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RPL8B

S. cerevisiae

60S ribosomal protein eL8 RPL8B

What the model saw

Gene: RPL8B
Organism: Saccharomyces cerevisiae
Known functions: 60S ribosomal protein eL8 RPL8B. RNA binding. structural constituent of ribosome.
View unredacted entry
60S ribosomal protein eL8 RPL8B. RNA binding. structural constituent of ribosome.

Solver output

Predicted influence
Anti-longevity
Confidence
72%
Mechanism
Deregulated nutrient sensing
Reasoning

RPL8B encodes a structural component of the 60S ribosomal large subunit (eL8), directly contributing to ribosome biogenesis and translational capacity. In yeast, ribosomal protein genes are among the most strongly regulated targets of the TORC1/nutrient-sensing pathway; high ribosomal activity is associated with pro-growth signaling and shortened lifespan. Deletion of many large ribosomal subunit protein genes, including paralogs of RPL8B, has been shown to extend chronological and replicative lifespan in S. cerevisiae, consistent with the idea that reducing translational output mimics dietary restriction and downregulates TOR signaling. The normal function of RPL8B—maintaining full ribosomal assembly and robust protein synthesis—therefore opposes longevity by sustaining high anabolic flux downstream of TORC1. This places RPL8B in the deregulated nutrient-sensing hallmark, as ribosome biogenesis is a primary effector of TOR-driven growth signaling.

Key pathways
TORC1/nutrient-sensing signalingribosome biogenesis and translational regulationdietary restriction mimicry via ribosomal protein deletion
Longevity influence
Anti-longevity
Lifespan effect
Increase

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

Answer
Correct
Mechanism
Correct
Reasoning quality
4/5
Failure mode
Correct
Notes

The model correctly predicted anti_longevity for RPL8B. The mechanistic reasoning is sound: RPL8B is a 60S ribosomal protein, and deletion of ribosomal protein genes in yeast is well-established to extend lifespan, meaning the wild-type gene opposes longevity (anti_longevity). The connection to TORC1/nutrient-sensing is appropriate and well-supported in the literature. The mechanism class of "deregulated_nutrient_sensing" is reasonable, though one could argue it's more directly about translational capacity/ribosome biogenesis. The confidence of 0.72 is appropriate given the general pattern of ribosomal protein deletions extending lifespan in yeast. Overall a high-quality prediction with solid reasoning.

Raw API responses

solver

{
  "reasoning": "RPL8B encodes a structural component of the 60S ribosomal large subunit (eL8), directly contributing to ribosome biogenesis and translational capacity. In yeast, ribosomal protein genes are among the most strongly regulated targets of the TORC1/nutrient-sensing pathway; high ribosomal activity is associated with pro-growth signaling and shortened lifespan. Deletion of many large ribosomal subunit protein genes, including paralogs of RPL8B, has been shown to extend chronological and replicative lifespan in S. cerevisiae, consistent with the idea that reducing translational output mimics dietary restriction and downregulates TOR signaling. The normal function of RPL8B—maintaining full ribosomal assembly and robust protein synthesis—therefore opposes longevity by sustaining high anabolic flux downstream of TORC1. This places RPL8B in the deregulated nutrient-sensing hallmark, as ribosome biogenesis is a primary effector of TOR-driven growth signaling.",
  "confidence": 0.72,
  "key_pathways": [
    "TORC1/nutrient-sensing signaling",
    "ribosome biogenesis and translational regulation",
    "dietary restriction mimicry via ribosomal protein deletion"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for RPL8B. The mechanistic reasoning is sound: RPL8B is a 60S ribosomal protein, and deletion of ribosomal protein genes in yeast is well-established to extend lifespan, meaning the wild-type gene opposes longevity (anti_longevity). The connection to TORC1/nutrient-sensing is appropriate and well-supported in the literature. The mechanism class of \"deregulated_nutrient_sensing\" is reasonable, though one could argue it's more directly about translational capacity/ribosome biogenesis. The confidence of 0.72 is appropriate given the general pattern of ribosomal protein deletions extending lifespan in yeast. Overall a high-quality prediction with solid reasoning.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}