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RPS4B

S. cerevisiae

40S ribosomal protein eS4 RPS4B

What the model saw

Gene: RPS4B
Organism: Saccharomyces cerevisiae
Known functions: 40S ribosomal protein eS4 RPS4B. RNA binding. structural constituent of ribosome.
View unredacted entry
40S ribosomal protein eS4 RPS4B. RNA binding. structural constituent of ribosome.

Solver output

Predicted influence
Anti-longevity
Confidence
72%
Mechanism
Deregulated nutrient sensing
Reasoning

RPS4B encodes a structural component of the 40S ribosomal small subunit (eS4), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — including deletion of paralogous 40S subunit components — is well established to extend both replicative and chronological lifespan, largely through attenuation of TORC1-driven protein synthesis. Elevated ribosome abundance and translational activity downstream of TOR/nutrient-sensing pathways accelerates aging, while its reduction mimics dietary restriction. As a structural constituent of the ribosome, RPS4B's normal function sustains high translational output, which promotes cellular growth at the cost of longevity. The RNA-binding activity of eS4 is integral to rRNA association and 40S assembly, reinforcing its pro-growth, anti-longevity role. Deletion of RPS4B is therefore predicted to extend lifespan, meaning its normal function is anti-longevity.

Key pathways
TORC1-driven ribosome biogenesis40S small ribosomal subunit assemblytranslational regulation and protein synthesis
Longevity influence
Anti-longevity
Lifespan effect
Increase and Decrease

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

Answer
Correct
Mechanism
Correct
Reasoning quality
4/5
Failure mode
Correct
Notes

The model correctly predicted anti_longevity for RPS4B. The mechanistic reasoning is sound: ribosomal protein genes in yeast are well-established anti-longevity genes, as their deletion extends lifespan through reduced translational output and attenuation of TORC1-driven protein synthesis. The model correctly identifies the TOR/nutrient-sensing pathway connection and the logic that deletion of RPS4B extends lifespan, making its normal function anti-longevity. The reasoning is well-articulated and biologically accurate. Confidence of 0.72 is appropriate given the general knowledge about ribosomal protein genes in yeast aging.

Raw API responses

solver

{
  "reasoning": "RPS4B encodes a structural component of the 40S ribosomal small subunit (eS4), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — including deletion of paralogous 40S subunit components — is well established to extend both replicative and chronological lifespan, largely through attenuation of TORC1-driven protein synthesis. Elevated ribosome abundance and translational activity downstream of TOR/nutrient-sensing pathways accelerates aging, while its reduction mimics dietary restriction. As a structural constituent of the ribosome, RPS4B's normal function sustains high translational output, which promotes cellular growth at the cost of longevity. The RNA-binding activity of eS4 is integral to rRNA association and 40S assembly, reinforcing its pro-growth, anti-longevity role. Deletion of RPS4B is therefore predicted to extend lifespan, meaning its normal function is anti-longevity.",
  "confidence": 0.72,
  "key_pathways": [
    "TORC1-driven ribosome biogenesis",
    "40S small ribosomal subunit assembly",
    "translational regulation and protein synthesis"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for RPS4B. The mechanistic reasoning is sound: ribosomal protein genes in yeast are well-established anti-longevity genes, as their deletion extends lifespan through reduced translational output and attenuation of TORC1-driven protein synthesis. The model correctly identifies the TOR/nutrient-sensing pathway connection and the logic that deletion of RPS4B extends lifespan, making its normal function anti-longevity. The reasoning is well-articulated and biologically accurate. Confidence of 0.72 is appropriate given the general knowledge about ribosomal protein genes in yeast aging.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}