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rps-5

C. elegans

Small ribosomal subunit protein uS7

What the model saw

Gene: rps-5
Organism: Caenorhabditis elegans
Known functions: Small ribosomal subunit protein uS7. RNA binding. mRNA binding. rRNA binding. structural constituent of ribosome.
View unredacted entry
Small ribosomal subunit protein uS7. RNA binding. mRNA binding. rRNA binding. structural constituent of ribosome.

Solver output

Predicted influence
Pro-longevity
Confidence
55%
Mechanism
Deregulated nutrient sensing
Reasoning

rps-5 encodes the small ribosomal subunit protein uS7, a core structural component of the 40S ribosome involved in mRNA and rRNA binding. In C. elegans, partial reduction of ribosomal protein function (including small subunit components) is well-documented to extend lifespan, likely by attenuating global translation rates and mimicking dietary restriction or reduced TOR/nutrient-sensing signaling. However, rps-5 itself is a constitutive structural component required for ribosome assembly and translation initiation; its normal (full) function sustains high translational output, which is associated with shortened lifespan via hyperactive TOR-like signaling. Thus, the gene's normal activity promotes translation and opposes longevity, while its reduction is pro-longevity. Classifying the normal function as anti-longevity aligns with the broader ribosomal biogenesis/TOR axis in aging. The mechanism maps most closely to deregulated nutrient sensing, as ribosome activity is a key downstream effector of TOR signaling.

Key pathways
TOR/nutrient-sensing signalingribosome biogenesis and translational regulationdietary restriction mimicry via reduced translation
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
Confident wrong
Notes

The model's mechanistic reasoning is actually correct and well-articulated: ribosomal proteins like rps-5 promote translation, and their reduction extends lifespan via TOR/nutrient-sensing pathways. This correctly identifies rps-5 as anti-longevity in its normal function. However, the model then contradicts its own reasoning by predicting "pro_longevity" instead of "anti_longevity." The model essentially reasoned its way to the correct answer but then selected the wrong classification label. The reasoning explicitly states "the gene's normal activity promotes translation and opposes longevity" and "Classifying the normal function as anti-longevity aligns with the broader ribosomal biogenesis/TOR axis" — yet the final prediction is "pro_longevity." This is a clear internal contradiction where the model's stated conclusion doesn't match its final answer. Confidence was only 0.55, showing appropriate uncertainty, but the final label is still wrong.

Raw API responses

solver

{
  "reasoning": "rps-5 encodes the small ribosomal subunit protein uS7, a core structural component of the 40S ribosome involved in mRNA and rRNA binding. In C. elegans, partial reduction of ribosomal protein function (including small subunit components) is well-documented to extend lifespan, likely by attenuating global translation rates and mimicking dietary restriction or reduced TOR/nutrient-sensing signaling. However, rps-5 itself is a constitutive structural component required for ribosome assembly and translation initiation; its normal (full) function sustains high translational output, which is associated with shortened lifespan via hyperactive TOR-like signaling. Thus, the gene's normal activity promotes translation and opposes longevity, while its reduction is pro-longevity. Classifying the normal function as anti-longevity aligns with the broader ribosomal biogenesis/TOR axis in aging. The mechanism maps most closely to deregulated nutrient sensing, as ribosome activity is a key downstream effector of TOR signaling.",
  "confidence": 0.55,
  "key_pathways": [
    "TOR/nutrient-sensing signaling",
    "ribosome biogenesis and translational regulation",
    "dietary restriction mimicry via reduced translation"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model's mechanistic reasoning is actually correct and well-articulated: ribosomal proteins like rps-5 promote translation, and their reduction extends lifespan via TOR/nutrient-sensing pathways. This correctly identifies rps-5 as anti-longevity in its normal function. However, the model then contradicts its own reasoning by predicting \"pro_longevity\" instead of \"anti_longevity.\" The model essentially reasoned its way to the correct answer but then selected the wrong classification label. The reasoning explicitly states \"the gene's normal activity promotes translation and opposes longevity\" and \"Classifying the normal function as anti-longevity aligns with the broader ribosomal biogenesis/TOR axis\" — yet the final prediction is \"pro_longevity.\" This is a clear internal contradiction where the model's stated conclusion doesn't match its final answer. Confidence was only 0.55, showing appropriate uncertainty, but the final label is still wrong.",
  "failure_mode": "confident_wrong",
  "answer_correct": false,
  "mechanism_correct": true,
  "reasoning_quality": 3,
  "ground_truth_questionable": false
}
rps-5 · Caenorhabditis elegans | Aging biology eval