RPL35A
S. cerevisiae
60S ribosomal protein uL29 RPL35A
What the model saw
Gene: RPL35A Organism: Saccharomyces cerevisiae Known functions: 60S ribosomal protein uL29 RPL35A. mRNA binding. structural constituent of ribosome.
View unredacted entry
60S ribosomal protein uL29 RPL35A. mRNA binding. structural constituent of ribosome.
Solver output
RPL35A encodes a structural component of the 60S ribosomal large subunit (uL29), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of large subunit components — is well established to extend chronological and replicative lifespan, largely through attenuation of TOR (TORC1) signaling and reduced global translation rates. TORC1 promotes ribosome biogenesis and protein synthesis; dampening this axis mimics caloric restriction and extends lifespan. Deletion of RPL35A would reduce ribosomal output, decrease translational activity, and relieve anabolic pressure, consistent with the pro-longevity effects seen for many rpl mutants in S. cerevisiae. Therefore, the normal (wild-type) function of RPL35A — supporting full ribosomal assembly and translation — opposes longevity by sustaining high TORC1-driven anabolism.
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 RPL35A. The mechanistic reasoning is sound and well-articulated: RPL35A encodes a 60S ribosomal large subunit protein, and its deletion reduces translational capacity, which extends lifespan in yeast by mimicking caloric restriction and attenuating TORC1-driven anabolism. This is consistent with the well-established literature on ribosomal protein deletions extending lifespan in S. cerevisiae. The model correctly identifies that the wild-type function of RPL35A (supporting full ribosomal assembly and translation) is anti-longevity. The confidence level of 0.72 is appropriate given the general pattern of ribosomal protein deletions extending lifespan. The mechanism class "deregulated_nutrient_sensing" is a reasonable categorization, though "reduced translation/ribosome biogenesis" might be more precise — this is a minor quibble.
Raw API responses
solver
{
"reasoning": "RPL35A encodes a structural component of the 60S ribosomal large subunit (uL29), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of large subunit components — is well established to extend chronological and replicative lifespan, largely through attenuation of TOR (TORC1) signaling and reduced global translation rates. TORC1 promotes ribosome biogenesis and protein synthesis; dampening this axis mimics caloric restriction and extends lifespan. Deletion of RPL35A would reduce ribosomal output, decrease translational activity, and relieve anabolic pressure, consistent with the pro-longevity effects seen for many rpl mutants in S. cerevisiae. Therefore, the normal (wild-type) function of RPL35A — supporting full ribosomal assembly and translation — opposes longevity by sustaining high TORC1-driven anabolism.",
"confidence": 0.72,
"key_pathways": [
"TORC1 signaling / ribosome biogenesis",
"mRNA translation / 60S ribosomal large subunit assembly",
"Caloric restriction mimicry via reduced translational capacity"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for RPL35A. The mechanistic reasoning is sound and well-articulated: RPL35A encodes a 60S ribosomal large subunit protein, and its deletion reduces translational capacity, which extends lifespan in yeast by mimicking caloric restriction and attenuating TORC1-driven anabolism. This is consistent with the well-established literature on ribosomal protein deletions extending lifespan in S. cerevisiae. The model correctly identifies that the wild-type function of RPL35A (supporting full ribosomal assembly and translation) is anti-longevity. The confidence level of 0.72 is appropriate given the general pattern of ribosomal protein deletions extending lifespan. The mechanism class \"deregulated_nutrient_sensing\" is a reasonable categorization, though \"reduced translation/ribosome biogenesis\" might be more precise — this is a minor quibble.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}