Egm
D. melanogaster
Enigma
What the model saw
Gene: Egm Organism: Drosophila melanogaster Known functions: Enigma. enigma. flavin adenine dinucleotide binding. medium-chain fatty acyl-CoA dehydrogenase activity. oxidoreductase activity, acting on the CH-CH group of donors. protein-macromolecule adaptor activity. very-long-chain fatty acyl-CoA dehydrogenase activity.
View unredacted entry
Enigma. enigma. flavin adenine dinucleotide binding. medium-chain fatty acyl-CoA dehydrogenase activity. oxidoreductase activity, acting on the CH-CH group of donors. protein-macromolecule adaptor activity. very-long-chain fatty acyl-CoA dehydrogenase activity.
Solver output
Egm (Enigma) encodes a flavin adenine dinucleotide (FAD)-dependent acyl-CoA dehydrogenase with both medium-chain and very-long-chain fatty acyl-CoA dehydrogenase activities, catalyzing the first oxidation step (CH-CH bond formation) in mitochondrial fatty acid β-oxidation. This activity is essential for efficient mitochondrial energy metabolism by feeding electrons into the electron transport chain via the electron-transferring flavoprotein (ETF) complex. Proper fatty acid β-oxidation supports mitochondrial membrane potential, reduces lipotoxic acyl-CoA accumulation, and limits reactive oxygen species production from incomplete fatty acid catabolism. Loss of such dehydrogenase function in model organisms is associated with mitochondrial dysfunction, lipid accumulation, and shortened lifespan. The additional protein-macromolecule adaptor activity (LIM domain-like scaffold function characteristic of Enigma family proteins) may further support mitochondrial or cytoskeletal organization relevant to metabolic homeostasis.
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
The model predicted pro_longevity with 0.72 confidence, but the ground truth is anti_longevity. The model's reasoning focused on the idea that loss of fatty acid β-oxidation function would cause mitochondrial dysfunction and shortened lifespan, which would make Egm pro_longevity (i.e., its presence extends life). However, the ground truth indicates Egm is anti_longevity, meaning its presence shortens lifespan (or its loss extends lifespan). The model's mechanistic reasoning was internally consistent but led to the wrong conclusion. The model failed to consider that Egm might promote aging through lipid metabolism dysregulation or other mechanisms when overexpressed/active. The confidence of 0.72 for the wrong answer is notably high.
Raw API responses
solver
{
"reasoning": "Egm (Enigma) encodes a flavin adenine dinucleotide (FAD)-dependent acyl-CoA dehydrogenase with both medium-chain and very-long-chain fatty acyl-CoA dehydrogenase activities, catalyzing the first oxidation step (CH-CH bond formation) in mitochondrial fatty acid β-oxidation. This activity is essential for efficient mitochondrial energy metabolism by feeding electrons into the electron transport chain via the electron-transferring flavoprotein (ETF) complex. Proper fatty acid β-oxidation supports mitochondrial membrane potential, reduces lipotoxic acyl-CoA accumulation, and limits reactive oxygen species production from incomplete fatty acid catabolism. Loss of such dehydrogenase function in model organisms is associated with mitochondrial dysfunction, lipid accumulation, and shortened lifespan. The additional protein-macromolecule adaptor activity (LIM domain-like scaffold function characteristic of Enigma family proteins) may further support mitochondrial or cytoskeletal organization relevant to metabolic homeostasis.",
"confidence": 0.72,
"key_pathways": [
"mitochondrial fatty acid beta-oxidation",
"FAD-dependent electron transfer to ETF complex",
"lipid metabolic homeostasis"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity with 0.72 confidence, but the ground truth is anti_longevity. The model's reasoning focused on the idea that loss of fatty acid β-oxidation function would cause mitochondrial dysfunction and shortened lifespan, which would make Egm pro_longevity (i.e., its presence extends life). However, the ground truth indicates Egm is anti_longevity, meaning its presence shortens lifespan (or its loss extends lifespan). The model's mechanistic reasoning was internally consistent but led to the wrong conclusion. The model failed to consider that Egm might promote aging through lipid metabolism dysregulation or other mechanisms when overexpressed/active. The confidence of 0.72 for the wrong answer is notably high.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}