RPL9B

solver

{
  "reasoning": "RPL9B encodes a structural component of the 60S ribosomal large subunit (uL6) that binds rRNA and is required for ribosome assembly and translational capacity. In yeast, reduced ribosomal protein gene dosage — particularly of large subunit components — is well established to extend both replicative and chronological lifespan, largely through attenuation of TOR (TORC1)-driven protein synthesis. Deletion of many RPL genes mimics the pro-longevity effects of rapamycin or caloric restriction by decreasing global translation rates and reducing the burden of misfolded proteins. RPL9B's normal function therefore promotes ribosome biogenesis and high translational output, which is associated with accelerated aging rather than longevity. This places its primary mechanism within deregulated nutrient sensing (TOR/ribosome biogenesis axis), a canonical hallmark of aging.",
  "confidence": 0.72,
  "key_pathways": [
    "TORC1-driven ribosome biogenesis",
    "60S 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 RPL9B. The mechanistic reasoning is sound and well-articulated: RPL9B encodes a 60S ribosomal large subunit protein, and deletion of RPL genes in yeast is well-established to extend lifespan by reducing translational output via the TOR/ribosome biogenesis axis. The model correctly identifies that the gene's normal function promotes aging (anti-longevity), and the mechanism class of deregulated nutrient sensing (TOR pathway) is appropriate. The confidence of 0.72 is reasonable given the general pattern of RPL gene deletions extending lifespan in yeast.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}