rps-23
C. elegans
Small ribosomal subunit protein uS12
What the model saw
Gene: rps-23 Organism: Caenorhabditis elegans Known functions: Small ribosomal subunit protein uS12. structural constituent of ribosome.
View unredacted entry
Small ribosomal subunit protein uS12. structural constituent of ribosome.
Solver output
RPS-23 encodes the small ribosomal subunit protein uS12, a core structural component of the 40S ribosome. In C. elegans, partial loss-of-function of ribosomal small subunit proteins — including rps-23 — has been shown to extend lifespan, likely by reducing global translation rates and mimicking dietary restriction or dampening TOR/TORC1 signaling, which is a central nutrient-sensing pathway that regulates longevity. Reduced ribosomal activity decreases protein synthesis flux, alleviating proteotoxic stress and activating downstream longevity effectors such as DAF-16/FOXO. However, the normal (wild-type) function of rps-23 is to sustain full translational capacity, which supports growth and reproduction at the cost of longevity — placing its normal activity in opposition to lifespan extension. Thus, the gene's normal function is anti-longevity, as high ribosomal output promotes anabolic signaling that shortens lifespan in this organism.
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
The model predicted "pro_longevity" but the ground truth is "anti_longevity." Interestingly, the model's own reasoning actually arrives at the correct mechanistic conclusion — it explicitly states "the gene's normal function is anti-longevity, as high ribosomal output promotes anabolic signaling that shortens lifespan" — but then contradicts itself by outputting "pro_longevity" as the final answer. This is a self-contradictory response where the reasoning correctly identifies the anti-longevity nature of rps-23's normal function, but the final classification label is wrong. The mechanism discussion about TOR/TORC1 and translation reduction extending lifespan is generally correct for ribosomal proteins in C. elegans, but the model failed to translate this into the correct final answer. The confidence of 0.62 is also misplaced given the internal contradiction in the reasoning.
Raw API responses
solver
{
"reasoning": "RPS-23 encodes the small ribosomal subunit protein uS12, a core structural component of the 40S ribosome. In C. elegans, partial loss-of-function of ribosomal small subunit proteins — including rps-23 — has been shown to extend lifespan, likely by reducing global translation rates and mimicking dietary restriction or dampening TOR/TORC1 signaling, which is a central nutrient-sensing pathway that regulates longevity. Reduced ribosomal activity decreases protein synthesis flux, alleviating proteotoxic stress and activating downstream longevity effectors such as DAF-16/FOXO. However, the normal (wild-type) function of rps-23 is to sustain full translational capacity, which supports growth and reproduction at the cost of longevity — placing its normal activity in opposition to lifespan extension. Thus, the gene's normal function is anti-longevity, as high ribosomal output promotes anabolic signaling that shortens lifespan in this organism.",
"confidence": 0.62,
"key_pathways": [
"TOR/TORC1 nutrient sensing",
"ribosome biogenesis and global translation",
"DAF-16/FOXO longevity signaling"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted \"pro_longevity\" but the ground truth is \"anti_longevity.\" Interestingly, the model's own reasoning actually arrives at the correct mechanistic conclusion — it explicitly states \"the gene's normal function is anti-longevity, as high ribosomal output promotes anabolic signaling that shortens lifespan\" — but then contradicts itself by outputting \"pro_longevity\" as the final answer. This is a self-contradictory response where the reasoning correctly identifies the anti-longevity nature of rps-23's normal function, but the final classification label is wrong. The mechanism discussion about TOR/TORC1 and translation reduction extending lifespan is generally correct for ribosomal proteins in C. elegans, but the model failed to translate this into the correct final answer. The confidence of 0.62 is also misplaced given the internal contradiction in the reasoning.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}