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RPS24A

S. cerevisiae

40S ribosomal protein eS24 RPS24A

What the model saw

Gene: RPS24A
Organism: Saccharomyces cerevisiae
Known functions: 40S ribosomal protein eS24 RPS24A. structural constituent of ribosome.
View unredacted entry
40S ribosomal protein eS24 RPS24A. structural constituent of ribosome.

Solver output

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

RPS24A encodes the 40S ribosomal small subunit protein eS24, a structural constituent of the ribosome. Ribosomal protein genes in yeast are well-established modulators of longevity: deletion of many small ribosomal subunit proteins (e.g., Rps6, Rps26) extends both replicative and chronological lifespan in S. cerevisiae. The ribosome is the central effector of translational output, which is tightly coupled to TOR (Target of Rapamycin) nutrient-sensing signaling. Reduced ribosome abundance or activity dampens global protein synthesis rates, mimicking the pro-longevity effects of TOR inhibition or dietary restriction. As a structural component of the 40S subunit, RPS24A's normal function sustains high translational capacity, which in the context of aging promotes anabolic drive and opposes lifespan extension. Thus, the normal (wild-type) function of RPS24A is anti-longevity, as its loss is associated with lifespan extension through reduced ribosomal activity and attenuated TOR-dependent translation.

Key pathways
TOR signaling / translational control40S ribosome biogenesisdietary restriction mimicry via reduced protein synthesis
Longevity influence
Anti-longevity
Lifespan effect
Increase and Decrease

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 RPS24A. The mechanistic reasoning is sound and well-articulated: RPS24A is a structural component of the 40S ribosomal subunit, and deletion of small ribosomal subunit proteins in yeast is well-established to extend lifespan through reduced translational output, mimicking TOR inhibition/dietary restriction effects. The model correctly identifies that the wild-type function of RPS24A sustains high translational capacity (anti-longevity), and its loss leads to lifespan extension. The confidence level of 0.72 is appropriate given the general knowledge about ribosomal protein deletions in yeast. The mechanism class of "deregulated_nutrient_sensing" is a reasonable categorization, though "translational control" might be more precise — however, TOR signaling and nutrient sensing are intimately linked to ribosome function, so this is acceptable.

Raw API responses

solver

{
  "reasoning": "RPS24A encodes the 40S ribosomal small subunit protein eS24, a structural constituent of the ribosome. Ribosomal protein genes in yeast are well-established modulators of longevity: deletion of many small ribosomal subunit proteins (e.g., Rps6, Rps26) extends both replicative and chronological lifespan in S. cerevisiae. The ribosome is the central effector of translational output, which is tightly coupled to TOR (Target of Rapamycin) nutrient-sensing signaling. Reduced ribosome abundance or activity dampens global protein synthesis rates, mimicking the pro-longevity effects of TOR inhibition or dietary restriction. As a structural component of the 40S subunit, RPS24A's normal function sustains high translational capacity, which in the context of aging promotes anabolic drive and opposes lifespan extension. Thus, the normal (wild-type) function of RPS24A is anti-longevity, as its loss is associated with lifespan extension through reduced ribosomal activity and attenuated TOR-dependent translation.",
  "confidence": 0.72,
  "key_pathways": [
    "TOR signaling / translational control",
    "40S ribosome biogenesis",
    "dietary restriction mimicry via reduced protein synthesis"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for RPS24A. The mechanistic reasoning is sound and well-articulated: RPS24A is a structural component of the 40S ribosomal subunit, and deletion of small ribosomal subunit proteins in yeast is well-established to extend lifespan through reduced translational output, mimicking TOR inhibition/dietary restriction effects. The model correctly identifies that the wild-type function of RPS24A sustains high translational capacity (anti-longevity), and its loss leads to lifespan extension. The confidence level of 0.72 is appropriate given the general knowledge about ribosomal protein deletions in yeast. The mechanism class of \"deregulated_nutrient_sensing\" is a reasonable categorization, though \"translational control\" might be more precise — however, TOR signaling and nutrient sensing are intimately linked to ribosome function, so this is acceptable.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}