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RPL13A

S. cerevisiae

60S ribosomal protein eL13 RPL13A

What the model saw

Gene: RPL13A
Organism: Saccharomyces cerevisiae
Known functions: 60S ribosomal protein eL13 RPL13A. RNA binding. structural constituent of ribosome.
View unredacted entry
60S ribosomal protein eL13 RPL13A. RNA binding. structural constituent of ribosome.

Solver output

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

RPL13A encodes a structural component of the 60S ribosomal large subunit (eL13), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of 60S subunit components — is well-established to extend chronological and replicative lifespan, largely through attenuation of TORC1-driven protein synthesis. Decreased ribosome abundance mimics dietary restriction by dampening anabolic signaling downstream of TOR, reducing global translation rates and associated proteotoxic stress. RPL13A's normal function thus promotes ribosome assembly and high translational output, which is associated with accelerated aging in yeast. Deletion or reduction of RPL13A would be expected to extend lifespan, meaning its normal presence is anti-longevity.

Key pathways
TORC1-ribosome biogenesis axis60S ribosomal 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
4/5
Failure mode
Correct
Notes

The model correctly predicted anti_longevity for RPL13A in S. cerevisiae. The mechanistic reasoning is sound: ribosomal protein genes, particularly 60S subunit components, are well-established anti-longevity factors in yeast, where their deletion extends lifespan through reduced translational output and TOR pathway attenuation. The model correctly frames RPL13A's normal function as promoting ribosome assembly and high translation, making it anti-longevity. The mechanism class "deregulated_nutrient_sensing" is a reasonable but slightly imprecise label — the more direct mechanism is ribosome biogenesis/translation rate reduction rather than nutrient sensing per se, though these are closely linked. Overall, the reasoning is well-grounded and the confidence level (0.72) is appropriate.

Raw API responses

solver

{
  "reasoning": "RPL13A encodes a structural component of the 60S ribosomal large subunit (eL13), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of 60S subunit components — is well-established to extend chronological and replicative lifespan, largely through attenuation of TORC1-driven protein synthesis. Decreased ribosome abundance mimics dietary restriction by dampening anabolic signaling downstream of TOR, reducing global translation rates and associated proteotoxic stress. RPL13A's normal function thus promotes ribosome assembly and high translational output, which is associated with accelerated aging in yeast. Deletion or reduction of RPL13A would be expected to extend lifespan, meaning its normal presence is anti-longevity.",
  "confidence": 0.72,
  "key_pathways": [
    "TORC1-ribosome biogenesis axis",
    "60S ribosomal subunit assembly",
    "translational regulation"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for RPL13A in S. cerevisiae. The mechanistic reasoning is sound: ribosomal protein genes, particularly 60S subunit components, are well-established anti-longevity factors in yeast, where their deletion extends lifespan through reduced translational output and TOR pathway attenuation. The model correctly frames RPL13A's normal function as promoting ribosome assembly and high translation, making it anti-longevity. The mechanism class \"deregulated_nutrient_sensing\" is a reasonable but slightly imprecise label — the more direct mechanism is ribosome biogenesis/translation rate reduction rather than nutrient sensing per se, though these are closely linked. Overall, the reasoning is well-grounded and the confidence level (0.72) is appropriate.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}
RPL13A · Saccharomyces cerevisiae | Aging biology eval