acs-20
C. elegans
long-chain-fatty-acid--CoA ligase
What the model saw
Gene: acs-20 Organism: Caenorhabditis elegans Known functions: long-chain-fatty-acid--CoA ligase. long-chain fatty acid transmembrane transporter activity. long-chain fatty acid-CoA ligase activity.
View unredacted entry
long-chain-fatty-acid--CoA ligase. long-chain fatty acid transmembrane transporter activity. long-chain fatty acid-CoA ligase activity.
Solver output
ACS-20 encodes a long-chain fatty acid-CoA ligase (acyl-CoA synthetase) that activates long-chain fatty acids by conjugating them to CoA, a critical step for fatty acid β-oxidation, lipid biosynthesis, and membrane remodeling. In C. elegans, proper fatty acid activation and trafficking are essential for maintaining lipid homeostasis, which is tightly coupled to nutrient-sensing pathways such as insulin/IGF-1 signaling and AMPK. Long-chain fatty acid transport and activation feed into mitochondrial β-oxidation, supporting energy metabolism and reducing lipotoxic lipid accumulation. Disruption of acyl-CoA synthetase activity in worms has been associated with impaired fat utilization and shortened lifespan, suggesting the normal function is required for metabolic fitness. The role of ACS-20 in channeling fatty acids into productive metabolic routes rather than allowing their accumulation as toxic species places it in the deregulated nutrient-sensing hallmark, acting pro-longevity by sustaining lipid metabolic balance.
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 acs-20. The mechanistic reasoning is plausible and generally sound - connecting long-chain fatty acid activation via acyl-CoA synthetase to lipid homeostasis, beta-oxidation, and nutrient sensing pathways. However, the reasoning is somewhat generic and speculative, relying on general principles about acyl-CoA synthetases rather than specific knowledge about acs-20 in C. elegans. The model appropriately hedged with 0.62 confidence. The mechanism class of "deregulated_nutrient_sensing" is reasonable but could also be classified under lipid metabolism more directly. Overall a correct prediction with adequate but not exceptional reasoning.
Raw API responses
solver
{
"reasoning": "ACS-20 encodes a long-chain fatty acid-CoA ligase (acyl-CoA synthetase) that activates long-chain fatty acids by conjugating them to CoA, a critical step for fatty acid β-oxidation, lipid biosynthesis, and membrane remodeling. In C. elegans, proper fatty acid activation and trafficking are essential for maintaining lipid homeostasis, which is tightly coupled to nutrient-sensing pathways such as insulin/IGF-1 signaling and AMPK. Long-chain fatty acid transport and activation feed into mitochondrial β-oxidation, supporting energy metabolism and reducing lipotoxic lipid accumulation. Disruption of acyl-CoA synthetase activity in worms has been associated with impaired fat utilization and shortened lifespan, suggesting the normal function is required for metabolic fitness. The role of ACS-20 in channeling fatty acids into productive metabolic routes rather than allowing their accumulation as toxic species places it in the deregulated nutrient-sensing hallmark, acting pro-longevity by sustaining lipid metabolic balance.",
"confidence": 0.62,
"key_pathways": [
"long-chain fatty acid activation and beta-oxidation",
"lipid homeostasis and nutrient sensing (insulin/IGF-1, AMPK)",
"fatty acid transmembrane transport"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for acs-20. The mechanistic reasoning is plausible and generally sound - connecting long-chain fatty acid activation via acyl-CoA synthetase to lipid homeostasis, beta-oxidation, and nutrient sensing pathways. However, the reasoning is somewhat generic and speculative, relying on general principles about acyl-CoA synthetases rather than specific knowledge about acs-20 in C. elegans. The model appropriately hedged with 0.62 confidence. The mechanism class of \"deregulated_nutrient_sensing\" is reasonable but could also be classified under lipid metabolism more directly. Overall a correct prediction with adequate but not exceptional reasoning.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}