MRX14
S. cerevisiae
mitochondrial 54S ribosomal protein bL34m MRX14
What the model saw
Gene: MRX14 Organism: Saccharomyces cerevisiae Known functions: mitochondrial 54S ribosomal protein bL34m MRX14. structural constituent of ribosome.
View unredacted entry
mitochondrial 54S ribosomal protein bL34m MRX14. structural constituent of ribosome.
Solver output
MRX14 encodes the mitochondrial large ribosomal subunit protein bL34m, a structural component of the 54S mitoribosome in S. cerevisiae. Proper assembly and function of the mitoribosome is essential for translation of the mitochondrially-encoded subunits of the oxidative phosphorylation complexes (e.g., Cox1, Cox2, Cox3, Cytb, Atp6/8/9). Loss of MRX14 would impair mitochondrial translation, leading to defective OXPHOS complex assembly, reduced respiratory capacity, and increased reactive oxygen species production — hallmarks of mitochondrial dysfunction associated with accelerated aging. Maintenance of mitochondrial ribosome integrity thus supports mitochondrial function and bioenergetic homeostasis, which are well-established pro-longevity factors in yeast. Consistent with this, many mitoribosomal protein deletions in yeast result in petite/respiratory-deficient phenotypes, which are generally associated with shortened chronological or replicative lifespan under standard 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 predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is internally coherent but leads to the wrong conclusion. The model correctly identifies that MRX14 loss impairs mitochondrial translation and OXPHOS, but then incorrectly concludes that maintaining MRX14 function is pro-longevity. In reality, MRX14 is anti_longevity, meaning its deletion or loss extends lifespan. This is consistent with the known phenomenon in yeast where mitochondrial ribosomal protein deletions (petite mutants) can actually extend replicative lifespan — a well-documented paradox. The model even mentions petite/respiratory-deficient phenotypes but then contradicts itself by saying these are 'generally associated with shortened lifespan,' which is incorrect for replicative lifespan in yeast. The model's mechanistic reasoning about mitochondrial dysfunction is partially correct in identifying the pathway, but the directionality of the longevity effect is wrong. The model had moderate confidence (0.62) but was still clearly wrong.
Raw API responses
solver
{
"reasoning": "MRX14 encodes the mitochondrial large ribosomal subunit protein bL34m, a structural component of the 54S mitoribosome in S. cerevisiae. Proper assembly and function of the mitoribosome is essential for translation of the mitochondrially-encoded subunits of the oxidative phosphorylation complexes (e.g., Cox1, Cox2, Cox3, Cytb, Atp6/8/9). Loss of MRX14 would impair mitochondrial translation, leading to defective OXPHOS complex assembly, reduced respiratory capacity, and increased reactive oxygen species production — hallmarks of mitochondrial dysfunction associated with accelerated aging. Maintenance of mitochondrial ribosome integrity thus supports mitochondrial function and bioenergetic homeostasis, which are well-established pro-longevity factors in yeast. Consistent with this, many mitoribosomal protein deletions in yeast result in petite/respiratory-deficient phenotypes, which are generally associated with shortened chronological or replicative lifespan under standard conditions.",
"confidence": 0.62,
"key_pathways": [
"mitochondrial translation",
"oxidative phosphorylation",
"mitoribosome assembly"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is internally coherent but leads to the wrong conclusion. The model correctly identifies that MRX14 loss impairs mitochondrial translation and OXPHOS, but then incorrectly concludes that maintaining MRX14 function is pro-longevity. In reality, MRX14 is anti_longevity, meaning its deletion or loss extends lifespan. This is consistent with the known phenomenon in yeast where mitochondrial ribosomal protein deletions (petite mutants) can actually extend replicative lifespan — a well-documented paradox. The model even mentions petite/respiratory-deficient phenotypes but then contradicts itself by saying these are 'generally associated with shortened lifespan,' which is incorrect for replicative lifespan in yeast. The model's mechanistic reasoning about mitochondrial dysfunction is partially correct in identifying the pathway, but the directionality of the longevity effect is wrong. The model had moderate confidence (0.62) but was still clearly wrong.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}