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cgt-2

C. elegans

Ceramide glucosyltransferase 2

What the model saw

Gene: cgt-2
Organism: Caenorhabditis elegans
Known functions: Ceramide glucosyltransferase 2. ceramide glucosyltransferase activity. glycosyltransferase activity.
View unredacted entry
Ceramide glucosyltransferase 2. ceramide glucosyltransferase activity. glycosyltransferase activity.

Solver output

Predicted influence
Anti-longevity
Confidence
62%
Mechanism
Deregulated nutrient sensing
Reasoning

CGT-2 encodes a ceramide glucosyltransferase that catalyzes the conversion of ceramide to glucosylceramide, the first and committed step in glycosphingolipid biosynthesis. In C. elegans, ceramide itself is a pro-longevity lipid mediator that promotes stress resistance and lifespan extension, in part by modulating insulin/IGF-1 signaling (DAF-2/DAF-16 pathway) and germline signaling. By consuming ceramide to produce glucosylceramide, CGT-2 activity reduces the bioavailable pool of ceramide, thereby attenuating ceramide-mediated longevity signals. Loss-of-function of ceramide glucosyltransferases in C. elegans has been associated with altered sphingolipid homeostasis that can extend lifespan, consistent with the normal function of cgt-2 being anti-longevity. The glycosphingolipid products also influence membrane composition and nutrient-sensing pathway activity, further linking this enzyme to aging regulation.

Key pathways
sphingolipid metabolism / ceramide-glucosylceramide conversioninsulin/IGF-1 signaling (DAF-2/DAF-16)glycosphingolipid biosynthesis
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 cgt-2. The mechanistic reasoning is sound: CGT-2 converts ceramide to glucosylceramide, depleting the pro-longevity ceramide pool, and loss of cgt-2 function would extend lifespan by preserving ceramide levels. The mechanism class "deregulated_nutrient_sensing" is a somewhat loose fit — sphingolipid metabolism is more directly the mechanism — but the core reasoning about ceramide/glucosylceramide balance and its connection to longevity pathways is biologically plausible and well-articulated. The confidence of 0.62 is appropriately moderate. Overall a good prediction with minor imprecision in mechanism classification.

Raw API responses

solver

{
  "reasoning": "CGT-2 encodes a ceramide glucosyltransferase that catalyzes the conversion of ceramide to glucosylceramide, the first and committed step in glycosphingolipid biosynthesis. In C. elegans, ceramide itself is a pro-longevity lipid mediator that promotes stress resistance and lifespan extension, in part by modulating insulin/IGF-1 signaling (DAF-2/DAF-16 pathway) and germline signaling. By consuming ceramide to produce glucosylceramide, CGT-2 activity reduces the bioavailable pool of ceramide, thereby attenuating ceramide-mediated longevity signals. Loss-of-function of ceramide glucosyltransferases in C. elegans has been associated with altered sphingolipid homeostasis that can extend lifespan, consistent with the normal function of cgt-2 being anti-longevity. The glycosphingolipid products also influence membrane composition and nutrient-sensing pathway activity, further linking this enzyme to aging regulation.",
  "confidence": 0.62,
  "key_pathways": [
    "sphingolipid metabolism / ceramide-glucosylceramide conversion",
    "insulin/IGF-1 signaling (DAF-2/DAF-16)",
    "glycosphingolipid biosynthesis"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for cgt-2. The mechanistic reasoning is sound: CGT-2 converts ceramide to glucosylceramide, depleting the pro-longevity ceramide pool, and loss of cgt-2 function would extend lifespan by preserving ceramide levels. The mechanism class \"deregulated_nutrient_sensing\" is a somewhat loose fit — sphingolipid metabolism is more directly the mechanism — but the core reasoning about ceramide/glucosylceramide balance and its connection to longevity pathways is biologically plausible and well-articulated. The confidence of 0.62 is appropriately moderate. Overall a good prediction with minor imprecision in mechanism classification.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}
cgt-2 · Caenorhabditis elegans | Aging biology eval