mrpl-10
C. elegans
Large ribosomal subunit protein uL10m
What the model saw
Gene: mrpl-10 Organism: Caenorhabditis elegans Known functions: Large ribosomal subunit protein uL10m. structural constituent of ribosome.
View unredacted entry
Large ribosomal subunit protein uL10m. structural constituent of ribosome.
Solver output
mrpl-10 encodes the mitochondrial large ribosomal subunit protein uL10m, which is a structural component of the mitoribosome responsible for translating mitochondrially-encoded proteins. In C. elegans, partial loss-of-function of mitochondrial ribosomal proteins (including components of the large subunit) has been repeatedly shown to extend lifespan, likely through a mitochondrial unfolded protein response (UPRmt) and/or reduced mitochondrial translation that mimics dietary restriction signaling. Reduced mitoribosome activity decreases OXPHOS complex assembly, attenuating mitochondrial respiration and activating compensatory stress responses (UPRmt via ATFS-1) that promote longevity. This places mrpl-10's normal function in supporting full mitochondrial translation capacity, meaning its wild-type activity opposes the lifespan-extending effect of mitoribosome impairment. However, since the gene's normal function is to maintain mitochondrial proteostasis and OXPHOS, complete loss is detrimental; the pro-longevity effect is observed with partial reduction, suggesting the normal function is net anti-longevity in the context 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 identified the mechanistic pathway (mitoribosome, UPRmt, reduced mitochondrial translation extending lifespan) but arrived at the wrong final answer. The ground truth is "anti_longevity" (meaning the gene's normal function promotes longevity, or loss of function shortens lifespan), but the model predicted "pro_longevity." Interestingly, the model's own reasoning actually describes the anti_longevity logic correctly in the last sentence ("the normal function is net anti-longevity in the context of aging"), yet it still labeled the gene as "pro_longevity." This is a contradiction within the model's own reasoning. The model understood the biology but confused itself about the directionality convention, ultimately selecting the wrong classification. The mechanistic understanding of mitoribosomal proteins and UPRmt is sound, but the final answer is incorrect.
Raw API responses
solver
{
"reasoning": "mrpl-10 encodes the mitochondrial large ribosomal subunit protein uL10m, which is a structural component of the mitoribosome responsible for translating mitochondrially-encoded proteins. In C. elegans, partial loss-of-function of mitochondrial ribosomal proteins (including components of the large subunit) has been repeatedly shown to extend lifespan, likely through a mitochondrial unfolded protein response (UPRmt) and/or reduced mitochondrial translation that mimics dietary restriction signaling. Reduced mitoribosome activity decreases OXPHOS complex assembly, attenuating mitochondrial respiration and activating compensatory stress responses (UPRmt via ATFS-1) that promote longevity. This places mrpl-10's normal function in supporting full mitochondrial translation capacity, meaning its wild-type activity opposes the lifespan-extending effect of mitoribosome impairment. However, since the gene's normal function is to maintain mitochondrial proteostasis and OXPHOS, complete loss is detrimental; the pro-longevity effect is observed with partial reduction, suggesting the normal function is net anti-longevity in the context of aging.",
"confidence": 0.65,
"key_pathways": [
"mitochondrial translation / mitoribosome assembly",
"mitochondrial unfolded protein response (UPRmt / ATFS-1)",
"OXPHOS complex biogenesis"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly identified the mechanistic pathway (mitoribosome, UPRmt, reduced mitochondrial translation extending lifespan) but arrived at the wrong final answer. The ground truth is \"anti_longevity\" (meaning the gene's normal function promotes longevity, or loss of function shortens lifespan), but the model predicted \"pro_longevity.\" Interestingly, the model's own reasoning actually describes the anti_longevity logic correctly in the last sentence (\"the normal function is net anti-longevity in the context of aging\"), yet it still labeled the gene as \"pro_longevity.\" This is a contradiction within the model's own reasoning. The model understood the biology but confused itself about the directionality convention, ultimately selecting the wrong classification. The mechanistic understanding of mitoribosomal proteins and UPRmt is sound, but the final answer is incorrect.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": false,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}