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RPL2B

S. cerevisiae

60S ribosomal protein uL2 RPL2B

What the model saw

Gene: RPL2B
Organism: Saccharomyces cerevisiae
Known functions: 60S ribosomal protein uL2 RPL2B. RNA binding. structural constituent of ribosome.
View unredacted entry
60S ribosomal protein uL2 RPL2B. RNA binding. structural constituent of ribosome.

Solver output

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

RPL2B encodes a core structural component of the 60S ribosomal large subunit (uL2), 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 TORC1-driven protein synthesis. Downregulation of ribosome biogenesis mimics dietary restriction and dampens TOR signaling output, a key pro-longevity intervention. RPL2B's normal function sustains high translational activity, which promotes growth but accelerates aging via nutrient-sensing pathway hyperactivation. Deletion of RPL2B or its paralog RPL2A has been shown to extend replicative lifespan in genome-wide screens, consistent with the broader pattern that ribosomal protein deletions are enriched among longevity-extending mutations in S. cerevisiae.

Key pathways
TORC1/ribosome biogenesis axistranslational regulationribosomal large subunit assembly
Longevity influence
Anti-longevity
Lifespan effect
Increase

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
5/5
Failure mode
Correct
Notes

The model correctly predicted anti_longevity for RPL2B. The reasoning is well-grounded: RPL2B is a 60S ribosomal protein, and deletion of ribosomal protein genes in yeast is well-established to extend lifespan, making the wild-type gene anti-longevity. The model correctly identifies the TORC1/ribosome biogenesis axis as the key mechanism, noting that reduced ribosomal protein dosage mimics dietary restriction and attenuates TOR signaling. The mechanism classification as "deregulated_nutrient_sensing" is appropriate given the TOR pathway connection. The model also correctly notes genome-wide screen evidence for RPL2B/RPL2A deletion extending replicative lifespan. Confidence of 0.72 is reasonable and well-calibrated.

Raw API responses

solver

{
  "reasoning": "RPL2B encodes a core structural component of the 60S ribosomal large subunit (uL2), 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 TORC1-driven protein synthesis. Downregulation of ribosome biogenesis mimics dietary restriction and dampens TOR signaling output, a key pro-longevity intervention. RPL2B's normal function sustains high translational activity, which promotes growth but accelerates aging via nutrient-sensing pathway hyperactivation. Deletion of RPL2B or its paralog RPL2A has been shown to extend replicative lifespan in genome-wide screens, consistent with the broader pattern that ribosomal protein deletions are enriched among longevity-extending mutations in S. cerevisiae.",
  "confidence": 0.72,
  "key_pathways": [
    "TORC1/ribosome biogenesis axis",
    "translational regulation",
    "ribosomal large subunit assembly"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for RPL2B. The reasoning is well-grounded: RPL2B is a 60S ribosomal protein, and deletion of ribosomal protein genes in yeast is well-established to extend lifespan, making the wild-type gene anti-longevity. The model correctly identifies the TORC1/ribosome biogenesis axis as the key mechanism, noting that reduced ribosomal protein dosage mimics dietary restriction and attenuates TOR signaling. The mechanism classification as \"deregulated_nutrient_sensing\" is appropriate given the TOR pathway connection. The model also correctly notes genome-wide screen evidence for RPL2B/RPL2A deletion extending replicative lifespan. Confidence of 0.72 is reasonable and well-calibrated.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}
RPL2B · Saccharomyces cerevisiae | Aging biology eval