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rplp-0

C. elegans

Large ribosomal subunit protein uL10

What the model saw

Gene: rplp-0
Organism: Caenorhabditis elegans
Known functions: Large ribosomal subunit protein uL10. large ribosomal subunit rRNA binding. structural constituent of ribosome.
View unredacted entry
Large ribosomal subunit protein uL10. large ribosomal subunit rRNA binding. structural constituent of ribosome.

Solver output

Predicted influence
Anti-longevity
Confidence
75%
Mechanism
Loss of proteostasis
Reasoning

rplp-0 encodes the large ribosomal subunit protein uL10, a structural component of the 60S ribosomal subunit that binds rRNA and is essential for ribosome assembly and translational activity. In C. elegans, reduced ribosomal function — particularly through knockdown of large subunit components — is well established to extend lifespan, as demonstrated by RNAi screens targeting ribosomal proteins. Downregulation of ribosome biogenesis and translation rate is thought to promote longevity by reducing the burden of misfolded proteins, activating stress-response pathways, and mimicking dietary restriction effects on the TOR/mTOR nutrient-sensing axis. The normal (full) function of rplp-0 thus sustains high translational output, which opposes longevity. This places its mechanism within proteostasis, as elevated ribosomal activity increases the load on protein quality-control systems and accelerates aging-associated proteotoxic stress.

Key pathways
ribosome biogenesis and translationmTOR/TOR nutrient-sensing pathwayproteostasis and protein quality control
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
5/5
Failure mode
Correct
Notes

The model correctly predicted anti_longevity for rplp-0 in C. elegans. The mechanistic reasoning is sound and well-articulated: rplp-0 encodes a large ribosomal subunit protein, and knockdown of ribosomal proteins in C. elegans is well-established to extend lifespan. The model correctly identifies that the normal function of rplp-0 (promoting translation) opposes longevity, making it anti-longevity. The pathways cited (ribosome biogenesis, mTOR/TOR, proteostasis) are all relevant and accurate. The confidence level of 0.75 is appropriate given the well-established literature on ribosomal protein knockdown and longevity in C. elegans.

Raw API responses

solver

{
  "reasoning": "rplp-0 encodes the large ribosomal subunit protein uL10, a structural component of the 60S ribosomal subunit that binds rRNA and is essential for ribosome assembly and translational activity. In C. elegans, reduced ribosomal function — particularly through knockdown of large subunit components — is well established to extend lifespan, as demonstrated by RNAi screens targeting ribosomal proteins. Downregulation of ribosome biogenesis and translation rate is thought to promote longevity by reducing the burden of misfolded proteins, activating stress-response pathways, and mimicking dietary restriction effects on the TOR/mTOR nutrient-sensing axis. The normal (full) function of rplp-0 thus sustains high translational output, which opposes longevity. This places its mechanism within proteostasis, as elevated ribosomal activity increases the load on protein quality-control systems and accelerates aging-associated proteotoxic stress.",
  "confidence": 0.75,
  "key_pathways": [
    "ribosome biogenesis and translation",
    "mTOR/TOR nutrient-sensing pathway",
    "proteostasis and protein quality control"
  ],
  "mechanism_class": "loss_of_proteostasis",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for rplp-0 in C. elegans. The mechanistic reasoning is sound and well-articulated: rplp-0 encodes a large ribosomal subunit protein, and knockdown of ribosomal proteins in C. elegans is well-established to extend lifespan. The model correctly identifies that the normal function of rplp-0 (promoting translation) opposes longevity, making it anti-longevity. The pathways cited (ribosome biogenesis, mTOR/TOR, proteostasis) are all relevant and accurate. The confidence level of 0.75 is appropriate given the well-established literature on ribosomal protein knockdown and longevity in C. elegans.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}