mrpl-1
C. elegans
39S ribosomal protein L1, mitochondrial
What the model saw
Gene: mrpl-1 Organism: Caenorhabditis elegans Known functions: 39S ribosomal protein L1, mitochondrial. mRNA binding. structural constituent of ribosome.
View unredacted entry
39S ribosomal protein L1, mitochondrial. mRNA binding. structural constituent of ribosome.
Solver output
mrpl-1 encodes the mitochondrial large ribosomal subunit protein L1 (39S), which is a structural constituent of the mitochondrial ribosome responsible for translating the 13 mitochondrially-encoded OXPHOS subunits. In C. elegans, partial loss-of-function of mitochondrial ribosomal proteins (e.g., via RNAi) reduces mitochondrial translation and OXPHOS activity, which paradoxically extends lifespan through the mitochondrial unfolded protein response (UPRmt) and reduced reactive oxygen species production — a well-characterized pro-longevity pathway in this organism. This places mrpl-1 in the category where its normal function (full mitochondrial translation) is associated with shorter lifespan, meaning knockdown is pro-longevity; however, the gene's normal function sustains mitochondrial homeostasis. Because the dominant experimental evidence in C. elegans shows that reducing mitochondrial ribosome activity (including mrpl-1 RNAi) extends lifespan via UPRmt activation and reduced electron transport chain activity, the gene's normal full activity is net anti-longevity in this context. Reassigning: the normal function of mrpl-1 supports full mitochondrial translation and OXPHOS, which in C. elegans is associated with normal (shorter) lifespan relative to knockdown conditions.
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 mrpl-1 knockdown extends lifespan via UPRmt and reduced OXPHOS, meaning the gene's normal function is anti-longevity. However, the model's final prediction is "pro_longevity" despite its own reasoning concluding the gene is anti-longevity. The model appears to have confused itself mid-reasoning, starting with "pro_longevity" and then correcting its reasoning to conclude anti-longevity, but failing to update the final prediction field. This is a self-contradictory answer where the reasoning correctly identifies the anti-longevity classification but the submitted prediction says pro_longevity. The ground truth is anti_longevity, so the prediction is wrong.
Raw API responses
solver
{
"reasoning": "mrpl-1 encodes the mitochondrial large ribosomal subunit protein L1 (39S), which is a structural constituent of the mitochondrial ribosome responsible for translating the 13 mitochondrially-encoded OXPHOS subunits. In C. elegans, partial loss-of-function of mitochondrial ribosomal proteins (e.g., via RNAi) reduces mitochondrial translation and OXPHOS activity, which paradoxically extends lifespan through the mitochondrial unfolded protein response (UPRmt) and reduced reactive oxygen species production — a well-characterized pro-longevity pathway in this organism. This places mrpl-1 in the category where its normal function (full mitochondrial translation) is associated with shorter lifespan, meaning knockdown is pro-longevity; however, the gene's normal function sustains mitochondrial homeostasis. Because the dominant experimental evidence in C. elegans shows that reducing mitochondrial ribosome activity (including mrpl-1 RNAi) extends lifespan via UPRmt activation and reduced electron transport chain activity, the gene's normal full activity is net anti-longevity in this context. Reassigning: the normal function of mrpl-1 supports full mitochondrial translation and OXPHOS, which in C. elegans is associated with normal (shorter) lifespan relative to knockdown conditions.",
"confidence": 0.72,
"key_pathways": [
"mitochondrial translation / OXPHOS",
"mitochondrial unfolded protein response (UPRmt)",
"electron transport chain activity"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model's mechanistic reasoning is actually correct - it correctly identifies that mrpl-1 knockdown extends lifespan via UPRmt and reduced OXPHOS, meaning the gene's normal function is anti-longevity. However, the model's final prediction is \"pro_longevity\" despite its own reasoning concluding the gene is anti-longevity. The model appears to have confused itself mid-reasoning, starting with \"pro_longevity\" and then correcting its reasoning to conclude anti-longevity, but failing to update the final prediction field. This is a self-contradictory answer where the reasoning correctly identifies the anti-longevity classification but the submitted prediction says pro_longevity. The ground truth is anti_longevity, so the prediction is wrong.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": false,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}