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RPL19B

S. cerevisiae

60S ribosomal protein eL19 RPL19B

What the model saw

Gene: RPL19B
Organism: Saccharomyces cerevisiae
Known functions: 60S ribosomal protein eL19 RPL19B. RNA binding. structural constituent of ribosome.
View unredacted entry
60S ribosomal protein eL19 RPL19B. RNA binding. structural constituent of ribosome.

Solver output

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

RPL19B encodes a structural component of the 60S ribosomal large subunit (eL19), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of 60S subunit components — is well established to extend chronological and replicative lifespan, largely through attenuation of TORC1-driven protein synthesis. Deletion of large-subunit ribosomal protein genes mimics the pro-longevity effects of rapamycin or dietary restriction by decreasing global translation rates and reducing proteotoxic burden. The normal function of RPL19B thus promotes high translational output, which is associated with accelerated aging in yeast. This places its primary mechanism within deregulated nutrient sensing (TOR pathway), where ribosome abundance is a key downstream effector of TORC1 signaling.

Key pathways
TORC1-ribosome biogenesis axis60S ribosomal large subunit assemblytranslational regulation and proteostasis
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 RPL19B. The mechanistic reasoning is sound and well-articulated: RPL19B encodes a 60S ribosomal protein, and deletion of ribosomal protein genes in yeast is well-established to extend lifespan by reducing translational output and attenuating TORC1 signaling. Therefore, the wild-type gene promotes aging (anti_longevity). The mechanism class of "deregulated_nutrient_sensing" is reasonable given the TOR pathway connection, though one could argue "protein synthesis/translation" is more direct. The confidence of 0.72 is appropriate given the general knowledge about ribosomal proteins in yeast aging. Overall, this is a high-quality, well-reasoned prediction.

Raw API responses

solver

{
  "reasoning": "RPL19B encodes a structural component of the 60S ribosomal large subunit (eL19), directly contributing to ribosome biogenesis and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of 60S subunit components — is well established to extend chronological and replicative lifespan, largely through attenuation of TORC1-driven protein synthesis. Deletion of large-subunit ribosomal protein genes mimics the pro-longevity effects of rapamycin or dietary restriction by decreasing global translation rates and reducing proteotoxic burden. The normal function of RPL19B thus promotes high translational output, which is associated with accelerated aging in yeast. This places its primary mechanism within deregulated nutrient sensing (TOR pathway), where ribosome abundance is a key downstream effector of TORC1 signaling.",
  "confidence": 0.72,
  "key_pathways": [
    "TORC1-ribosome biogenesis axis",
    "60S ribosomal large subunit assembly",
    "translational regulation and proteostasis"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for RPL19B. The mechanistic reasoning is sound and well-articulated: RPL19B encodes a 60S ribosomal protein, and deletion of ribosomal protein genes in yeast is well-established to extend lifespan by reducing translational output and attenuating TORC1 signaling. Therefore, the wild-type gene promotes aging (anti_longevity). The mechanism class of \"deregulated_nutrient_sensing\" is reasonable given the TOR pathway connection, though one could argue \"protein synthesis/translation\" is more direct. The confidence of 0.72 is appropriate given the general knowledge about ribosomal proteins in yeast aging. Overall, this is a high-quality, well-reasoned prediction.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}