rpl-3
C. elegans
Large ribosomal subunit protein uL3
What the model saw
Gene: rpl-3 Organism: Caenorhabditis elegans Known functions: Large ribosomal subunit protein uL3. RNA binding. structural constituent of ribosome.
View unredacted entry
Large ribosomal subunit protein uL3. RNA binding. structural constituent of ribosome.
Solver output
RPL-3 encodes the large ribosomal subunit protein uL3, a core structural component of the 60S ribosomal subunit required for mRNA translation. In C. elegans, partial loss-of-function of large ribosomal subunit components (including rpl genes) has been shown to extend lifespan by reducing global translation rates, which mimics dietary restriction and downregulates TOR/TORC1 signaling — a key nutrient-sensing pathway linked to longevity. Reduced ribosomal activity lowers the production of pro-aging proteins while potentially upregulating stress-response and proteostasis pathways. However, the normal (wild-type) function of rpl-3 is to support full translational capacity, which under nutrient-rich conditions promotes growth over longevity via TOR activation. Thus, the gene's normal function is net anti-longevity, but given the well-established paradigm that ribosomal subunit knockdowns extend life, the wild-type activity opposes longevity by sustaining high translation and TOR-coupled anabolic signaling. Classifying the normal function as anti-longevity is therefore the most consistent interpretation with the ribosome-reduction longevity literature in C. elegans.
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 correctly identified the mechanistic framework — that rpl-3 encodes a large ribosomal subunit protein, and that knockdown of ribosomal subunit genes extends lifespan in C. elegans by reducing translation rates and mimicking dietary restriction. The model even explicitly stated "the gene's normal function is net anti-longevity" in its reasoning, which matches the ground truth. However, the final prediction was labeled "pro_longevity" — directly contradicting both the ground truth (anti_longevity) and the model's own reasoning. This is a self-contradictory answer where the reasoning correctly arrives at anti_longevity but the final classification field says pro_longevity. The model appears to have confused itself in the final step, possibly conflating "knockdown extends life" with "gene is pro-longevity." The confidence of 0.62 is moderate but the answer is definitively wrong.
Raw API responses
solver
{
"reasoning": "RPL-3 encodes the large ribosomal subunit protein uL3, a core structural component of the 60S ribosomal subunit required for mRNA translation. In C. elegans, partial loss-of-function of large ribosomal subunit components (including rpl genes) has been shown to extend lifespan by reducing global translation rates, which mimics dietary restriction and downregulates TOR/TORC1 signaling — a key nutrient-sensing pathway linked to longevity. Reduced ribosomal activity lowers the production of pro-aging proteins while potentially upregulating stress-response and proteostasis pathways. However, the normal (wild-type) function of rpl-3 is to support full translational capacity, which under nutrient-rich conditions promotes growth over longevity via TOR activation. Thus, the gene's normal function is net anti-longevity, but given the well-established paradigm that ribosomal subunit knockdowns extend life, the wild-type activity opposes longevity by sustaining high translation and TOR-coupled anabolic signaling. Classifying the normal function as anti-longevity is therefore the most consistent interpretation with the ribosome-reduction longevity literature in C. elegans.",
"confidence": 0.62,
"key_pathways": [
"TOR/TORC1 nutrient sensing",
"ribosomal translation rate regulation",
"dietary restriction mimicry via reduced protein synthesis"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly identified the mechanistic framework — that rpl-3 encodes a large ribosomal subunit protein, and that knockdown of ribosomal subunit genes extends lifespan in C. elegans by reducing translation rates and mimicking dietary restriction. The model even explicitly stated \"the gene's normal function is net anti-longevity\" in its reasoning, which matches the ground truth. However, the final prediction was labeled \"pro_longevity\" — directly contradicting both the ground truth (anti_longevity) and the model's own reasoning. This is a self-contradictory answer where the reasoning correctly arrives at anti_longevity but the final classification field says pro_longevity. The model appears to have confused itself in the final step, possibly conflating \"knockdown extends life\" with \"gene is pro-longevity.\" The confidence of 0.62 is moderate but the answer is definitively wrong.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}