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rpl-10a

C. elegans

Large ribosomal subunit protein uL1

What the model saw

Gene: rpl-10a
Organism: Caenorhabditis elegans
Known functions: Large ribosomal subunit protein uL1. RNA binding. structural constituent of ribosome.
View unredacted entry
Large ribosomal subunit protein uL1. RNA binding. structural constituent of ribosome.

Solver output

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

rpl-10a encodes the large ribosomal subunit protein uL1, a core structural component of the 60S ribosomal subunit required for mRNA translation. Ribosomal protein genes in C. elegans are well-established modulators of longevity: partial loss-of-function of large subunit ribosomal proteins (e.g., rpl-4, rpl-11, rpl-25) consistently extends lifespan by reducing global translational capacity, which mimics dietary restriction and downregulates TOR/TORC1 signaling. The normal function of rpl-10a is to sustain high translational output, which promotes anabolic growth but accelerates aging. Reduced ribosome activity also activates stress-response pathways and proteostasis networks that are pro-longevity. Therefore, the wild-type (full) activity of rpl-10a opposes longevity by maintaining elevated protein synthesis rates downstream of nutrient-sensing/TOR signaling.

Key pathways
TOR/TORC1 nutrient sensingribosome biogenesis and translational regulationdietary restriction mimicry via reduced protein synthesis
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 rpl-10a. The mechanistic reasoning is sound: ribosomal protein genes in C. elegans are well-known anti-longevity factors because their knockdown reduces translational output, mimicking dietary restriction and extending lifespan. The model correctly identifies that wild-type rpl-10a activity promotes aging by sustaining high protein synthesis. The mechanism class "deregulated_nutrient_sensing" is a reasonable (if slightly imprecise) categorization — the more direct mechanism is translational regulation/ribosome function, but TOR/nutrient sensing is closely linked. The reasoning is well-supported by the literature on ribosomal protein RNAi in C. elegans. Confidence of 0.72 is appropriate given the general pattern of ribosomal proteins in this organism.

Raw API responses

solver

{
  "reasoning": "rpl-10a encodes the large ribosomal subunit protein uL1, a core structural component of the 60S ribosomal subunit required for mRNA translation. Ribosomal protein genes in C. elegans are well-established modulators of longevity: partial loss-of-function of large subunit ribosomal proteins (e.g., rpl-4, rpl-11, rpl-25) consistently extends lifespan by reducing global translational capacity, which mimics dietary restriction and downregulates TOR/TORC1 signaling. The normal function of rpl-10a is to sustain high translational output, which promotes anabolic growth but accelerates aging. Reduced ribosome activity also activates stress-response pathways and proteostasis networks that are pro-longevity. Therefore, the wild-type (full) activity of rpl-10a opposes longevity by maintaining elevated protein synthesis rates downstream of nutrient-sensing/TOR signaling.",
  "confidence": 0.72,
  "key_pathways": [
    "TOR/TORC1 nutrient sensing",
    "ribosome biogenesis and translational regulation",
    "dietary restriction mimicry via reduced protein synthesis"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for rpl-10a. The mechanistic reasoning is sound: ribosomal protein genes in C. elegans are well-known anti-longevity factors because their knockdown reduces translational output, mimicking dietary restriction and extending lifespan. The model correctly identifies that wild-type rpl-10a activity promotes aging by sustaining high protein synthesis. The mechanism class \"deregulated_nutrient_sensing\" is a reasonable (if slightly imprecise) categorization — the more direct mechanism is translational regulation/ribosome function, but TOR/nutrient sensing is closely linked. The reasoning is well-supported by the literature on ribosomal protein RNAi in C. elegans. Confidence of 0.72 is appropriate given the general pattern of ribosomal proteins in this organism.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}