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YDC1

S. cerevisiae

alkaline dihydroceramidase

What the model saw

Gene: YDC1
Organism: Saccharomyces cerevisiae
Known functions: alkaline dihydroceramidase. N-acylsphingosine amidohydrolase activity.
View unredacted entry
alkaline dihydroceramidase. N-acylsphingosine amidohydrolase activity.

Solver output

Predicted influence
Anti-longevity
Confidence
65%
Mechanism
Altered intercellular communication
Reasoning

YDC1 encodes an alkaline dihydroceramidase (N-acylsphingosine amidohydrolase) that hydrolyzes dihydroceramide into sphingosine and fatty acid, thereby reducing cellular ceramide levels. Ceramide is a pro-apoptotic and pro-senescence bioactive sphingolipid in yeast; elevated ceramide promotes growth arrest and cell death, while its reduction by YDC1 activity shifts the sphingolipid rheostat toward sphingosine and away from ceramide. However, ceramide also plays a protective role in stress responses and has been linked to lifespan extension in yeast — loss of ceramide synthesis or excess ceramide catabolism is associated with shortened chronological lifespan. By catabolizing dihydroceramide, YDC1 reduces the pool of ceramide available for pro-longevity signaling (e.g., via Sit4 phosphatase and TORC1 inhibition), thus its normal activity is predicted to be anti-longevity. This places YDC1 in the sphingolipid signaling arm of nutrient/stress sensing pathways that modulate aging.

Key pathways
sphingolipid metabolismceramide signalingchronological lifespan regulation
Longevity influence
Anti-longevity
Lifespan effect
Increase and 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
Correct
Mechanism
Correct
Reasoning quality
4/5
Failure mode
Correct
Notes

The model correctly predicted anti_longevity for YDC1. The mechanistic reasoning is sound: YDC1 encodes an alkaline dihydroceramidase that catabolizes dihydroceramide, reducing ceramide levels. The model correctly identifies that ceramide has pro-longevity roles in yeast (via stress signaling, TORC1 inhibition, etc.), so YDC1 activity that depletes ceramide would be anti-longevity. The mechanism class of "altered_intercellular_communication" is somewhat questionable — sphingolipid metabolism/signaling would be more accurate — but the core biochemical reasoning about ceramide's role in yeast longevity is correct. Confidence of 0.65 is appropriately calibrated given the complexity of sphingolipid biology.

Raw API responses

solver

{
  "reasoning": "YDC1 encodes an alkaline dihydroceramidase (N-acylsphingosine amidohydrolase) that hydrolyzes dihydroceramide into sphingosine and fatty acid, thereby reducing cellular ceramide levels. Ceramide is a pro-apoptotic and pro-senescence bioactive sphingolipid in yeast; elevated ceramide promotes growth arrest and cell death, while its reduction by YDC1 activity shifts the sphingolipid rheostat toward sphingosine and away from ceramide. However, ceramide also plays a protective role in stress responses and has been linked to lifespan extension in yeast — loss of ceramide synthesis or excess ceramide catabolism is associated with shortened chronological lifespan. By catabolizing dihydroceramide, YDC1 reduces the pool of ceramide available for pro-longevity signaling (e.g., via Sit4 phosphatase and TORC1 inhibition), thus its normal activity is predicted to be anti-longevity. This places YDC1 in the sphingolipid signaling arm of nutrient/stress sensing pathways that modulate aging.",
  "confidence": 0.65,
  "key_pathways": [
    "sphingolipid metabolism",
    "ceramide signaling",
    "chronological lifespan regulation"
  ],
  "mechanism_class": "altered_intercellular_communication",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for YDC1. The mechanistic reasoning is sound: YDC1 encodes an alkaline dihydroceramidase that catabolizes dihydroceramide, reducing ceramide levels. The model correctly identifies that ceramide has pro-longevity roles in yeast (via stress signaling, TORC1 inhibition, etc.), so YDC1 activity that depletes ceramide would be anti-longevity. The mechanism class of \"altered_intercellular_communication\" is somewhat questionable — sphingolipid metabolism/signaling would be more accurate — but the core biochemical reasoning about ceramide's role in yeast longevity is correct. Confidence of 0.65 is appropriately calibrated given the complexity of sphingolipid biology.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}