f13g3.7
C. elegans
SLC (SoLute Carrier) homolog
What the model saw
Gene: F13G3.7 Organism: Caenorhabditis elegans Known functions: SLC (SoLute Carrier) homolog. branched-chain amino acid transmembrane transporter activity.
View unredacted entry
SLC (SoLute Carrier) homolog. branched-chain amino acid transmembrane transporter activity.
Solver output
F13G3.7 encodes a branched-chain amino acid (BCAA) transmembrane transporter (SLC homolog), which facilitates cellular uptake of BCAAs such as leucine, isoleucine, and valine. Elevated intracellular BCAA levels, particularly leucine, are well-established activators of the mTORC1 (mechanistic target of rapamycin complex 1) nutrient-sensing pathway. In C. elegans, hyperactivation of the TOR/TORC1 pathway suppresses autophagy and promotes anabolic growth at the expense of longevity, while reduced TOR signaling (e.g., via dietary restriction or genetic inhibition) robustly extends lifespan. By importing BCAAs into cells, this transporter would be expected to promote mTORC1 activation and thus oppose longevity. This places its primary mechanism within the deregulated nutrient-sensing hallmark of 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 anti_longevity for F13G3.7. The mechanistic reasoning is sound and well-articulated: BCAA transporter → increased intracellular BCAAs → mTORC1 activation → reduced longevity. This is a plausible and well-supported mechanistic pathway in C. elegans biology. The confidence of 0.62 is appropriately calibrated given the limited direct evidence for this specific gene. The reasoning quality is good but not perfect since it's largely inferential rather than based on direct experimental evidence for this specific gene.
Raw API responses
solver
{
"reasoning": "F13G3.7 encodes a branched-chain amino acid (BCAA) transmembrane transporter (SLC homolog), which facilitates cellular uptake of BCAAs such as leucine, isoleucine, and valine. Elevated intracellular BCAA levels, particularly leucine, are well-established activators of the mTORC1 (mechanistic target of rapamycin complex 1) nutrient-sensing pathway. In C. elegans, hyperactivation of the TOR/TORC1 pathway suppresses autophagy and promotes anabolic growth at the expense of longevity, while reduced TOR signaling (e.g., via dietary restriction or genetic inhibition) robustly extends lifespan. By importing BCAAs into cells, this transporter would be expected to promote mTORC1 activation and thus oppose longevity. This places its primary mechanism within the deregulated nutrient-sensing hallmark of aging.",
"confidence": 0.62,
"key_pathways": [
"mTORC1/TOR nutrient sensing",
"branched-chain amino acid (BCAA) import",
"dietary restriction / amino acid signaling"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for F13G3.7. The mechanistic reasoning is sound and well-articulated: BCAA transporter → increased intracellular BCAAs → mTORC1 activation → reduced longevity. This is a plausible and well-supported mechanistic pathway in C. elegans biology. The confidence of 0.62 is appropriately calibrated given the limited direct evidence for this specific gene. The reasoning quality is good but not perfect since it's largely inferential rather than based on direct experimental evidence for this specific gene.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}