RPL10
S. cerevisiae
60S ribosomal protein uL16 RPL10
What the model saw
Gene: RPL10 Organism: Saccharomyces cerevisiae Known functions: 60S ribosomal protein uL16 RPL10. protein binding. structural constituent of ribosome.
View unredacted entry
60S ribosomal protein uL16 RPL10. protein binding. structural constituent of ribosome.
Solver output
RPL10 encodes the 60S ribosomal protein uL16, a structural component of the large ribosomal subunit essential for ribosome assembly and translational activity. Ribosomal protein genes in yeast are tightly coupled to the TOR (Target of Rapamycin) nutrient-sensing pathway, which upregulates ribosome biogenesis and global translation under nutrient-rich conditions. Elevated ribosomal activity driven by TOR signaling is a well-established pro-aging mechanism in yeast; conversely, reduced translation via ribosome attenuation (e.g., deletion of ribosomal protein genes) extends chronological and replicative lifespan. Deletion of RPL10 or reduction in 60S ribosomal function has been associated with lifespan extension in yeast screens, consistent with the broader finding that partial impairment of ribosome function reduces protein synthesis rates and mimics dietary restriction. Thus, the normal (wild-type) function of RPL10—promoting full ribosomal capacity and translation—acts to shorten lifespan rather than extend it.
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 RPL10. The mechanistic reasoning is sound and well-grounded: RPL10 encodes a 60S ribosomal protein, and the model correctly connects ribosomal protein function to TOR signaling, ribosome biogenesis, and the established finding that reduced translation/ribosome function extends lifespan in yeast. The mechanism class "deregulated_nutrient_sensing" is a reasonable fit, though "protein synthesis/translation" might be more precise. The reasoning about deletion of ribosomal protein genes extending lifespan is well-supported in the literature. Confidence of 0.65 is appropriately calibrated. Overall a strong, well-reasoned prediction.
Raw API responses
solver
{
"reasoning": "RPL10 encodes the 60S ribosomal protein uL16, a structural component of the large ribosomal subunit essential for ribosome assembly and translational activity. Ribosomal protein genes in yeast are tightly coupled to the TOR (Target of Rapamycin) nutrient-sensing pathway, which upregulates ribosome biogenesis and global translation under nutrient-rich conditions. Elevated ribosomal activity driven by TOR signaling is a well-established pro-aging mechanism in yeast; conversely, reduced translation via ribosome attenuation (e.g., deletion of ribosomal protein genes) extends chronological and replicative lifespan. Deletion of RPL10 or reduction in 60S ribosomal function has been associated with lifespan extension in yeast screens, consistent with the broader finding that partial impairment of ribosome function reduces protein synthesis rates and mimics dietary restriction. Thus, the normal (wild-type) function of RPL10—promoting full ribosomal capacity and translation—acts to shorten lifespan rather than extend it.",
"confidence": 0.65,
"key_pathways": [
"TOR signaling / ribosome biogenesis",
"60S ribosomal subunit assembly",
"translational regulation"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for RPL10. The mechanistic reasoning is sound and well-grounded: RPL10 encodes a 60S ribosomal protein, and the model correctly connects ribosomal protein function to TOR signaling, ribosome biogenesis, and the established finding that reduced translation/ribosome function extends lifespan in yeast. The mechanism class \"deregulated_nutrient_sensing\" is a reasonable fit, though \"protein synthesis/translation\" might be more precise. The reasoning about deletion of ribosomal protein genes extending lifespan is well-supported in the literature. Confidence of 0.65 is appropriately calibrated. Overall a strong, well-reasoned prediction.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}