c33f10.12
C. elegans
Phosphate carrier protein, mitochondrial
What the model saw
Gene: C33F10.12 Organism: Caenorhabditis elegans Known functions: Phosphate carrier protein, mitochondrial. phosphate transmembrane transporter activity.
View unredacted entry
Phosphate carrier protein, mitochondrial. phosphate transmembrane transporter activity.
Solver output
C33F10.12 encodes the mitochondrial phosphate carrier protein (PiC), which transports inorganic phosphate from the cytosol into the mitochondrial matrix via the inner mitochondrial membrane. This phosphate is essential for ATP synthesis by the F1F0-ATP synthase, directly supporting oxidative phosphorylation efficiency. Proper mitochondrial phosphate import is required to maintain the proton motive force and ATP production capacity; loss of this function impairs mitochondrial bioenergetics. However, there is a nuanced consideration: in C. elegans, mild mitochondrial dysfunction (mitohormesis) can paradoxically extend lifespan by activating the mitochondrial unfolded protein response (UPRmt) and stress-response pathways. The phosphate carrier is a core component of normal OXPHOS function, and its normal activity supports mitochondrial homeostasis, which is generally considered pro-longevity in the context of maintaining energy metabolism and reducing ROS from dysfunctional electron transport.
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 acknowledged the mitohormesis concept (mild mitochondrial dysfunction extending lifespan) but then concluded the gene is pro_longevity because it maintains mitochondrial homeostasis. This is backwards - if C33F10.12 is anti_longevity, it likely means that loss/reduction of this phosphate carrier extends lifespan, consistent with the mitohormesis/mild mitochondrial dysfunction paradigm the model itself mentioned. The model correctly identified the gene's function as a mitochondrial phosphate carrier involved in OXPHOS, but drew the wrong conclusion about its longevity influence. The model even had the right mechanistic framework (mitohormesis) but failed to apply it correctly to reach the right answer. Confidence was 0.62, which is moderate but still wrong.
Raw API responses
solver
{
"reasoning": "C33F10.12 encodes the mitochondrial phosphate carrier protein (PiC), which transports inorganic phosphate from the cytosol into the mitochondrial matrix via the inner mitochondrial membrane. This phosphate is essential for ATP synthesis by the F1F0-ATP synthase, directly supporting oxidative phosphorylation efficiency. Proper mitochondrial phosphate import is required to maintain the proton motive force and ATP production capacity; loss of this function impairs mitochondrial bioenergetics. However, there is a nuanced consideration: in C. elegans, mild mitochondrial dysfunction (mitohormesis) can paradoxically extend lifespan by activating the mitochondrial unfolded protein response (UPRmt) and stress-response pathways. The phosphate carrier is a core component of normal OXPHOS function, and its normal activity supports mitochondrial homeostasis, which is generally considered pro-longevity in the context of maintaining energy metabolism and reducing ROS from dysfunctional electron transport.",
"confidence": 0.62,
"key_pathways": [
"oxidative phosphorylation / mitochondrial ATP synthesis",
"mitochondrial inner membrane transport (SLC25 family)",
"mitochondrial homeostasis / UPRmt"
],
"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 acknowledged the mitohormesis concept (mild mitochondrial dysfunction extending lifespan) but then concluded the gene is pro_longevity because it maintains mitochondrial homeostasis. This is backwards - if C33F10.12 is anti_longevity, it likely means that loss/reduction of this phosphate carrier extends lifespan, consistent with the mitohormesis/mild mitochondrial dysfunction paradigm the model itself mentioned. The model correctly identified the gene's function as a mitochondrial phosphate carrier involved in OXPHOS, but drew the wrong conclusion about its longevity influence. The model even had the right mechanistic framework (mitohormesis) but failed to apply it correctly to reach the right answer. Confidence was 0.62, which is moderate but still wrong.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}