← Browse entries

rpl-7

C. elegans

Large ribosomal subunit protein uL30

What the model saw

Gene: rpl-7
Organism: Caenorhabditis elegans
Known functions: Large ribosomal subunit protein uL30. RNA binding. structural constituent of ribosome.
View unredacted entry
Large ribosomal subunit protein uL30. RNA binding. structural constituent of ribosome.

Solver output

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

RPL-7 encodes the large ribosomal subunit protein uL30, a core structural component of the 60S ribosomal subunit responsible for mRNA translation. In C. elegans, partial loss-of-function of large ribosomal subunit proteins (including rpl genes) has been repeatedly shown to extend lifespan by reducing global translation rates, which mimics dietary restriction and downregulates TOR/TORC1 signaling — a key nutrient-sensing pathway linked to longevity. Reduced ribosomal activity lowers the production of pro-aging proteins and alleviates proteostatic burden. The normal (wild-type) function of rpl-7 therefore promotes robust translation and high TOR activity, which is associated with accelerated aging; thus the gene's normal function is anti-longevity. However, since RNAi knockdown of ribosomal proteins extends life, the gene's normal full activity opposes longevity by sustaining high translational output and nutrient-sensing signaling.

Key pathways
mTOR/TORC1 nutrient sensingribosome biogenesis and global translationdietary 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
Incorrect
Mechanism
Correct
Reasoning quality
3/5
Failure mode
Right answer, wrong reasoning
Notes

The model's mechanistic reasoning is actually correct — it correctly identifies that rpl-7 encodes a large ribosomal subunit protein, that knockdown extends lifespan, and that the normal function of the gene sustains high translational output which is anti-longevity. However, the model contradicts itself in its final prediction: despite reasoning that the gene's "normal function is anti-longevity," it outputs "pro_longevity" as the longevity_influence. The reasoning clearly supports "anti_longevity" (which is the ground truth), but the final answer label is wrong. This is a self-contradictory prediction where the reasoning is correct but the final answer label is incorrect.

Raw API responses

solver

{
  "reasoning": "RPL-7 encodes the large ribosomal subunit protein uL30, a core structural component of the 60S ribosomal subunit responsible for mRNA translation. In C. elegans, partial loss-of-function of large ribosomal subunit proteins (including rpl genes) has been repeatedly shown to extend lifespan by reducing global translation rates, which mimics dietary restriction and downregulates TOR/TORC1 signaling — a key nutrient-sensing pathway linked to longevity. Reduced ribosomal activity lowers the production of pro-aging proteins and alleviates proteostatic burden. The normal (wild-type) function of rpl-7 therefore promotes robust translation and high TOR activity, which is associated with accelerated aging; thus the gene's normal function is anti-longevity. However, since RNAi knockdown of ribosomal proteins extends life, the gene's normal full activity opposes longevity by sustaining high translational output and nutrient-sensing signaling.",
  "confidence": 0.62,
  "key_pathways": [
    "mTOR/TORC1 nutrient sensing",
    "ribosome biogenesis and global translation",
    "dietary restriction mimicry via reduced protein synthesis"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model's mechanistic reasoning is actually correct — it correctly identifies that rpl-7 encodes a large ribosomal subunit protein, that knockdown extends lifespan, and that the normal function of the gene sustains high translational output which is anti-longevity. However, the model contradicts itself in its final prediction: despite reasoning that the gene's \"normal function is anti-longevity,\" it outputs \"pro_longevity\" as the longevity_influence. The reasoning clearly supports \"anti_longevity\" (which is the ground truth), but the final answer label is wrong. This is a self-contradictory prediction where the reasoning is correct but the final answer label is incorrect.",
  "failure_mode": "right_answer_wrong_reasoning",
  "answer_correct": false,
  "mechanism_correct": true,
  "reasoning_quality": 3,
  "ground_truth_questionable": false
}