rpl-9
C. elegans
Large ribosomal subunit protein uL6
What the model saw
Gene: rpl-9 Organism: Caenorhabditis elegans Known functions: Large ribosomal subunit protein uL6. rRNA binding. structural constituent of ribosome.
View unredacted entry
Large ribosomal subunit protein uL6. rRNA binding. structural constituent of ribosome.
Solver output
RPL-9 encodes the large ribosomal subunit protein uL6, a structural component of the 60S ribosome that binds rRNA. Ribosomal protein levels are tightly coupled to TOR (Target of Rapamycin) signaling, the master regulator of nutrient-sensing and anabolic growth. In C. elegans, partial reduction of ribosomal protein function — including large subunit components — is well-established to extend lifespan, likely by attenuating global translation rates and mimicking dietary restriction or TOR inhibition. Reduced translational capacity via ribosomal protein knockdown activates downstream longevity pathways including DAF-16/FOXO and stress-response programs. Therefore, the normal (full) function of rpl-9 promotes high translational output downstream of TOR, opposing longevity; its loss-of-function is pro-longevity, making the wild-type gene anti-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 rpl-9. The mechanistic reasoning is sound: ribosomal protein knockdown in C. elegans is well-known to extend lifespan by reducing translational output, mimicking TOR inhibition/dietary restriction, and activating DAF-16/FOXO. The model correctly frames the wild-type gene as anti-longevity because its loss-of-function is pro-longevity. The mechanism class "deregulated_nutrient_sensing" is a reasonable fit given the TOR connection, though "translational regulation" might be more precise. Overall, the reasoning is thorough, accurate, and well-supported.
Raw API responses
solver
{
"reasoning": "RPL-9 encodes the large ribosomal subunit protein uL6, a structural component of the 60S ribosome that binds rRNA. Ribosomal protein levels are tightly coupled to TOR (Target of Rapamycin) signaling, the master regulator of nutrient-sensing and anabolic growth. In C. elegans, partial reduction of ribosomal protein function — including large subunit components — is well-established to extend lifespan, likely by attenuating global translation rates and mimicking dietary restriction or TOR inhibition. Reduced translational capacity via ribosomal protein knockdown activates downstream longevity pathways including DAF-16/FOXO and stress-response programs. Therefore, the normal (full) function of rpl-9 promotes high translational output downstream of TOR, opposing longevity; its loss-of-function is pro-longevity, making the wild-type gene anti-longevity.",
"confidence": 0.72,
"key_pathways": [
"TOR/mTOR nutrient-sensing and translational control",
"60S ribosome biogenesis and global protein synthesis",
"DAF-16/FOXO longevity pathway (activated upon ribosomal attenuation)"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for rpl-9. The mechanistic reasoning is sound: ribosomal protein knockdown in C. elegans is well-known to extend lifespan by reducing translational output, mimicking TOR inhibition/dietary restriction, and activating DAF-16/FOXO. The model correctly frames the wild-type gene as anti-longevity because its loss-of-function is pro-longevity. The mechanism class \"deregulated_nutrient_sensing\" is a reasonable fit given the TOR connection, though \"translational regulation\" might be more precise. Overall, the reasoning is thorough, accurate, and well-supported.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}