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RPS18B

S. cerevisiae

40S ribosomal protein uS13 RPS18B

What the model saw

Gene: RPS18B
Organism: Saccharomyces cerevisiae
Known functions: 40S ribosomal protein uS13 RPS18B. RNA binding. nucleic acid binding. structural constituent of ribosome.
View unredacted entry
40S ribosomal protein uS13 RPS18B. RNA binding. nucleic acid binding. structural constituent of ribosome.

Solver output

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

RPS18B encodes a structural component of the 40S ribosomal small subunit (uS13), directly contributing to ribosome biogenesis and translational capacity. In yeast, ribosomal protein genes are major downstream effectors of the TOR (Target of Rapamycin) nutrient-sensing pathway; high ribosome abundance and elevated translation rates are associated with shortened lifespan. Partial loss-of-function of ribosomal protein genes, including 40S subunit components, is well-documented to extend chronological and replicative lifespan in S. cerevisiae by mimicking reduced TOR signaling. The normal function of RPS18B — promoting ribosome assembly and global protein synthesis — therefore opposes longevity by sustaining anabolic signaling that accelerates aging. This places it squarely within the deregulated nutrient-sensing hallmark, specifically the TOR-ribosome biogenesis axis.

Key pathways
TOR signaling / ribosome biogenesis40S ribosomal small subunit assemblytranslational regulation
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 RPS18B. The mechanistic reasoning is sound and well-articulated: RPS18B encodes a 40S ribosomal protein, and deletion/reduction of ribosomal protein genes in yeast is well-established to extend lifespan by mimicking reduced TOR signaling. The model correctly identifies the TOR-ribosome biogenesis axis as the key pathway, and appropriately classifies the mechanism as deregulated nutrient sensing. Confidence of 0.72 is reasonable given the gene-specific uncertainty. Overall, this is an excellent prediction with correct answer and correct mechanistic reasoning.

Raw API responses

solver

{
  "reasoning": "RPS18B encodes a structural component of the 40S ribosomal small subunit (uS13), directly contributing to ribosome biogenesis and translational capacity. In yeast, ribosomal protein genes are major downstream effectors of the TOR (Target of Rapamycin) nutrient-sensing pathway; high ribosome abundance and elevated translation rates are associated with shortened lifespan. Partial loss-of-function of ribosomal protein genes, including 40S subunit components, is well-documented to extend chronological and replicative lifespan in S. cerevisiae by mimicking reduced TOR signaling. The normal function of RPS18B — promoting ribosome assembly and global protein synthesis — therefore opposes longevity by sustaining anabolic signaling that accelerates aging. This places it squarely within the deregulated nutrient-sensing hallmark, specifically the TOR-ribosome biogenesis axis.",
  "confidence": 0.72,
  "key_pathways": [
    "TOR signaling / ribosome biogenesis",
    "40S ribosomal small subunit assembly",
    "translational regulation"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for RPS18B. The mechanistic reasoning is sound and well-articulated: RPS18B encodes a 40S ribosomal protein, and deletion/reduction of ribosomal protein genes in yeast is well-established to extend lifespan by mimicking reduced TOR signaling. The model correctly identifies the TOR-ribosome biogenesis axis as the key pathway, and appropriately classifies the mechanism as deregulated nutrient sensing. Confidence of 0.72 is reasonable given the gene-specific uncertainty. Overall, this is an excellent prediction with correct answer and correct mechanistic reasoning.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}