rpl-4
C. elegans
Large ribosomal subunit protein uL4
What the model saw
Gene: rpl-4 Organism: Caenorhabditis elegans Known functions: Large ribosomal subunit protein uL4. RNA binding. structural constituent of ribosome.
View unredacted entry
Large ribosomal subunit protein uL4. RNA binding. structural constituent of ribosome.
Solver output
RPL-4 encodes the large ribosomal subunit protein uL4, a core structural component of the 60S ribosomal subunit involved in mRNA translation. In C. elegans, partial loss-of-function of large ribosomal subunit proteins, including rpl-4, has been shown to extend lifespan by reducing global translation rates, which mimics the effects of dietary restriction and downregulation of the TOR/mTOR nutrient-sensing pathway. Reduced ribosomal activity decreases overall protein synthesis, alleviating proteotoxic stress and improving proteostasis. However, since the gene's *normal* (wild-type) function is to sustain full translational capacity — which is associated with pro-growth, pro-aging signaling — the wild-type gene itself promotes aging rather than longevity. Nonetheless, in the context of the hallmarks framework, ribosome biogenesis and translational output are canonically regulated downstream of TOR/nutrient-sensing, placing this gene in the deregulated nutrient-sensing class. The net effect of the normal gene function (supporting high translation) is anti-longevity, as reduction of rpl-4 activity extends lifespan in worms.
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
The model's mechanistic reasoning is actually correct - it correctly identifies that rpl-4 knockdown extends lifespan, and that the wild-type gene's normal function supports high translation which promotes aging (anti-longevity). However, the model contradicts itself: after correctly reasoning that the wild-type gene is anti-longevity, it outputs "pro_longevity" as its final prediction. This is a clear internal contradiction where the reasoning leads to the correct conclusion (anti_longevity) but the final answer field says the opposite (pro_longevity). The mechanism class of deregulated nutrient sensing / TOR signaling is reasonable. The confidence of 0.65 for the wrong answer is also notable. This appears to be a failure where the model got confused between "the gene promotes longevity when knocked down" vs "the gene's normal function is anti-longevity."
Raw API responses
solver
{
"reasoning": "RPL-4 encodes the large ribosomal subunit protein uL4, a core structural component of the 60S ribosomal subunit involved in mRNA translation. In C. elegans, partial loss-of-function of large ribosomal subunit proteins, including rpl-4, has been shown to extend lifespan by reducing global translation rates, which mimics the effects of dietary restriction and downregulation of the TOR/mTOR nutrient-sensing pathway. Reduced ribosomal activity decreases overall protein synthesis, alleviating proteotoxic stress and improving proteostasis. However, since the gene's *normal* (wild-type) function is to sustain full translational capacity — which is associated with pro-growth, pro-aging signaling — the wild-type gene itself promotes aging rather than longevity. Nonetheless, in the context of the hallmarks framework, ribosome biogenesis and translational output are canonically regulated downstream of TOR/nutrient-sensing, placing this gene in the deregulated nutrient-sensing class. The net effect of the normal gene function (supporting high translation) is anti-longevity, as reduction of rpl-4 activity extends lifespan in worms.",
"confidence": 0.65,
"key_pathways": [
"mTOR/TOR signaling and translational control",
"ribosome biogenesis",
"dietary restriction mimicry via reduced protein synthesis"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model's mechanistic reasoning is actually correct - it correctly identifies that rpl-4 knockdown extends lifespan, and that the wild-type gene's normal function supports high translation which promotes aging (anti-longevity). However, the model contradicts itself: after correctly reasoning that the wild-type gene is anti-longevity, it outputs \"pro_longevity\" as its final prediction. This is a clear internal contradiction where the reasoning leads to the correct conclusion (anti_longevity) but the final answer field says the opposite (pro_longevity). The mechanism class of deregulated nutrient sensing / TOR signaling is reasonable. The confidence of 0.65 for the wrong answer is also notable. This appears to be a failure where the model got confused between \"the gene promotes longevity when knocked down\" vs \"the gene's normal function is anti-longevity.\"",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": false,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}