RPL35B
S. cerevisiae
60S ribosomal protein uL29 RPL35B
What the model saw
Gene: RPL35B Organism: Saccharomyces cerevisiae Known functions: 60S ribosomal protein uL29 RPL35B. mRNA binding. structural constituent of ribosome.
View unredacted entry
60S ribosomal protein uL29 RPL35B. mRNA binding. structural constituent of ribosome.
Solver output
RPL35B encodes a 60S ribosomal large subunit protein (uL29), a structural constituent of the ribosome involved in mRNA binding and translation. Ribosomal protein genes in yeast are well-established regulators of chronological and replicative lifespan: deletion of many large ribosomal subunit genes (including RPL components) extends lifespan in S. cerevisiae by reducing overall translational capacity and mimicking the effects of dietary restriction or TOR pathway downregulation. Reduced ribosome biogenesis and translation rate downstream of TORC1 inhibition is a conserved pro-longevity mechanism. As a structural component of the 60S subunit, RPL35B contributes to ribosome assembly and global protein synthesis rates; its normal function thus supports the high-translation, nutrient-sensing state that opposes longevity. Loss of RPL35B would be expected to reduce ribosomal output, lower TORC1-driven anabolic signaling, and extend lifespan, placing its normal (wild-type) function in the anti-longevity category.
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 RPL35B. The mechanistic reasoning is sound and well-grounded: deletion of large ribosomal subunit genes (RPL components) in yeast is known to extend lifespan by reducing translational capacity, mimicking dietary restriction or TOR pathway downregulation. The model correctly identifies that the wild-type function of RPL35B (supporting high translation/ribosome activity) is anti-longevity. The mechanism class "deregulated_nutrient_sensing" is a reasonable fit, though "translational regulation" might be more precise. Overall, the reasoning is coherent and well-supported by the literature on yeast ribosomal protein deletions and lifespan extension.
Raw API responses
solver
{
"reasoning": "RPL35B encodes a 60S ribosomal large subunit protein (uL29), a structural constituent of the ribosome involved in mRNA binding and translation. Ribosomal protein genes in yeast are well-established regulators of chronological and replicative lifespan: deletion of many large ribosomal subunit genes (including RPL components) extends lifespan in S. cerevisiae by reducing overall translational capacity and mimicking the effects of dietary restriction or TOR pathway downregulation. Reduced ribosome biogenesis and translation rate downstream of TORC1 inhibition is a conserved pro-longevity mechanism. As a structural component of the 60S subunit, RPL35B contributes to ribosome assembly and global protein synthesis rates; its normal function thus supports the high-translation, nutrient-sensing state that opposes longevity. Loss of RPL35B would be expected to reduce ribosomal output, lower TORC1-driven anabolic signaling, and extend lifespan, placing its normal (wild-type) function in the anti-longevity category.",
"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 RPL35B. The mechanistic reasoning is sound and well-grounded: deletion of large ribosomal subunit genes (RPL components) in yeast is known to extend lifespan by reducing translational capacity, mimicking dietary restriction or TOR pathway downregulation. The model correctly identifies that the wild-type function of RPL35B (supporting high translation/ribosome activity) is anti-longevity. The mechanism class \"deregulated_nutrient_sensing\" is a reasonable fit, though \"translational regulation\" might be more precise. Overall, the reasoning is coherent and well-supported by the literature on yeast ribosomal protein deletions and lifespan extension.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}