RPL16B
S. cerevisiae
60S ribosomal protein uL13 RPL16B
What the model saw
Gene: RPL16B Organism: Saccharomyces cerevisiae Known functions: 60S ribosomal protein uL13 RPL16B. RNA binding. mRNA binding. structural constituent of ribosome.
View unredacted entry
60S ribosomal protein uL13 RPL16B. RNA binding. mRNA binding. structural constituent of ribosome.
Solver output
RPL16B encodes a structural component of the 60S ribosomal large subunit (uL13), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of large subunit components — is well established to extend chronological and replicative lifespan, largely through attenuation of TORC1-driven protein synthesis. Deletion or reduction of 60S ribosomal proteins like RPL16B decreases global translation rates, mimicking caloric restriction and dampening TOR signaling output. This connects ribosome function to the deregulated nutrient-sensing hallmark, as TOR pathway hyperactivation promotes aging via excessive anabolic signaling. The normal (wild-type) function of RPL16B therefore sustains high translational output, which is pro-aging in yeast, making the gene itself anti-longevity in its normal role.
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 RPL16B. The mechanistic reasoning is sound: RPL16B encodes a 60S ribosomal large subunit protein, and deletion of ribosomal protein genes in yeast is well-established to extend lifespan by reducing translational output and attenuating TOR signaling. The connection to deregulated nutrient sensing via TORC1 is a reasonable and well-supported mechanistic framework. The reasoning is coherent and consistent with the literature on ribosomal protein deletions extending yeast lifespan. Confidence of 0.72 is appropriate given the general pattern for 60S ribosomal proteins in yeast.
Raw API responses
solver
{
"reasoning": "RPL16B encodes a structural component of the 60S ribosomal large subunit (uL13), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of large subunit components — is well established to extend chronological and replicative lifespan, largely through attenuation of TORC1-driven protein synthesis. Deletion or reduction of 60S ribosomal proteins like RPL16B decreases global translation rates, mimicking caloric restriction and dampening TOR signaling output. This connects ribosome function to the deregulated nutrient-sensing hallmark, as TOR pathway hyperactivation promotes aging via excessive anabolic signaling. The normal (wild-type) function of RPL16B therefore sustains high translational output, which is pro-aging in yeast, making the gene itself anti-longevity in its normal role.",
"confidence": 0.72,
"key_pathways": [
"TORC1/nutrient-sensing signaling",
"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 RPL16B. The mechanistic reasoning is sound: RPL16B encodes a 60S ribosomal large subunit protein, and deletion of ribosomal protein genes in yeast is well-established to extend lifespan by reducing translational output and attenuating TOR signaling. The connection to deregulated nutrient sensing via TORC1 is a reasonable and well-supported mechanistic framework. The reasoning is coherent and consistent with the literature on ribosomal protein deletions extending yeast lifespan. Confidence of 0.72 is appropriate given the general pattern for 60S ribosomal proteins in yeast.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}