tars-1
C. elegans
Threonine--tRNA ligase, cytoplasmic;threonine--tRNA ligase
What the model saw
Gene: tars-1 Organism: Caenorhabditis elegans Known functions: Threonine--tRNA ligase, cytoplasmic;threonine--tRNA ligase. ATP binding. aminoacyl-tRNA ligase activity. nucleotide binding. threonine-tRNA ligase activity.
View unredacted entry
Threonine--tRNA ligase, cytoplasmic;threonine--tRNA ligase. ATP binding. aminoacyl-tRNA ligase activity. nucleotide binding. threonine-tRNA ligase activity.
Solver output
tars-1 encodes the cytoplasmic threonyl-tRNA synthetase (ThrRS), which charges tRNA^Thr with threonine in an ATP-dependent reaction, directly fueling translational elongation. Aminoacyl-tRNA synthetases are rate-limiting components of the global protein synthesis machinery; their activity is upregulated by nutrient/TOR signaling and downregulated during dietary restriction or reduced TOR activity, both of which extend lifespan in C. elegans. Elevated translational capacity driven by tars-1 activity promotes anabolic growth programs downstream of TOR (TORC1), which is a well-established pro-aging axis. Consistent with this, partial loss-of-function of ribosomal and translation-related genes—including aminoacyl-tRNA synthetases—extends lifespan in C. elegans by reducing global protein synthesis rates and mimicking dietary restriction. Thus, the normal (full) function of tars-1 supports high translational output, which opposes 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 tars-1. The mechanistic reasoning is sound and well-grounded: tars-1 encodes threonyl-tRNA synthetase, which supports global protein synthesis; reduced translation (via knockdown of aminoacyl-tRNA synthetases or ribosomal components) is known to extend lifespan in C. elegans, consistent with the anti-longevity classification. The model appropriately connects tars-1 activity to TOR/nutrient sensing and translational control. The confidence of 0.65 is reasonable given the indirect nature of the evidence. The mechanism class "deregulated_nutrient_sensing" is a reasonable fit, though "translational regulation" might be more precise. Overall, a well-reasoned and correct prediction.
Raw API responses
solver
{
"reasoning": "tars-1 encodes the cytoplasmic threonyl-tRNA synthetase (ThrRS), which charges tRNA^Thr with threonine in an ATP-dependent reaction, directly fueling translational elongation. Aminoacyl-tRNA synthetases are rate-limiting components of the global protein synthesis machinery; their activity is upregulated by nutrient/TOR signaling and downregulated during dietary restriction or reduced TOR activity, both of which extend lifespan in C. elegans. Elevated translational capacity driven by tars-1 activity promotes anabolic growth programs downstream of TOR (TORC1), which is a well-established pro-aging axis. Consistent with this, partial loss-of-function of ribosomal and translation-related genes—including aminoacyl-tRNA synthetases—extends lifespan in C. elegans by reducing global protein synthesis rates and mimicking dietary restriction. Thus, the normal (full) function of tars-1 supports high translational output, which opposes longevity.",
"confidence": 0.65,
"key_pathways": [
"mTORC1/TOR nutrient sensing and translational control",
"aminoacyl-tRNA biosynthesis and global protein synthesis",
"dietary restriction mimicry via reduced translation"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for tars-1. The mechanistic reasoning is sound and well-grounded: tars-1 encodes threonyl-tRNA synthetase, which supports global protein synthesis; reduced translation (via knockdown of aminoacyl-tRNA synthetases or ribosomal components) is known to extend lifespan in C. elegans, consistent with the anti-longevity classification. The model appropriately connects tars-1 activity to TOR/nutrient sensing and translational control. The confidence of 0.65 is reasonable given the indirect nature of the evidence. The mechanism class \"deregulated_nutrient_sensing\" is a reasonable fit, though \"translational regulation\" might be more precise. Overall, a well-reasoned and correct prediction.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}