rps-12
C. elegans
Small ribosomal subunit protein eS12
What the model saw
Gene: rps-12 Organism: Caenorhabditis elegans Known functions: Small ribosomal subunit protein eS12. structural constituent of ribosome.
View unredacted entry
Small ribosomal subunit protein eS12. structural constituent of ribosome.
Solver output
rps-12 encodes the small (40S) ribosomal subunit protein eS12, a structural component required for ribosome assembly and global mRNA translation. In C. elegans, reduced ribosomal activity — through RNAi knockdown of small subunit proteins including rps genes — consistently extends lifespan, acting downstream of or in parallel to the TOR/TORC1 nutrient-sensing pathway, which promotes ribosome biogenesis and protein synthesis. Full ribosomal function drives high translational output, which is associated with accelerated aging; conversely, partial ribosome insufficiency triggers a conserved longevity response linked to reduced TOR signaling and activation of stress-response programs. Therefore, the normal (full) function of rps-12 promotes translation and opposes longevity.
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 correctly predicted anti_longevity for rps-12. The mechanistic reasoning is sound: ribosomal protein knockdown in C. elegans extends lifespan, meaning full rps-12 function promotes translation and opposes longevity. The TOR/TORC1 connection is reasonable and well-established in the literature. The mechanism class "deregulated_nutrient_sensing" is a slight oversimplification — the primary mechanism is reduced translation/ribosome function rather than nutrient sensing per se — but it's not wrong given TOR's role in ribosome biogenesis. Overall, solid reasoning with appropriate confidence.
Raw API responses
solver
{
"reasoning": "rps-12 encodes the small (40S) ribosomal subunit protein eS12, a structural component required for ribosome assembly and global mRNA translation. In C. elegans, reduced ribosomal activity — through RNAi knockdown of small subunit proteins including rps genes — consistently extends lifespan, acting downstream of or in parallel to the TOR/TORC1 nutrient-sensing pathway, which promotes ribosome biogenesis and protein synthesis. Full ribosomal function drives high translational output, which is associated with accelerated aging; conversely, partial ribosome insufficiency triggers a conserved longevity response linked to reduced TOR signaling and activation of stress-response programs. Therefore, the normal (full) function of rps-12 promotes translation and opposes longevity.",
"confidence": 0.72,
"key_pathways": [
"TOR/TORC1 nutrient-sensing and ribosome biogenesis",
"mRNA translation via 40S ribosomal small subunit",
"ribosomal protein-mediated longevity regulation"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for rps-12. The mechanistic reasoning is sound: ribosomal protein knockdown in C. elegans extends lifespan, meaning full rps-12 function promotes translation and opposes longevity. The TOR/TORC1 connection is reasonable and well-established in the literature. The mechanism class \"deregulated_nutrient_sensing\" is a slight oversimplification — the primary mechanism is reduced translation/ribosome function rather than nutrient sensing per se — but it's not wrong given TOR's role in ribosome biogenesis. Overall, solid reasoning with appropriate confidence.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}