fmo-2
C. elegans
Flavin-containing monooxygenase
What the model saw
Gene: fmo-2 Organism: Caenorhabditis elegans Known functions: Flavin-containing monooxygenase. N,N-dimethylaniline monooxygenase activity. NAD(P)H oxidase H2O2-forming activity. NADP binding. flavin adenine dinucleotide binding. monooxygenase activity. trimethylamine monooxygenase activity.
View unredacted entry
Flavin-containing monooxygenase. N,N-dimethylaniline monooxygenase activity. NAD(P)H oxidase H2O2-forming activity. NADP binding. flavin adenine dinucleotide binding. monooxygenase activity. trimethylamine monooxygenase activity.
Solver output
fmo-2 encodes a flavin-containing monooxygenase in C. elegans that is transcriptionally upregulated downstream of multiple longevity pathways, including dietary restriction, hypoxia (HIF-1), and reduced insulin/IGF-1 signaling. The enzyme uses NADPH and FAD as cofactors to catalyze oxygenation reactions (e.g., N,N-dimethylaniline and trimethylamine monooxygenase activities), and its overexpression is sufficient to extend lifespan in C. elegans. Mechanistically, FMO-2 activity is linked to one-carbon metabolism and methionine cycle modulation, connecting nutrient-sensing pathways to longevity. The NAD(P)H oxidase H2O2-forming activity also suggests a role in redox signaling that may influence stress-response pathways. Its induction under dietary restriction places it as a key effector in the nutrient-sensing axis that promotes healthy aging.
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 correctly predicted pro_longevity for fmo-2 in C. elegans with high confidence (0.82). The mechanistic reasoning is accurate and detailed: fmo-2 is indeed upregulated downstream of dietary restriction, HIF-1/hypoxia, and reduced IIS signaling, and its overexpression extends lifespan. The connection to one-carbon/methionine metabolism is also well-established in the literature. The mechanism class of "deregulated_nutrient_sensing" is reasonable, though the primary classification might more precisely be "stress response" or "metabolic," but the nutrient-sensing framing is defensible given fmo-2's role downstream of dietary restriction pathways. Overall, this is an excellent prediction with accurate and well-supported reasoning.
Raw API responses
solver
{
"reasoning": "fmo-2 encodes a flavin-containing monooxygenase in C. elegans that is transcriptionally upregulated downstream of multiple longevity pathways, including dietary restriction, hypoxia (HIF-1), and reduced insulin/IGF-1 signaling. The enzyme uses NADPH and FAD as cofactors to catalyze oxygenation reactions (e.g., N,N-dimethylaniline and trimethylamine monooxygenase activities), and its overexpression is sufficient to extend lifespan in C. elegans. Mechanistically, FMO-2 activity is linked to one-carbon metabolism and methionine cycle modulation, connecting nutrient-sensing pathways to longevity. The NAD(P)H oxidase H2O2-forming activity also suggests a role in redox signaling that may influence stress-response pathways. Its induction under dietary restriction places it as a key effector in the nutrient-sensing axis that promotes healthy aging.",
"confidence": 0.82,
"key_pathways": [
"insulin/IGF-1 signaling (IIS) longevity pathway",
"dietary restriction / nutrient sensing",
"one-carbon / methionine metabolism"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for fmo-2 in C. elegans with high confidence (0.82). The mechanistic reasoning is accurate and detailed: fmo-2 is indeed upregulated downstream of dietary restriction, HIF-1/hypoxia, and reduced IIS signaling, and its overexpression extends lifespan. The connection to one-carbon/methionine metabolism is also well-established in the literature. The mechanism class of \"deregulated_nutrient_sensing\" is reasonable, though the primary classification might more precisely be \"stress response\" or \"metabolic,\" but the nutrient-sensing framing is defensible given fmo-2's role downstream of dietary restriction pathways. Overall, this is an excellent prediction with accurate and well-supported reasoning.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}