rpl-19
C. elegans
Large ribosomal subunit protein eL19
What the model saw
Gene: rpl-19 Organism: Caenorhabditis elegans Known functions: Large ribosomal subunit protein eL19. RNA binding. structural constituent of ribosome.
View unredacted entry
Large ribosomal subunit protein eL19. RNA binding. structural constituent of ribosome.
Solver output
RPL-19 encodes the large ribosomal subunit protein eL19, a 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 genes) has been repeatedly shown to extend lifespan by reducing global translation rates, which mimics dietary restriction and downregulates TOR (mTORC1) signaling — a key nutrient-sensing pathway. Reduced ribosomal activity lowers the production of potentially misfolded proteins and dampens anabolic signaling, both of which are associated with longevity. The normal (wild-type) function of rpl-19 is therefore to sustain high translational output, which promotes growth but opposes longevity; however, since the question asks about the gene's normal function, full ribosomal activity supports the pro-growth, pro-aging state. Nonetheless, the broader literature on ribosomal protein knockdowns in C. elegans consistently places rpl gene activity in the anti-longevity category when expressed at normal levels, as their reduction extends lifespan via TOR/translation axis modulation.
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-19 encodes a large ribosomal subunit protein, and that knockdown of rpl genes in C. elegans extends lifespan by reducing translation via TOR signaling. The model even explicitly states "the broader literature on ribosomal protein knockdowns in C. elegans consistently places rpl gene activity in the anti-longevity category when expressed at normal levels." However, the model then contradicts itself and outputs "pro_longevity" as its final prediction, which is the wrong answer. The ground truth is "anti_longevity." The model's reasoning correctly supports anti_longevity but the final label is wrong. This is a case where the model's own reasoning contradicts its final answer — it essentially argued for anti_longevity but labeled it pro_longevity. The confidence of 0.65 reflects some uncertainty, but the final answer is still incorrect.
Raw API responses
solver
{
"reasoning": "RPL-19 encodes the large ribosomal subunit protein eL19, a 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 genes) has been repeatedly shown to extend lifespan by reducing global translation rates, which mimics dietary restriction and downregulates TOR (mTORC1) signaling — a key nutrient-sensing pathway. Reduced ribosomal activity lowers the production of potentially misfolded proteins and dampens anabolic signaling, both of which are associated with longevity. The normal (wild-type) function of rpl-19 is therefore to sustain high translational output, which promotes growth but opposes longevity; however, since the question asks about the gene's normal function, full ribosomal activity supports the pro-growth, pro-aging state. Nonetheless, the broader literature on ribosomal protein knockdowns in C. elegans consistently places rpl gene activity in the anti-longevity category when expressed at normal levels, as their reduction extends lifespan via TOR/translation axis modulation.",
"confidence": 0.65,
"key_pathways": [
"mTOR/TOR signaling and translational control",
"ribosome biogenesis and global protein synthesis",
"dietary restriction mimicry via reduced translation"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model's mechanistic reasoning is actually correct — it correctly identifies that rpl-19 encodes a large ribosomal subunit protein, and that knockdown of rpl genes in C. elegans extends lifespan by reducing translation via TOR signaling. The model even explicitly states \"the broader literature on ribosomal protein knockdowns in C. elegans consistently places rpl gene activity in the anti-longevity category when expressed at normal levels.\" However, the model then contradicts itself and outputs \"pro_longevity\" as its final prediction, which is the wrong answer. The ground truth is \"anti_longevity.\" The model's reasoning correctly supports anti_longevity but the final label is wrong. This is a case where the model's own reasoning contradicts its final answer — it essentially argued for anti_longevity but labeled it pro_longevity. The confidence of 0.65 reflects some uncertainty, but the final answer is still incorrect.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": false,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}