RPL19A
S. cerevisiae
60S ribosomal protein eL19 RPL19A
What the model saw
Gene: RPL19A Organism: Saccharomyces cerevisiae Known functions: 60S ribosomal protein eL19 RPL19A. RNA binding. structural constituent of ribosome.
View unredacted entry
60S ribosomal protein eL19 RPL19A. RNA binding. structural constituent of ribosome.
Solver output
RPL19A encodes a structural component of the 60S ribosomal large subunit (eL19), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of 60S subunit components — is one of the most robust interventions known to extend chronological and replicative lifespan, acting downstream of the TOR/TORC1 nutrient-sensing pathway. TORC1 promotes ribosome biogenesis; its inhibition (e.g., by rapamycin) mimics dietary restriction and extends lifespan partly by reducing ribosomal protein expression. Deletion of individual large-subunit ribosomal protein genes, including paralogs of RPL19A, consistently appears among the longest-lived deletion strains in genome-wide yeast longevity screens. The normal function of RPL19A — supporting full ribosomal assembly and high translational output — therefore opposes longevity by sustaining anabolic signaling and protein synthesis rates that accelerate 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 correctly predicted anti_longevity for RPL19A with high confidence (0.72). The mechanistic reasoning is excellent: it correctly identifies that RPL19A encodes a 60S ribosomal large subunit protein, that deletion of ribosomal protein genes extends yeast lifespan, and that this operates downstream of the TORC1 nutrient-sensing pathway. The model accurately notes that the normal function of RPL19A (supporting ribosome assembly and high translational output) opposes longevity, making it anti-longevity. The mechanism class of "deregulated_nutrient_sensing" is a reasonable classification given the TOR/TORC1 connection, though "ribosome biogenesis" might be more precise — this is a minor quibble. Overall, the reasoning is well-grounded in established yeast aging biology.
Raw API responses
solver
{
"reasoning": "RPL19A encodes a structural component of the 60S ribosomal large subunit (eL19), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of 60S subunit components — is one of the most robust interventions known to extend chronological and replicative lifespan, acting downstream of the TOR/TORC1 nutrient-sensing pathway. TORC1 promotes ribosome biogenesis; its inhibition (e.g., by rapamycin) mimics dietary restriction and extends lifespan partly by reducing ribosomal protein expression. Deletion of individual large-subunit ribosomal protein genes, including paralogs of RPL19A, consistently appears among the longest-lived deletion strains in genome-wide yeast longevity screens. The normal function of RPL19A — supporting full ribosomal assembly and high translational output — therefore opposes longevity by sustaining anabolic signaling and protein synthesis rates that accelerate aging.",
"confidence": 0.72,
"key_pathways": [
"TORC1-ribosome biogenesis axis",
"60S ribosomal large subunit assembly",
"translational regulation of lifespan"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for RPL19A with high confidence (0.72). The mechanistic reasoning is excellent: it correctly identifies that RPL19A encodes a 60S ribosomal large subunit protein, that deletion of ribosomal protein genes extends yeast lifespan, and that this operates downstream of the TORC1 nutrient-sensing pathway. The model accurately notes that the normal function of RPL19A (supporting ribosome assembly and high translational output) opposes longevity, making it anti-longevity. The mechanism class of \"deregulated_nutrient_sensing\" is a reasonable classification given the TOR/TORC1 connection, though \"ribosome biogenesis\" might be more precise — this is a minor quibble. Overall, the reasoning is well-grounded in established yeast aging biology.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}