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rps-14

C. elegans

Small ribosomal subunit protein uS11

What the model saw

Gene: rps-14
Organism: Caenorhabditis elegans
Known functions: Small ribosomal subunit protein uS11. structural constituent of ribosome.
View unredacted entry
Small ribosomal subunit protein uS11. structural constituent of ribosome.

Solver output

Predicted influence
Pro-longevity
Confidence
62%
Mechanism
Deregulated nutrient sensing
Reasoning

rps-14 encodes the small ribosomal subunit protein uS11, a core structural component of the 40S ribosomal subunit required for mRNA translation. In C. elegans, partial loss-of-function of ribosomal small subunit proteins (including rps genes) has been repeatedly shown to extend lifespan, likely by reducing global translation rates and mimicking dietary restriction or dampening TOR/TORC1 signaling — a key nutrient-sensing pathway. Reduced ribosomal activity decreases the synthesis of pro-aging proteins while activating stress-response and proteostasis pathways. Thus, the normal (full) function of rps-14 — supporting maximal translational capacity — is associated with shorter lifespan, meaning its normal function is anti-longevity; however, since ribosome biogenesis and translation are downstream of TOR nutrient sensing, the best mechanistic classification is deregulated nutrient sensing. The gene's normal function sustains high TOR-driven translation, which opposes longevity.

Key pathways
TOR/TORC1 nutrient sensing and translational control40S ribosomal subunit assembly and global mRNA translationdietary restriction mimicry via ribosome 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
Incorrect
Mechanism
Correct
Reasoning quality
3/5
Failure mode
Right answer, wrong reasoning
Notes

The model's reasoning is actually correct - it correctly identifies that rps-14's normal function supports high translation and is therefore anti-longevity (loss of function extends lifespan). However, the model then contradicts itself by outputting "pro_longevity" as the final prediction, which is the opposite of the ground truth "anti_longevity". The reasoning correctly states "the normal (full) function of rps-14 — supporting maximal translational capacity — is associated with shorter lifespan, meaning its normal function is anti-longevity" but then the JSON output says "pro_longevity". This is a clear internal contradiction where the reasoning leads to the correct answer but the final prediction is wrong. The mechanistic reasoning about TOR/TORC1, ribosomal translation reduction extending lifespan, and dietary restriction mimicry is sound.

Raw API responses

solver

{
  "reasoning": "rps-14 encodes the small ribosomal subunit protein uS11, a core structural component of the 40S ribosomal subunit required for mRNA translation. In C. elegans, partial loss-of-function of ribosomal small subunit proteins (including rps genes) has been repeatedly shown to extend lifespan, likely by reducing global translation rates and mimicking dietary restriction or dampening TOR/TORC1 signaling — a key nutrient-sensing pathway. Reduced ribosomal activity decreases the synthesis of pro-aging proteins while activating stress-response and proteostasis pathways. Thus, the normal (full) function of rps-14 — supporting maximal translational capacity — is associated with shorter lifespan, meaning its normal function is anti-longevity; however, since ribosome biogenesis and translation are downstream of TOR nutrient sensing, the best mechanistic classification is deregulated nutrient sensing. The gene's normal function sustains high TOR-driven translation, which opposes longevity.",
  "confidence": 0.62,
  "key_pathways": [
    "TOR/TORC1 nutrient sensing and translational control",
    "40S ribosomal subunit assembly and global mRNA translation",
    "dietary restriction mimicry via ribosome attenuation"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model's reasoning is actually correct - it correctly identifies that rps-14's normal function supports high translation and is therefore anti-longevity (loss of function extends lifespan). However, the model then contradicts itself by outputting \"pro_longevity\" as the final prediction, which is the opposite of the ground truth \"anti_longevity\". The reasoning correctly states \"the normal (full) function of rps-14 — supporting maximal translational capacity — is associated with shorter lifespan, meaning its normal function is anti-longevity\" but then the JSON output says \"pro_longevity\". This is a clear internal contradiction where the reasoning leads to the correct answer but the final prediction is wrong. The mechanistic reasoning about TOR/TORC1, ribosomal translation reduction extending lifespan, and dietary restriction mimicry is sound.",
  "failure_mode": "right_answer_wrong_reasoning",
  "answer_correct": false,
  "mechanism_correct": true,
  "reasoning_quality": 3,
  "ground_truth_questionable": false
}