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RPS10B

S. cerevisiae

40S ribosomal protein eS10 RPS10B

What the model saw

Gene: RPS10B
Organism: Saccharomyces cerevisiae
Known functions: 40S ribosomal protein eS10 RPS10B. RNA binding. protein binding. structural constituent of ribosome.
View unredacted entry
40S ribosomal protein eS10 RPS10B. RNA binding. protein binding. structural constituent of ribosome.

Solver output

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

RPS10B encodes a structural component of the 40S ribosomal small subunit (eS10), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — including deletion of 40S subunit components — is well-established to extend chronological and replicative lifespan, largely through attenuation of TORC1-driven protein synthesis. Excess ribosomal activity promotes anabolic signaling downstream of TOR/Sch9, which accelerates aging. The structural constituent role of RPS10B in the 40S ribosome means its normal function sustains high translational output, opposing longevity. Additionally, ribosome abundance is a key readout of nutrient-sensing pathway activity (TOR/S6K axis), placing this gene squarely in the deregulated nutrient sensing hallmark. Loss-of-function of paralogous ribosomal protein genes in yeast consistently yields lifespan extension, supporting an anti-longevity classification for the wild-type gene.

Key pathways
TORC1-S6K translational control40S ribosome biogenesisribosomal protein-mediated nutrient sensing
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
5/5
Failure mode
Correct
Notes

The model correctly predicted anti_longevity for RPS10B. The mechanistic reasoning is sound and well-articulated: RPS10B encodes a 40S ribosomal subunit protein, and deletion of ribosomal protein genes in yeast is well-established to extend lifespan via attenuation of TOR/S6K-driven translational output. The model correctly identifies the TOR/nutrient sensing axis as the key pathway, and appropriately generalizes from known ribosomal protein deletion studies. The confidence level of 0.72 is reasonable given the gene-specific uncertainty. Overall, this is a high-quality prediction with correct answer and correct mechanistic reasoning.

Raw API responses

solver

{
  "reasoning": "RPS10B encodes a structural component of the 40S ribosomal small subunit (eS10), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — including deletion of 40S subunit components — is well-established to extend chronological and replicative lifespan, largely through attenuation of TORC1-driven protein synthesis. Excess ribosomal activity promotes anabolic signaling downstream of TOR/Sch9, which accelerates aging. The structural constituent role of RPS10B in the 40S ribosome means its normal function sustains high translational output, opposing longevity. Additionally, ribosome abundance is a key readout of nutrient-sensing pathway activity (TOR/S6K axis), placing this gene squarely in the deregulated nutrient sensing hallmark. Loss-of-function of paralogous ribosomal protein genes in yeast consistently yields lifespan extension, supporting an anti-longevity classification for the wild-type gene.",
  "confidence": 0.72,
  "key_pathways": [
    "TORC1-S6K translational control",
    "40S ribosome biogenesis",
    "ribosomal protein-mediated nutrient sensing"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for RPS10B. The mechanistic reasoning is sound and well-articulated: RPS10B encodes a 40S ribosomal subunit protein, and deletion of ribosomal protein genes in yeast is well-established to extend lifespan via attenuation of TOR/S6K-driven translational output. The model correctly identifies the TOR/nutrient sensing axis as the key pathway, and appropriately generalizes from known ribosomal protein deletion studies. The confidence level of 0.72 is reasonable given the gene-specific uncertainty. Overall, this is a high-quality prediction with correct answer and correct mechanistic reasoning.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}