← Browse entries

RPL6B

S. cerevisiae

60S ribosomal protein eL6 RPL6B

What the model saw

Gene: RPL6B
Organism: Saccharomyces cerevisiae
Known functions: 60S ribosomal protein eL6 RPL6B. RNA binding. structural constituent of ribosome.
View unredacted entry
60S ribosomal protein eL6 RPL6B. RNA binding. structural constituent of ribosome.

Solver output

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

RPL6B encodes a structural component of the 60S ribosomal large subunit (eL6), 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 RPL6B thus promotes high translational output, which is associated with accelerated aging in yeast. This places RPL6B's activity squarely within the deregulated nutrient-sensing hallmark, as ribosome abundance is a key downstream effector of TOR 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 RPL6B with high confidence (0.72). The mechanistic reasoning is sound and well-articulated: RPL6B encodes a 60S ribosomal large subunit protein, and deletion of ribosomal protein genes in yeast is well-known to extend lifespan by reducing translational output and mimicking dietary restriction/TOR inhibition. The model correctly identifies that the normal (wild-type) function of RPL6B promotes high translation rates, which accelerates aging — making it anti-longevity. The mechanism class of "deregulated_nutrient_sensing" is reasonable given the TOR-ribosome biogenesis connection, though one could also classify it under proteostasis or translational regulation. Overall, the prediction and reasoning are both correct and well-supported.

Raw API responses

solver

{
  "reasoning": "RPL6B encodes a structural component of the 60S ribosomal large subunit (eL6), 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 RPL6B thus promotes high translational output, which is associated with accelerated aging in yeast. This places RPL6B's activity squarely within the deregulated nutrient-sensing hallmark, as ribosome abundance is a key downstream effector of TOR 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 RPL6B with high confidence (0.72). The mechanistic reasoning is sound and well-articulated: RPL6B encodes a 60S ribosomal large subunit protein, and deletion of ribosomal protein genes in yeast is well-known to extend lifespan by reducing translational output and mimicking dietary restriction/TOR inhibition. The model correctly identifies that the normal (wild-type) function of RPL6B promotes high translation rates, which accelerates aging — making it anti-longevity. The mechanism class of \"deregulated_nutrient_sensing\" is reasonable given the TOR-ribosome biogenesis connection, though one could also classify it under proteostasis or translational regulation. Overall, the prediction and reasoning are both correct and well-supported.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}