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Dci

D. melanogaster

Dodecenoyl-CoA delta-isomerase

What the model saw

Gene: Dci
Organism: Drosophila melanogaster
Known functions: Dodecenoyl-CoA delta-isomerase. delta(3)-delta(2)-enoyl-CoA isomerase activity.
View unredacted entry
Dodecenoyl-CoA delta-isomerase. delta(3)-delta(2)-enoyl-CoA isomerase activity.

Solver output

Predicted influence
Pro-longevity
Confidence
65%
Mechanism
Mitochondrial dysfunction
Reasoning

Dci encodes dodecenoyl-CoA delta-isomerase, which catalyzes the conversion of delta(3)-enoyl-CoA to delta(2)-enoyl-CoA, an essential auxiliary step in the beta-oxidation of unsaturated fatty acids in mitochondria. Without this isomerase activity, unsaturated fatty acids with double bonds at odd-numbered positions cannot be fully oxidized, leading to incomplete fatty acid catabolism and accumulation of toxic intermediates. Efficient mitochondrial fatty acid beta-oxidation is critical for maintaining mitochondrial membrane potential, ATP production, and redox balance — all of which decline with age. Loss of Dci function would impair mitochondrial energy metabolism and potentially increase lipotoxic stress, accelerating aging-associated mitochondrial dysfunction. Therefore, the normal function of Dci supports mitochondrial integrity and metabolic efficiency, consistent with a pro-longevity role.

Key pathways
mitochondrial fatty acid beta-oxidationunsaturated fatty acid catabolismmitochondrial energy metabolism
Longevity influence
Pro-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 pro_longevity for Dci. The mechanistic reasoning is sound and well-articulated: Dci encodes dodecenoyl-CoA delta-isomerase, which is essential for beta-oxidation of unsaturated fatty acids in mitochondria. The model correctly identifies that loss of this enzyme would impair mitochondrial energy metabolism and lead to accumulation of toxic intermediates, supporting a pro-longevity role for the gene. The reasoning is biologically plausible and consistent with the known function of the gene. Confidence of 0.65 is appropriate given the limited direct evidence typically available for Drosophila longevity genes. The mechanism class "mitochondrial_dysfunction" is a reasonable categorization, though it describes the consequence of loss-of-function rather than the normal mechanism.

Raw API responses

solver

{
  "reasoning": "Dci encodes dodecenoyl-CoA delta-isomerase, which catalyzes the conversion of delta(3)-enoyl-CoA to delta(2)-enoyl-CoA, an essential auxiliary step in the beta-oxidation of unsaturated fatty acids in mitochondria. Without this isomerase activity, unsaturated fatty acids with double bonds at odd-numbered positions cannot be fully oxidized, leading to incomplete fatty acid catabolism and accumulation of toxic intermediates. Efficient mitochondrial fatty acid beta-oxidation is critical for maintaining mitochondrial membrane potential, ATP production, and redox balance — all of which decline with age. Loss of Dci function would impair mitochondrial energy metabolism and potentially increase lipotoxic stress, accelerating aging-associated mitochondrial dysfunction. Therefore, the normal function of Dci supports mitochondrial integrity and metabolic efficiency, consistent with a pro-longevity role.",
  "confidence": 0.65,
  "key_pathways": [
    "mitochondrial fatty acid beta-oxidation",
    "unsaturated fatty acid catabolism",
    "mitochondrial energy metabolism"
  ],
  "mechanism_class": "mitochondrial_dysfunction",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model correctly predicted pro_longevity for Dci. The mechanistic reasoning is sound and well-articulated: Dci encodes dodecenoyl-CoA delta-isomerase, which is essential for beta-oxidation of unsaturated fatty acids in mitochondria. The model correctly identifies that loss of this enzyme would impair mitochondrial energy metabolism and lead to accumulation of toxic intermediates, supporting a pro-longevity role for the gene. The reasoning is biologically plausible and consistent with the known function of the gene. Confidence of 0.65 is appropriate given the limited direct evidence typically available for Drosophila longevity genes. The mechanism class \"mitochondrial_dysfunction\" is a reasonable categorization, though it describes the consequence of loss-of-function rather than the normal mechanism.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}
Dci · Drosophila melanogaster | Aging biology eval