bcat-1
C. elegans
Branched-chain-amino-acid aminotransferase, cytosolic
What the model saw
Gene: bcat-1 Organism: Caenorhabditis elegans Known functions: Branched-chain-amino-acid aminotransferase, cytosolic. L-isoleucine:2-oxoglutarate transaminase activity. L-leucine:2-oxoglutarate transaminase activity. L-valine:2-oxoglutarate transaminase activity. branched-chain-amino-acid:2-oxoglutarate transaminase activity. catalytic activity.
View unredacted entry
Branched-chain-amino-acid aminotransferase, cytosolic. L-isoleucine:2-oxoglutarate transaminase activity. L-leucine:2-oxoglutarate transaminase activity. L-valine:2-oxoglutarate transaminase activity. branched-chain-amino-acid:2-oxoglutarate transaminase activity. catalytic activity.
Solver output
BCAT-1 is the cytosolic branched-chain amino acid aminotransferase in C. elegans, catalyzing the first step in the catabolism of leucine, isoleucine, and valine (BCAAs) by transaminating them to their respective alpha-keto acids. Knockdown of bcat-1 leads to accumulation of BCAAs, particularly leucine, which activates mTORC1 signaling — a central pro-aging nutrient-sensing pathway. Elevated BCAA levels and mTORC1 activity suppress autophagy and promote anabolic processes that shorten lifespan. Published RNAi studies in C. elegans have shown that bcat-1 knockdown extends lifespan, indicating that the normal function of BCAT-1 (degrading BCAAs and thus relieving BCAA-mediated mTORC1 suppression) is pro-aging. Therefore, the wild-type gene activity opposes longevity by maintaining BCAA catabolism and permitting mTORC1 activation.
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 bcat-1 in C. elegans with high confidence (0.78). The mechanistic reasoning is detailed and accurate: BCAT-1 degrades BCAAs (leucine, isoleucine, valine), and its knockdown leads to BCAA accumulation, which activates mTORC1 signaling, suppresses autophagy, and shortens lifespan. The model correctly identifies that the wild-type gene function is pro-aging (anti-longevity), as its loss of function extends lifespan. The pathway identification (mTORC1 nutrient sensing, BCAA catabolism, autophagy suppression) is all consistent with published literature on bcat-1 in C. elegans.
Raw API responses
solver
{
"reasoning": "BCAT-1 is the cytosolic branched-chain amino acid aminotransferase in C. elegans, catalyzing the first step in the catabolism of leucine, isoleucine, and valine (BCAAs) by transaminating them to their respective alpha-keto acids. Knockdown of bcat-1 leads to accumulation of BCAAs, particularly leucine, which activates mTORC1 signaling — a central pro-aging nutrient-sensing pathway. Elevated BCAA levels and mTORC1 activity suppress autophagy and promote anabolic processes that shorten lifespan. Published RNAi studies in C. elegans have shown that bcat-1 knockdown extends lifespan, indicating that the normal function of BCAT-1 (degrading BCAAs and thus relieving BCAA-mediated mTORC1 suppression) is pro-aging. Therefore, the wild-type gene activity opposes longevity by maintaining BCAA catabolism and permitting mTORC1 activation.",
"confidence": 0.78,
"key_pathways": [
"mTORC1 nutrient sensing via branched-chain amino acids",
"BCAA catabolism (leucine/isoleucine/valine transamination)",
"autophagy suppression downstream of mTORC1"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for bcat-1 in C. elegans with high confidence (0.78). The mechanistic reasoning is detailed and accurate: BCAT-1 degrades BCAAs (leucine, isoleucine, valine), and its knockdown leads to BCAA accumulation, which activates mTORC1 signaling, suppresses autophagy, and shortens lifespan. The model correctly identifies that the wild-type gene function is pro-aging (anti-longevity), as its loss of function extends lifespan. The pathway identification (mTORC1 nutrient sensing, BCAA catabolism, autophagy suppression) is all consistent with published literature on bcat-1 in C. elegans.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}