rps-20
C. elegans
Small ribosomal subunit protein uS10
What the model saw
Gene: rps-20 Organism: Caenorhabditis elegans Known functions: Small ribosomal subunit protein uS10. structural constituent of ribosome.
View unredacted entry
Small ribosomal subunit protein uS10. structural constituent of ribosome.
Solver output
rps-20 encodes the small ribosomal subunit protein uS10 (RPS20), a structural component of the 40S ribosomal subunit required for mRNA translation. In C. elegans, partial loss-of-function of ribosomal proteins, including small subunit components, has been repeatedly shown to extend lifespan by reducing global translation rates, which mimics dietary restriction and downregulates TOR/TORC1 signaling. Reduced ribosomal activity lowers anabolic output and activates stress-response pathways, including DAF-16/FOXO and HSF-1. Thus, the normal (full) function of rps-20 — sustaining high translational capacity — is associated with shorter lifespan, meaning its reduction is pro-longevity; however, the gene's normal function per se supports the nutrient-sensing/TOR axis that promotes growth at the expense of longevity. Ribosome biogenesis and translational output are canonically linked to deregulated nutrient sensing as a hallmark of aging.
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." The model's reasoning is internally confused: it correctly notes that reduction of ribosomal proteins extends lifespan, but then incorrectly labels rps-20 as "pro_longevity." In GenAge's framework, a gene is "anti_longevity" when its normal function promotes aging/shortens lifespan — meaning its reduction extends lifespan. The model's own mechanistic reasoning actually supports the anti_longevity classification (the gene's normal function sustains high translation and promotes aging), yet it arrives at the wrong label. The model conflated "reduction of the gene is pro-longevity" with "the gene itself is pro_longevity," which is the opposite of the correct interpretation. The mechanism described (reduced translation via TOR/ribosome pathway) is partially correct in biology, but the final classification is wrong and the reasoning is self-contradictory.
Raw API responses
solver
{
"reasoning": "rps-20 encodes the small ribosomal subunit protein uS10 (RPS20), a structural component of the 40S ribosomal subunit required for mRNA translation. In C. elegans, partial loss-of-function of ribosomal proteins, including small subunit components, has been repeatedly shown to extend lifespan by reducing global translation rates, which mimics dietary restriction and downregulates TOR/TORC1 signaling. Reduced ribosomal activity lowers anabolic output and activates stress-response pathways, including DAF-16/FOXO and HSF-1. Thus, the normal (full) function of rps-20 — sustaining high translational capacity — is associated with shorter lifespan, meaning its reduction is pro-longevity; however, the gene's normal function per se supports the nutrient-sensing/TOR axis that promotes growth at the expense of longevity. Ribosome biogenesis and translational output are canonically linked to deregulated nutrient sensing as a hallmark of aging.",
"confidence": 0.65,
"key_pathways": [
"TOR/TORC1 nutrient sensing",
"ribosomal translation rate regulation",
"DAF-16/FOXO stress response"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted \"pro_longevity\" but the ground truth is \"anti_longevity.\" The model's reasoning is internally confused: it correctly notes that reduction of ribosomal proteins extends lifespan, but then incorrectly labels rps-20 as \"pro_longevity.\" In GenAge's framework, a gene is \"anti_longevity\" when its normal function promotes aging/shortens lifespan — meaning its reduction extends lifespan. The model's own mechanistic reasoning actually supports the anti_longevity classification (the gene's normal function sustains high translation and promotes aging), yet it arrives at the wrong label. The model conflated \"reduction of the gene is pro-longevity\" with \"the gene itself is pro_longevity,\" which is the opposite of the correct interpretation. The mechanism described (reduced translation via TOR/ribosome pathway) is partially correct in biology, but the final classification is wrong and the reasoning is self-contradictory.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}