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rps-15

C. elegans

Small ribosomal subunit protein uS19

What the model saw

Gene: rps-15
Organism: Caenorhabditis elegans
Known functions: Small ribosomal subunit protein uS19. RNA binding. structural constituent of ribosome.
View unredacted entry
Small ribosomal subunit protein uS19. RNA binding. structural constituent of ribosome.

Solver output

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

rps-15 encodes the small ribosomal subunit protein uS19, a core structural component of the 40S ribosomal subunit required for mRNA translation. In C. elegans, ribosomal protein genes are downstream effectors of the TOR (Target of Rapamycin) nutrient-sensing pathway, which couples nutrient availability to global protein synthesis rates. Elevated ribosomal activity and translation capacity driven by TOR signaling is associated with accelerated aging, while partial reduction of ribosomal protein function (e.g., via RNAi knockdown of rps genes) has been shown to extend lifespan in C. elegans by reducing overall translational output and mimicking dietary restriction. Thus, the normal pro-translational function of rps-15 promotes anabolic activity that opposes longevity, placing it in the deregulated nutrient-sensing hallmark through TOR-mediated translational control.

Key pathways
TOR signaling / translational control40S ribosome biogenesisdietary restriction mimicry via ribosomal attenuation
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-15. The mechanistic reasoning is sound: ribosomal protein genes in C. elegans are well-established anti-longevity factors, as their knockdown extends lifespan by reducing translational output, often linked to TOR signaling and dietary restriction mimicry. The model correctly identifies that the normal function of rps-15 (promoting translation) opposes longevity. The mechanism class "deregulated_nutrient_sensing" is a reasonable framing, though "proteostasis/translation" might be a more direct classification. The reasoning is well-articulated and biologically accurate. Confidence of 0.72 is appropriate given the general knowledge about ribosomal proteins in C. elegans aging.

Raw API responses

solver

{
  "reasoning": "rps-15 encodes the small ribosomal subunit protein uS19, a core structural component of the 40S ribosomal subunit required for mRNA translation. In C. elegans, ribosomal protein genes are downstream effectors of the TOR (Target of Rapamycin) nutrient-sensing pathway, which couples nutrient availability to global protein synthesis rates. Elevated ribosomal activity and translation capacity driven by TOR signaling is associated with accelerated aging, while partial reduction of ribosomal protein function (e.g., via RNAi knockdown of rps genes) has been shown to extend lifespan in C. elegans by reducing overall translational output and mimicking dietary restriction. Thus, the normal pro-translational function of rps-15 promotes anabolic activity that opposes longevity, placing it in the deregulated nutrient-sensing hallmark through TOR-mediated translational control.",
  "confidence": 0.72,
  "key_pathways": [
    "TOR signaling / translational control",
    "40S ribosome biogenesis",
    "dietary restriction mimicry via ribosomal attenuation"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for rps-15. The mechanistic reasoning is sound: ribosomal protein genes in C. elegans are well-established anti-longevity factors, as their knockdown extends lifespan by reducing translational output, often linked to TOR signaling and dietary restriction mimicry. The model correctly identifies that the normal function of rps-15 (promoting translation) opposes longevity. The mechanism class \"deregulated_nutrient_sensing\" is a reasonable framing, though \"proteostasis/translation\" might be a more direct classification. The reasoning is well-articulated and biologically accurate. Confidence of 0.72 is appropriate given the general knowledge about ribosomal proteins in C. elegans aging.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}