rps-6
C. elegans
Small ribosomal subunit protein eS6
What the model saw
Gene: rps-6 Organism: Caenorhabditis elegans Known functions: Small ribosomal subunit protein eS6. structural constituent of ribosome.
View unredacted entry
Small ribosomal subunit protein eS6. structural constituent of ribosome.
Solver output
RPS-6 (eS6) is a core structural component of the 40S small ribosomal subunit and is a well-established downstream effector of the TOR (Target of Rapamycin) signaling pathway. S6 kinase (S6K/rsks-1 in C. elegans) phosphorylates RPS-6 to promote ribosome biogenesis and global protein synthesis in response to nutrient availability. Hyperactivation of TOR-S6K-RPS-6 signaling accelerates aging, while reduction of ribosomal activity — including partial loss of rps-6 function — extends lifespan in C. elegans and other model organisms. Reduced translation via ribosome attenuation is a conserved pro-longevity mechanism, meaning the normal (full) function of rps-6 in sustaining high translational capacity is anti-longevity. This places rps-6 squarely within the deregulated nutrient-sensing hallmark, specifically the mTORC1–S6K–ribosome axis that couples anabolic signaling to aging rate.
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-6. The mechanistic reasoning is excellent and well-grounded: RPS-6 is a downstream target of TOR-S6K signaling, and reduction of ribosomal/translational activity is a well-established pro-longevity mechanism in C. elegans. The model correctly identifies that full rps-6 function promotes high translational capacity which accelerates aging, making it anti-longevity. The mechanism class of "deregulated_nutrient_sensing" is appropriate given the TOR-S6K-RPS-6 axis connection. Confidence of 0.72 is reasonable.
Raw API responses
solver
{
"reasoning": "RPS-6 (eS6) is a core structural component of the 40S small ribosomal subunit and is a well-established downstream effector of the TOR (Target of Rapamycin) signaling pathway. S6 kinase (S6K/rsks-1 in C. elegans) phosphorylates RPS-6 to promote ribosome biogenesis and global protein synthesis in response to nutrient availability. Hyperactivation of TOR-S6K-RPS-6 signaling accelerates aging, while reduction of ribosomal activity — including partial loss of rps-6 function — extends lifespan in C. elegans and other model organisms. Reduced translation via ribosome attenuation is a conserved pro-longevity mechanism, meaning the normal (full) function of rps-6 in sustaining high translational capacity is anti-longevity. This places rps-6 squarely within the deregulated nutrient-sensing hallmark, specifically the mTORC1–S6K–ribosome axis that couples anabolic signaling to aging rate.",
"confidence": 0.72,
"key_pathways": [
"TOR-S6K signaling",
"ribosome biogenesis and translational regulation",
"mTORC1-mediated nutrient sensing"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for rps-6. The mechanistic reasoning is excellent and well-grounded: RPS-6 is a downstream target of TOR-S6K signaling, and reduction of ribosomal/translational activity is a well-established pro-longevity mechanism in C. elegans. The model correctly identifies that full rps-6 function promotes high translational capacity which accelerates aging, making it anti-longevity. The mechanism class of \"deregulated_nutrient_sensing\" is appropriate given the TOR-S6K-RPS-6 axis connection. Confidence of 0.72 is reasonable.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}