mrpl-24
C. elegans
Large ribosomal subunit protein uL24m
What the model saw
Gene: mrpl-24 Organism: Caenorhabditis elegans Known functions: Large ribosomal subunit protein uL24m. RNA binding. structural constituent of ribosome.
View unredacted entry
Large ribosomal subunit protein uL24m. RNA binding. structural constituent of ribosome.
Solver output
mrpl-24 encodes the mitochondrial large ribosomal subunit protein uL24m, which is a structural component of the mitochondrial ribosome responsible for translating mitochondrially-encoded proteins. In C. elegans, partial loss-of-function of mitochondrial ribosomal proteins (MRPs) is well-documented to extend lifespan through a mechanism involving mild mitochondrial translation impairment, which triggers the mitochondrial unfolded protein response (UPRmt) and reduces electron transport chain activity. This mild mitochondrial stress activates retrograde signaling pathways (including ATFS-1/UPRmt) that reprogram nuclear gene expression toward stress resistance and longevity. The effect mirrors the lifespan extension seen with other mitochondrial ribosomal subunit knockdowns (e.g., mrps-5, mrpl-2), placing this gene's normal function as a promoter of mitochondrial translation that, when fully active, does not trigger the pro-longevity UPRmt signal — meaning its normal (full) activity is anti-longevity relative to the reduced-function state. However, since the question asks about the gene's normal function, full mitochondrial ribosome activity supports robust OXPHOS and nutrient sensing via mTORC1/TOR signaling, which is generally associated with reduced longevity in this framework.
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 predicted "pro_longevity" but the ground truth is "anti_longevity." The model's reasoning is internally contradictory and ultimately lands on the wrong answer. The model correctly identifies that knockdown of mitochondrial ribosomal proteins extends lifespan in C. elegans (which would make the gene anti_longevity — its normal function opposes longevity), but then confusingly concludes "pro_longevity" for the gene's influence. The model even explicitly states "its normal (full) activity is anti-longevity relative to the reduced-function state," which is the correct answer, yet still outputs "pro_longevity." The mechanism discussion about UPRmt and mitochondrial translation is partially correct in concept, but the final classification is wrong. The model's confidence of 0.65 is somewhat appropriate given the uncertainty, but the final answer is incorrect despite the reasoning pointing toward the right answer at one point.
Raw API responses
solver
{
"reasoning": "mrpl-24 encodes the mitochondrial large ribosomal subunit protein uL24m, which is a structural component of the mitochondrial ribosome responsible for translating mitochondrially-encoded proteins. In C. elegans, partial loss-of-function of mitochondrial ribosomal proteins (MRPs) is well-documented to extend lifespan through a mechanism involving mild mitochondrial translation impairment, which triggers the mitochondrial unfolded protein response (UPRmt) and reduces electron transport chain activity. This mild mitochondrial stress activates retrograde signaling pathways (including ATFS-1/UPRmt) that reprogram nuclear gene expression toward stress resistance and longevity. The effect mirrors the lifespan extension seen with other mitochondrial ribosomal subunit knockdowns (e.g., mrps-5, mrpl-2), placing this gene's normal function as a promoter of mitochondrial translation that, when fully active, does not trigger the pro-longevity UPRmt signal — meaning its normal (full) activity is anti-longevity relative to the reduced-function state. However, since the question asks about the gene's normal function, full mitochondrial ribosome activity supports robust OXPHOS and nutrient sensing via mTORC1/TOR signaling, which is generally associated with reduced longevity in this framework.",
"confidence": 0.65,
"key_pathways": [
"mitochondrial translation / UPRmt",
"TOR/nutrient sensing signaling",
"mitochondrial ribosome biogenesis"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted \"pro_longevity\" but the ground truth is \"anti_longevity.\" The model's reasoning is internally contradictory and ultimately lands on the wrong answer. The model correctly identifies that knockdown of mitochondrial ribosomal proteins extends lifespan in C. elegans (which would make the gene anti_longevity — its normal function opposes longevity), but then confusingly concludes \"pro_longevity\" for the gene's influence. The model even explicitly states \"its normal (full) activity is anti-longevity relative to the reduced-function state,\" which is the correct answer, yet still outputs \"pro_longevity.\" The mechanism discussion about UPRmt and mitochondrial translation is partially correct in concept, but the final classification is wrong. The model's confidence of 0.65 is somewhat appropriate given the uncertainty, but the final answer is incorrect despite the reasoning pointing toward the right answer at one point.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 3,
"ground_truth_questionable": false
}