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rps-3

C. elegans

Small ribosomal subunit protein uS3

What the model saw

Gene: rps-3
Organism: Caenorhabditis elegans
Known functions: Small ribosomal subunit protein uS3. RNA binding. structural constituent of ribosome.
View unredacted entry
Small ribosomal subunit protein uS3. RNA binding. structural constituent of ribosome.

Solver output

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

RPS-3 (uS3) is a core structural component of the 40S small ribosomal subunit in C. elegans, directly contributing to translational capacity. Ribosomal protein levels set the overall rate of mRNA translation, which is tightly coupled to nutrient-sensing pathways such as TOR/mTORC1 signaling. In multiple model organisms including C. elegans, partial reduction of ribosomal protein function (e.g., via RNAi knockdown of rps or rpl genes) extends lifespan by reducing global translation rates, mimicking dietary restriction and dampening TOR activity. The normal (full) function of rps-3 therefore promotes high translational output, which is associated with accelerated aging and shortened lifespan. This places its pro-aging role squarely within the deregulated nutrient-sensing hallmark, specifically through TOR-driven ribosome biogenesis and translational upregulation.

Key pathways
mTOR/TOR signaling and translational controlribosome biogenesisdietary restriction mimicry via reduced translation
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 rps-3. The mechanistic reasoning is sound: ribosomal proteins like RPS-3 contribute to translational capacity, and their reduction extends lifespan in C. elegans by mimicking dietary restriction and reducing TOR-driven translation. The mechanism class "deregulated_nutrient_sensing" is a reasonable framing, though one could argue the more direct mechanism is reduced translation/protein synthesis rather than nutrient sensing per se. The reasoning is well-articulated and consistent with the known biology of ribosomal protein knockdowns in C. elegans. Confidence of 0.72 is appropriate given the general knowledge about ribosomal proteins in aging.

Raw API responses

solver

{
  "reasoning": "RPS-3 (uS3) is a core structural component of the 40S small ribosomal subunit in C. elegans, directly contributing to translational capacity. Ribosomal protein levels set the overall rate of mRNA translation, which is tightly coupled to nutrient-sensing pathways such as TOR/mTORC1 signaling. In multiple model organisms including C. elegans, partial reduction of ribosomal protein function (e.g., via RNAi knockdown of rps or rpl genes) extends lifespan by reducing global translation rates, mimicking dietary restriction and dampening TOR activity. The normal (full) function of rps-3 therefore promotes high translational output, which is associated with accelerated aging and shortened lifespan. This places its pro-aging role squarely within the deregulated nutrient-sensing hallmark, specifically through TOR-driven ribosome biogenesis and translational upregulation.",
  "confidence": 0.72,
  "key_pathways": [
    "mTOR/TOR signaling and translational control",
    "ribosome biogenesis",
    "dietary restriction mimicry via reduced translation"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for rps-3. The mechanistic reasoning is sound: ribosomal proteins like RPS-3 contribute to translational capacity, and their reduction extends lifespan in C. elegans by mimicking dietary restriction and reducing TOR-driven translation. The mechanism class \"deregulated_nutrient_sensing\" is a reasonable framing, though one could argue the more direct mechanism is reduced translation/protein synthesis rather than nutrient sensing per se. The reasoning is well-articulated and consistent with the known biology of ribosomal protein knockdowns in C. elegans. Confidence of 0.72 is appropriate given the general knowledge about ribosomal proteins in aging.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}