slc-36.1
C. elegans
Amino acid transporter transmembrane domain-containing protein
What the model saw
Gene: slc-36.1 Organism: Caenorhabditis elegans Known functions: Amino acid transporter transmembrane domain-containing protein. L-amino acid transmembrane transporter activity.
View unredacted entry
Amino acid transporter transmembrane domain-containing protein. L-amino acid transmembrane transporter activity.
Solver output
slc-36.1 encodes a proton-coupled amino acid transporter (PAT family/SLC36) that mediates L-amino acid uptake across membranes, including lysosomal membranes. In C. elegans, SLC-36.1 is the ortholog of mammalian PAT1 (SLC36A1), which transports amino acids out of the lysosome into the cytoplasm, directly activating mTORC1 (TORC1 in worms) by supplying amino acid signals at the lysosomal surface. TORC1 activation suppresses autophagy and promotes anabolic growth, both of which are well-established anti-longevity effects in C. elegans. Reduced amino acid sensing through TORC1 (e.g., via dietary restriction or TORC1 inhibition) extends lifespan, so a transporter that fuels TORC1 activation would oppose longevity. Loss of slc-36.1 function has been shown to reduce TORC1 activity and extend lifespan in C. elegans, consistent with its normal function being pro-growth and anti-longevity.
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 slc-36.1. The mechanistic reasoning is detailed and accurate: SLC-36.1 is a lysosomal amino acid transporter that activates TORC1 signaling, which suppresses autophagy and promotes anabolic growth, thereby opposing longevity. The model correctly identifies that loss of slc-36.1 reduces TORC1 activity and extends lifespan, making the normal gene function anti-longevity. The confidence level of 0.65 is reasonable given the specificity of the gene. Overall, this is an excellent prediction with correct answer and sound mechanistic reasoning.
Raw API responses
solver
{
"reasoning": "slc-36.1 encodes a proton-coupled amino acid transporter (PAT family/SLC36) that mediates L-amino acid uptake across membranes, including lysosomal membranes. In C. elegans, SLC-36.1 is the ortholog of mammalian PAT1 (SLC36A1), which transports amino acids out of the lysosome into the cytoplasm, directly activating mTORC1 (TORC1 in worms) by supplying amino acid signals at the lysosomal surface. TORC1 activation suppresses autophagy and promotes anabolic growth, both of which are well-established anti-longevity effects in C. elegans. Reduced amino acid sensing through TORC1 (e.g., via dietary restriction or TORC1 inhibition) extends lifespan, so a transporter that fuels TORC1 activation would oppose longevity. Loss of slc-36.1 function has been shown to reduce TORC1 activity and extend lifespan in C. elegans, consistent with its normal function being pro-growth and anti-longevity.",
"confidence": 0.65,
"key_pathways": [
"mTORC1/TORC1 amino acid sensing",
"lysosomal amino acid transport",
"autophagy suppression"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for slc-36.1. The mechanistic reasoning is detailed and accurate: SLC-36.1 is a lysosomal amino acid transporter that activates TORC1 signaling, which suppresses autophagy and promotes anabolic growth, thereby opposing longevity. The model correctly identifies that loss of slc-36.1 reduces TORC1 activity and extends lifespan, making the normal gene function anti-longevity. The confidence level of 0.65 is reasonable given the specificity of the gene. Overall, this is an excellent prediction with correct answer and sound mechanistic reasoning.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}