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RPL7A

S. cerevisiae

60S ribosomal protein uL30 RPL7A

What the model saw

Gene: RPL7A
Organism: Saccharomyces cerevisiae
Known functions: 60S ribosomal protein uL30 RPL7A. RNA binding. structural constituent of ribosome.
View unredacted entry
60S ribosomal protein uL30 RPL7A. RNA binding. structural constituent of ribosome.

Solver output

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

RPL7A encodes the 60S ribosomal protein uL30, a structural component of the large ribosomal subunit essential for translation. In yeast, ribosome biogenesis and translational activity are tightly coupled to the TOR (Target of Rapamycin) nutrient-sensing pathway; high TOR activity upregulates ribosome production and promotes aging, while reduced ribosomal protein gene dosage (e.g., deletion of one copy of RPL genes) extends chronological and replicative lifespan. Deletion of RPL7A or reduction in 60S ribosomal subunit availability decreases global translation rates, mimicking the pro-longevity effects of TOR inhibition. Multiple studies in S. cerevisiae have shown that heterozygous deletion of large-subunit ribosomal protein genes, including paralogs of RPL7A, extends replicative lifespan. Therefore, the normal function of RPL7A—promoting full ribosomal assembly and high translational output—opposes longevity by sustaining elevated protein synthesis rates downstream of nutrient-sensing pathways.

Key pathways
TOR signaling / ribosome biogenesis60S ribosomal subunit assemblytranslational regulation
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 RPL7A. The mechanistic reasoning is well-grounded: RPL7A encodes a 60S ribosomal protein, and deletion of ribosomal protein genes in yeast is well-established to extend lifespan by reducing translational output, mimicking TOR inhibition. The model correctly identifies that the normal function of RPL7A (promoting ribosome assembly and high translation) opposes longevity, making it anti-longevity. The mechanism class "deregulated_nutrient_sensing" is a reasonable classification given the TOR-ribosome biogenesis connection, though "protein synthesis/translation" might be more direct. Overall, the reasoning is accurate and well-supported by the literature.

Raw API responses

solver

{
  "reasoning": "RPL7A encodes the 60S ribosomal protein uL30, a structural component of the large ribosomal subunit essential for translation. In yeast, ribosome biogenesis and translational activity are tightly coupled to the TOR (Target of Rapamycin) nutrient-sensing pathway; high TOR activity upregulates ribosome production and promotes aging, while reduced ribosomal protein gene dosage (e.g., deletion of one copy of RPL genes) extends chronological and replicative lifespan. Deletion of RPL7A or reduction in 60S ribosomal subunit availability decreases global translation rates, mimicking the pro-longevity effects of TOR inhibition. Multiple studies in S. cerevisiae have shown that heterozygous deletion of large-subunit ribosomal protein genes, including paralogs of RPL7A, extends replicative lifespan. Therefore, the normal function of RPL7A—promoting full ribosomal assembly and high translational output—opposes longevity by sustaining elevated protein synthesis rates downstream of nutrient-sensing pathways.",
  "confidence": 0.72,
  "key_pathways": [
    "TOR signaling / ribosome biogenesis",
    "60S ribosomal subunit assembly",
    "translational regulation"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for RPL7A. The mechanistic reasoning is well-grounded: RPL7A encodes a 60S ribosomal protein, and deletion of ribosomal protein genes in yeast is well-established to extend lifespan by reducing translational output, mimicking TOR inhibition. The model correctly identifies that the normal function of RPL7A (promoting ribosome assembly and high translation) opposes longevity, making it anti-longevity. The mechanism class \"deregulated_nutrient_sensing\" is a reasonable classification given the TOR-ribosome biogenesis connection, though \"protein synthesis/translation\" might be more direct. Overall, the reasoning is accurate and well-supported by the literature.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}