hpo-31
C. elegans
CCA tRNA nucleotidyltransferase 1, mitochondrial
What the model saw
Gene: hpo-31 Organism: Caenorhabditis elegans Known functions: CCA tRNA nucleotidyltransferase 1, mitochondrial. RNA binding. nucleotidyltransferase activity. tRNA binding.
View unredacted entry
CCA tRNA nucleotidyltransferase 1, mitochondrial. RNA binding. nucleotidyltransferase activity. tRNA binding.
Solver output
hpo-31 encodes a mitochondrial CCA tRNA nucleotidyltransferase, which adds the universal CCA trinucleotide to the 3' end of mitochondrial tRNAs, an essential post-transcriptional maturation step required for aminoacylation and participation in mitochondrial translation. Without functional CCA addition, mitochondrial tRNAs cannot be charged with amino acids, impairing synthesis of the 13 OXPHOS subunits encoded by the mitochondrial genome. Proper mitochondrial translation is critical for maintaining electron transport chain integrity and ATP production. Loss of this enzyme would compromise mitochondrial function, consistent with the pattern seen in C. elegans where mild mitochondrial perturbations can extend lifespan via the mitochondrial unfolded protein response (UPRmt), but the gene's normal function is to sustain mitochondrial proteostasis and bioenergetics, which supports organismal health and longevity. The maintenance of mitochondrial tRNA integrity also prevents accumulation of dysfunctional mitochondria, a hallmark of aging.
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 predicted pro_longevity for hpo-31. The mechanistic reasoning is sound and well-grounded: hpo-31 encodes a mitochondrial CCA tRNA nucleotidyltransferase, and the model correctly identifies its role in mitochondrial tRNA maturation, translation, and OXPHOS maintenance. The model also appropriately notes the nuance that mild mitochondrial perturbations in C. elegans can extend lifespan via UPRmt, while the gene's normal function supports mitochondrial health. The reasoning is slightly hedged/complex (trying to explain both why loss might extend lifespan AND why the gene is pro-longevity), but ultimately arrives at the correct conclusion with reasonable mechanistic justification. Confidence of 0.72 is appropriate given the complexity.
Raw API responses
solver
{
"reasoning": "hpo-31 encodes a mitochondrial CCA tRNA nucleotidyltransferase, which adds the universal CCA trinucleotide to the 3' end of mitochondrial tRNAs, an essential post-transcriptional maturation step required for aminoacylation and participation in mitochondrial translation. Without functional CCA addition, mitochondrial tRNAs cannot be charged with amino acids, impairing synthesis of the 13 OXPHOS subunits encoded by the mitochondrial genome. Proper mitochondrial translation is critical for maintaining electron transport chain integrity and ATP production. Loss of this enzyme would compromise mitochondrial function, consistent with the pattern seen in C. elegans where mild mitochondrial perturbations can extend lifespan via the mitochondrial unfolded protein response (UPRmt), but the gene's normal function is to sustain mitochondrial proteostasis and bioenergetics, which supports organismal health and longevity. The maintenance of mitochondrial tRNA integrity also prevents accumulation of dysfunctional mitochondria, a hallmark of aging.",
"confidence": 0.72,
"key_pathways": [
"mitochondrial tRNA maturation (CCA addition)",
"mitochondrial translation / OXPHOS",
"mitochondrial unfolded protein response (UPRmt)"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for hpo-31. The mechanistic reasoning is sound and well-grounded: hpo-31 encodes a mitochondrial CCA tRNA nucleotidyltransferase, and the model correctly identifies its role in mitochondrial tRNA maturation, translation, and OXPHOS maintenance. The model also appropriately notes the nuance that mild mitochondrial perturbations in C. elegans can extend lifespan via UPRmt, while the gene's normal function supports mitochondrial health. The reasoning is slightly hedged/complex (trying to explain both why loss might extend lifespan AND why the gene is pro-longevity), but ultimately arrives at the correct conclusion with reasonable mechanistic justification. Confidence of 0.72 is appropriate given the complexity.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}