RPS6A
S. cerevisiae
40S ribosomal protein eS6 RPS6A
What the model saw
Gene: RPS6A Organism: Saccharomyces cerevisiae Known functions: 40S ribosomal protein eS6 RPS6A. structural constituent of ribosome.
View unredacted entry
40S ribosomal protein eS6 RPS6A. structural constituent of ribosome.
Solver output
RPS6A encodes the 40S ribosomal small subunit protein eS6, a well-known downstream phosphorylation target of the TOR (Target of Rapamycin) / S6 Kinase (Sch9 in yeast) signaling axis. As a structural constituent of the ribosome, it directly supports translational capacity and ribosome biogenesis, both of which are upregulated by active TORC1 signaling. Elevated TORC1/S6K activity and increased ribosomal output are strongly associated with reduced lifespan in yeast and other organisms; conversely, reducing ribosomal protein gene dosage (including RPS6) extends chronological and replicative lifespan in S. cerevisiae. The pro-growth, pro-translation function of RPS6A thus opposes longevity by sustaining high anabolic flux downstream of nutrient-sensing pathways. Deletion or reduction of RPS6A mimics partial TOR inhibition, which is a canonical longevity intervention.
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 RPS6A with high confidence (0.72). The mechanistic reasoning is excellent and well-grounded: RPS6A encodes a 40S ribosomal protein that is a downstream target of TOR/S6K signaling, and deletion of ribosomal protein genes (including RPS6) is known to extend lifespan in yeast by mimicking partial TOR inhibition. The model correctly identifies that the pro-growth, pro-translation function of RPS6A opposes longevity. The mechanism class of "deregulated_nutrient_sensing" is appropriate given the TOR/S6K connection. The reasoning is detailed, accurate, and well-supported by the literature on yeast aging.
Raw API responses
solver
{
"reasoning": "RPS6A encodes the 40S ribosomal small subunit protein eS6, a well-known downstream phosphorylation target of the TOR (Target of Rapamycin) / S6 Kinase (Sch9 in yeast) signaling axis. As a structural constituent of the ribosome, it directly supports translational capacity and ribosome biogenesis, both of which are upregulated by active TORC1 signaling. Elevated TORC1/S6K activity and increased ribosomal output are strongly associated with reduced lifespan in yeast and other organisms; conversely, reducing ribosomal protein gene dosage (including RPS6) extends chronological and replicative lifespan in S. cerevisiae. The pro-growth, pro-translation function of RPS6A thus opposes longevity by sustaining high anabolic flux downstream of nutrient-sensing pathways. Deletion or reduction of RPS6A mimics partial TOR inhibition, which is a canonical longevity intervention.",
"confidence": 0.72,
"key_pathways": [
"TOR/S6 Kinase signaling",
"ribosome biogenesis",
"translational regulation"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for RPS6A with high confidence (0.72). The mechanistic reasoning is excellent and well-grounded: RPS6A encodes a 40S ribosomal protein that is a downstream target of TOR/S6K signaling, and deletion of ribosomal protein genes (including RPS6) is known to extend lifespan in yeast by mimicking partial TOR inhibition. The model correctly identifies that the pro-growth, pro-translation function of RPS6A opposes longevity. The mechanism class of \"deregulated_nutrient_sensing\" is appropriate given the TOR/S6K connection. The reasoning is detailed, accurate, and well-supported by the literature on yeast aging.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}