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RPL1B

S. cerevisiae

60S ribosomal protein uL1 RPL1B

What the model saw

Gene: RPL1B
Organism: Saccharomyces cerevisiae
Known functions: 60S ribosomal protein uL1 RPL1B. RNA binding. structural constituent of ribosome.
View unredacted entry
60S ribosomal protein uL1 RPL1B. RNA binding. structural constituent of ribosome.

Solver output

Predicted influence
Anti-longevity
Confidence
75%
Mechanism
Deregulated nutrient sensing
Reasoning

RPL1B encodes a core structural component of the 60S ribosomal large subunit (uL1), 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. Decreased ribosome abundance mimics dietary restriction by dampening anabolic signaling downstream of TOR, reducing global translation rates and associated proteotoxic stress. Deletion of RPL1B (one of two paralogs) has been shown to extend replicative lifespan in genome-wide screens. Thus, the normal pro-translational function of RPL1B opposes longevity by sustaining high ribosomal output and TOR-coupled anabolic activity.

Key pathways
TORC1-ribosome biogenesis axis60S large ribosomal subunit assemblytranslational regulation and nutrient sensing
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 RPL1B. The mechanistic reasoning is sound and well-articulated: RPL1B encodes a 60S ribosomal large subunit protein, and deletion of ribosomal protein genes in yeast is well-established to extend lifespan by reducing translational output and mimicking dietary restriction via attenuation of TORC1 signaling. The model correctly identifies that the wild-type gene opposes longevity (anti_longevity) by sustaining high ribosomal output. The confidence level of 0.75 is appropriate. The mechanism classification as "deregulated_nutrient_sensing" is reasonable given the TOR/ribosome biogenesis connection, though "translational_regulation" might be more precise — this is a minor quibble and does not detract from the overall quality.

Raw API responses

solver

{
  "reasoning": "RPL1B encodes a core structural component of the 60S ribosomal large subunit (uL1), 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. Decreased ribosome abundance mimics dietary restriction by dampening anabolic signaling downstream of TOR, reducing global translation rates and associated proteotoxic stress. Deletion of RPL1B (one of two paralogs) has been shown to extend replicative lifespan in genome-wide screens. Thus, the normal pro-translational function of RPL1B opposes longevity by sustaining high ribosomal output and TOR-coupled anabolic activity.",
  "confidence": 0.75,
  "key_pathways": [
    "TORC1-ribosome biogenesis axis",
    "60S large ribosomal subunit assembly",
    "translational regulation and nutrient sensing"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for RPL1B. The mechanistic reasoning is sound and well-articulated: RPL1B encodes a 60S ribosomal large subunit protein, and deletion of ribosomal protein genes in yeast is well-established to extend lifespan by reducing translational output and mimicking dietary restriction via attenuation of TORC1 signaling. The model correctly identifies that the wild-type gene opposes longevity (anti_longevity) by sustaining high ribosomal output. The confidence level of 0.75 is appropriate. The mechanism classification as \"deregulated_nutrient_sensing\" is reasonable given the TOR/ribosome biogenesis connection, though \"translational_regulation\" might be more precise — this is a minor quibble and does not detract from the overall quality.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}