CRC1
S. cerevisiae
carnitine:acyl carnitine antiporter
What the model saw
Gene: CRC1 Organism: Saccharomyces cerevisiae Known functions: carnitine:acyl carnitine antiporter. O-acyl-L-carnitine transmembrane transporter activity. carnitine:O-acyl-L-carnitine antiporter activity.
View unredacted entry
carnitine:acyl carnitine antiporter. O-acyl-L-carnitine transmembrane transporter activity. carnitine:O-acyl-L-carnitine antiporter activity.
Solver output
CRC1 encodes the mitochondrial inner membrane carnitine/acylcarnitine carrier in S. cerevisiae, which exchanges free carnitine for acylcarnitines across the mitochondrial inner membrane. This antiporter activity is essential for the carnitine shuttle, which transports activated fatty acyl groups (as acylcarnitines) into the mitochondrial matrix for beta-oxidation. By enabling efficient mitochondrial fatty acid oxidation, CRC1 supports mitochondrial metabolic function and energy homeostasis. Impaired fatty acid import into mitochondria leads to lipid accumulation, reduced respiratory capacity, and mitochondrial dysfunction — all hallmarks associated with accelerated aging. Proper carnitine shuttle activity also helps maintain acyl-CoA/CoA balance in the mitochondrial matrix, which is important for TCA cycle flux and NAD+ regeneration, both linked to longevity in yeast.
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 but the ground truth is anti_longevity. The model's reasoning assumes that CRC1 supports longevity by enabling mitochondrial fatty acid oxidation and energy homeostasis, but the actual GenAge classification indicates CRC1 is anti-longevity (meaning its deletion or loss extends lifespan). The mechanistic reasoning is plausible in isolation but leads to the wrong conclusion — the model failed to consider that CRC1 deletion might extend lifespan, possibly by reducing fatty acid oxidation flux or altering mitochondrial metabolism in ways that promote longevity (e.g., mimicking caloric restriction-like states). The model's confidence of 0.62 is moderate but still committed to the wrong answer.
Raw API responses
solver
{
"reasoning": "CRC1 encodes the mitochondrial inner membrane carnitine/acylcarnitine carrier in S. cerevisiae, which exchanges free carnitine for acylcarnitines across the mitochondrial inner membrane. This antiporter activity is essential for the carnitine shuttle, which transports activated fatty acyl groups (as acylcarnitines) into the mitochondrial matrix for beta-oxidation. By enabling efficient mitochondrial fatty acid oxidation, CRC1 supports mitochondrial metabolic function and energy homeostasis. Impaired fatty acid import into mitochondria leads to lipid accumulation, reduced respiratory capacity, and mitochondrial dysfunction — all hallmarks associated with accelerated aging. Proper carnitine shuttle activity also helps maintain acyl-CoA/CoA balance in the mitochondrial matrix, which is important for TCA cycle flux and NAD+ regeneration, both linked to longevity in yeast.",
"confidence": 0.62,
"key_pathways": [
"carnitine shuttle / fatty acid beta-oxidation",
"mitochondrial metabolic homeostasis",
"acyl-CoA/CoA balance and TCA cycle flux"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning assumes that CRC1 supports longevity by enabling mitochondrial fatty acid oxidation and energy homeostasis, but the actual GenAge classification indicates CRC1 is anti-longevity (meaning its deletion or loss extends lifespan). The mechanistic reasoning is plausible in isolation but leads to the wrong conclusion — the model failed to consider that CRC1 deletion might extend lifespan, possibly by reducing fatty acid oxidation flux or altering mitochondrial metabolism in ways that promote longevity (e.g., mimicking caloric restriction-like states). The model's confidence of 0.62 is moderate but still committed to the wrong answer.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}