RPP1B
S. cerevisiae
ribosomal protein P1 RPP1B
What the model saw
Gene: RPP1B Organism: Saccharomyces cerevisiae Known functions: ribosomal protein P1 RPP1B. protein binding. protein kinase activator activity. ribonucleoprotein complex binding. structural constituent of ribosome.
View unredacted entry
ribosomal protein P1 RPP1B. protein binding. protein kinase activator activity. ribonucleoprotein complex binding. structural constituent of ribosome.
Solver output
RPP1B encodes a ribosomal stalk protein (P1 family) that is a structural constituent of the large ribosomal subunit and acts as a protein kinase activator. The ribosomal P-stalk complex (comprising P0, P1, P2 proteins) directly activates translation elongation factor-dependent GTPase activity and stimulates overall translational output. Elevated ribosomal activity and enhanced translation are hallmarks of upregulated TOR/nutrient-sensing signaling, which is well-established as anti-longevity in yeast and other organisms. Reduced ribosomal protein gene dosage (including P-stalk components) is associated with lifespan extension in yeast, consistent with the idea that high translational capacity promotes aging. Additionally, the protein kinase activator activity of RPP1B may further amplify anabolic signaling. Thus, the normal pro-translational function of RPP1B is expected to oppose longevity by sustaining high ribosome activity downstream of nutrient-sensing pathways.
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 RPP1B. The mechanistic reasoning is sound and well-grounded: RPP1B is a ribosomal stalk protein that promotes translation, and reduced ribosomal protein gene dosage is indeed associated with lifespan extension in yeast. The connection to TOR/nutrient-sensing is reasonable, though it's somewhat indirect (the model correctly notes that high translational capacity promotes aging, which is consistent with the literature on ribosomal proteins and yeast longevity). The mechanism class "deregulated_nutrient_sensing" is a reasonable but slightly imprecise label - the more direct mechanism is through ribosome function and translational output rather than nutrient sensing per se, but the two are closely linked. Overall, solid reasoning with appropriate confidence (0.65).
Raw API responses
solver
{
"reasoning": "RPP1B encodes a ribosomal stalk protein (P1 family) that is a structural constituent of the large ribosomal subunit and acts as a protein kinase activator. The ribosomal P-stalk complex (comprising P0, P1, P2 proteins) directly activates translation elongation factor-dependent GTPase activity and stimulates overall translational output. Elevated ribosomal activity and enhanced translation are hallmarks of upregulated TOR/nutrient-sensing signaling, which is well-established as anti-longevity in yeast and other organisms. Reduced ribosomal protein gene dosage (including P-stalk components) is associated with lifespan extension in yeast, consistent with the idea that high translational capacity promotes aging. Additionally, the protein kinase activator activity of RPP1B may further amplify anabolic signaling. Thus, the normal pro-translational function of RPP1B is expected to oppose longevity by sustaining high ribosome activity downstream of nutrient-sensing pathways.",
"confidence": 0.65,
"key_pathways": [
"TOR signaling / ribosome biogenesis",
"translational elongation (P-stalk GTPase activation)",
"protein kinase activation (anabolic signaling)"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for RPP1B. The mechanistic reasoning is sound and well-grounded: RPP1B is a ribosomal stalk protein that promotes translation, and reduced ribosomal protein gene dosage is indeed associated with lifespan extension in yeast. The connection to TOR/nutrient-sensing is reasonable, though it's somewhat indirect (the model correctly notes that high translational capacity promotes aging, which is consistent with the literature on ribosomal proteins and yeast longevity). The mechanism class \"deregulated_nutrient_sensing\" is a reasonable but slightly imprecise label - the more direct mechanism is through ribosome function and translational output rather than nutrient sensing per se, but the two are closely linked. Overall, solid reasoning with appropriate confidence (0.65).",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}