from its transporter role rather than direct experimental evidence cited). Overall a strong prediction with solid mechanistic reasoning.

Raw API responses

solver

{
  "reasoning": "fdgt-1 encodes a facilitated glucose transporter (GLUT homolog) that mediates hexose uptake across membranes. Increased glucose import elevates intracellular glucose availability, which activates insulin/IGF-1 signaling (IIS) through elevated glucose metabolism and downstream DAF-2 pathway activation, suppressing the pro-longevity transcription factor DAF-16/FOXO. In C. elegans, dietary glucose supplementation is well-established to shorten lifespan via IIS hyperactivation and suppression of DAF-16 nuclear localization. Enhanced glucose transport also promotes glycolysis over mitochondrial respiration, reducing NAD+ levels and dampening sirtuin (SIR-2.1) activity, further opposing longevity. Thus, the normal pro-transport function of fdgt-1 is expected to be anti-longevity by fueling nutrient-sensing pathways that oppose stress resistance and lifespan extension.",
  "confidence": 0.68,
  "key_pathways": [
    "insulin/IGF-1 signaling (DAF-2/DAF-16 axis)",
    "glucose metabolism and glycolysis",
    "NAD+/sirtuin signaling (SIR-2.1)"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for fdgt-1. The mechanistic reasoning is sound and well-grounded: glucose transporters increase intracellular glucose, which activates IIS/DAF-2 pathway and suppresses DAF-16/FOXO, a well-established mechanism for lifespan shortening in C. elegans. The model also correctly notes the NAD+/sirtuin angle. The reasoning is biologically plausible and consistent with published literature on glucose and aging in C. elegans. Confidence of 0.68 is appropriately calibrated given the indirect nature of the inference (the gene's function is inferred from its transporter role rather than direct experimental evidence cited). Overall a strong prediction with solid mechanistic reasoning.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}