RPS26B
S. cerevisiae
40S ribosomal protein eS26 RPS26B
What the model saw
Gene: RPS26B Organism: Saccharomyces cerevisiae Known functions: 40S ribosomal protein eS26 RPS26B. mRNA binding. protein binding. structural constituent of ribosome. zinc ion binding.
View unredacted entry
40S ribosomal protein eS26 RPS26B. mRNA binding. protein binding. structural constituent of ribosome. zinc ion binding.
Solver output
RPS26B encodes a structural component of the 40S ribosomal small subunit (eS26), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of small subunit components — is well established to extend chronological and replicative lifespan, largely through attenuation of TORC1-driven protein synthesis and nutrient-sensing signaling. Deletion or reduction of 40S ribosomal proteins like RPS26 decreases global translation rates, mimicking dietary restriction and dampening TOR pathway activity, which is a canonical pro-longevity intervention. The mRNA binding and structural ribosome constituent functions confirm its role in promoting translational output, which when elevated accelerates aging. Thus, the normal (wild-type) function of RPS26B — supporting robust ribosome assembly and translation — opposes longevity.
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 RPS26B. The mechanistic reasoning is sound and well-grounded: ribosomal protein genes in yeast are well-established anti-longevity genes, and deletion of small subunit ribosomal proteins like RPS26B extends lifespan by reducing translational output and mimicking dietary restriction via TOR pathway attenuation. The model correctly identifies the key pathways (TORC1/nutrient-sensing, ribosome biogenesis) and explains why the wild-type function opposes longevity. The confidence of 0.72 is appropriate given the general knowledge about ribosomal proteins in yeast aging. Minor note: the model could have been more specific about whether this is replicative or chronological lifespan extension, but the overall reasoning is solid.
Raw API responses
solver
{
"reasoning": "RPS26B encodes a structural component of the 40S ribosomal small subunit (eS26), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of small subunit components — is well established to extend chronological and replicative lifespan, largely through attenuation of TORC1-driven protein synthesis and nutrient-sensing signaling. Deletion or reduction of 40S ribosomal proteins like RPS26 decreases global translation rates, mimicking dietary restriction and dampening TOR pathway activity, which is a canonical pro-longevity intervention. The mRNA binding and structural ribosome constituent functions confirm its role in promoting translational output, which when elevated accelerates aging. Thus, the normal (wild-type) function of RPS26B — supporting robust ribosome assembly and translation — opposes longevity.",
"confidence": 0.72,
"key_pathways": [
"TORC1/nutrient-sensing signaling",
"ribosome biogenesis and translation",
"dietary restriction mimicry via reduced protein synthesis"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for RPS26B. The mechanistic reasoning is sound and well-grounded: ribosomal protein genes in yeast are well-established anti-longevity genes, and deletion of small subunit ribosomal proteins like RPS26B extends lifespan by reducing translational output and mimicking dietary restriction via TOR pathway attenuation. The model correctly identifies the key pathways (TORC1/nutrient-sensing, ribosome biogenesis) and explains why the wild-type function opposes longevity. The confidence of 0.72 is appropriate given the general knowledge about ribosomal proteins in yeast aging. Minor note: the model could have been more specific about whether this is replicative or chronological lifespan extension, but the overall reasoning is solid.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}