RPL37B
S. cerevisiae
60S ribosomal protein eL37 RPL37B
What the model saw
Gene: RPL37B Organism: Saccharomyces cerevisiae Known functions: 60S ribosomal protein eL37 RPL37B. structural constituent of ribosome. zinc ion binding.
View unredacted entry
60S ribosomal protein eL37 RPL37B. structural constituent of ribosome. zinc ion binding.
Solver output
RPL37B encodes a structural component of the 60S ribosomal large subunit (eL37), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of 60S subunit components — is well established to extend chronological and replicative lifespan, largely through attenuation of TORC1-driven protein synthesis and downstream effects mimicking dietary restriction. Excess ribosomal activity promotes anabolic signaling via the TOR pathway, which is a central node of nutrient sensing whose hyperactivation shortens lifespan. The zinc ion binding activity of eL37 is intrinsic to its structural role in stabilizing the 60S subunit architecture, reinforcing its pro-translational function. Deletion or reduction of RPL37B would be expected to dampen global translation rates, reduce TORC1 output, and extend lifespan, meaning the normal (wild-type) function of RPL37B 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 RPL37B. The mechanistic reasoning is sound: ribosomal protein genes in yeast are well-established anti-longevity genes because their deletion reduces translational capacity and mimics dietary restriction, extending lifespan. The model correctly identifies the 60S ribosomal subunit role and links it to TOR/nutrient sensing pathways. The mechanism_class of "deregulated_nutrient_sensing" is a reasonable (if slightly indirect) classification — the more direct mechanism is reduced translation/ribosome biogenesis, but the TOR connection is valid. The reasoning is well-articulated and confident at an appropriate level (0.72). Minor quibble: the primary mechanism is really about reduced translation rates rather than nutrient sensing per se, but the two are closely linked in yeast aging biology.
Raw API responses
solver
{
"reasoning": "RPL37B encodes a structural component of the 60S ribosomal large subunit (eL37), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of 60S subunit components — is well established to extend chronological and replicative lifespan, largely through attenuation of TORC1-driven protein synthesis and downstream effects mimicking dietary restriction. Excess ribosomal activity promotes anabolic signaling via the TOR pathway, which is a central node of nutrient sensing whose hyperactivation shortens lifespan. The zinc ion binding activity of eL37 is intrinsic to its structural role in stabilizing the 60S subunit architecture, reinforcing its pro-translational function. Deletion or reduction of RPL37B would be expected to dampen global translation rates, reduce TORC1 output, and extend lifespan, meaning the normal (wild-type) function of RPL37B opposes longevity.",
"confidence": 0.72,
"key_pathways": [
"TORC1/nutrient sensing",
"ribosome biogenesis and translation",
"60S large subunit assembly"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for RPL37B. The mechanistic reasoning is sound: ribosomal protein genes in yeast are well-established anti-longevity genes because their deletion reduces translational capacity and mimics dietary restriction, extending lifespan. The model correctly identifies the 60S ribosomal subunit role and links it to TOR/nutrient sensing pathways. The mechanism_class of \"deregulated_nutrient_sensing\" is a reasonable (if slightly indirect) classification — the more direct mechanism is reduced translation/ribosome biogenesis, but the TOR connection is valid. The reasoning is well-articulated and confident at an appropriate level (0.72). Minor quibble: the primary mechanism is really about reduced translation rates rather than nutrient sensing per se, but the two are closely linked in yeast aging biology.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}