MIR1
S. cerevisiae
Mir1p
What the model saw
Gene: MIR1 Organism: Saccharomyces cerevisiae Known functions: Mir1p. phosphate transmembrane transporter activity.
View unredacted entry
Mir1p. phosphate transmembrane transporter activity.
Solver output
MIR1 encodes the mitochondrial phosphate carrier (Mir1p) in S. cerevisiae, responsible for transporting inorganic phosphate across the inner mitochondrial membrane into the matrix, where it is essential for oxidative phosphorylation and ATP synthesis. Adequate mitochondrial phosphate import supports efficient OXPHOS and mitochondrial function, which is linked to healthy aging. Phosphate homeostasis is tightly coupled to nutrient sensing pathways, including TOR signaling; proper phosphate transport helps maintain the balance between anabolic and catabolic states that favors longevity. Loss of mitochondrial phosphate transport would impair ATP production and mitochondrial membrane potential, contributing to mitochondrial dysfunction—a recognized hallmark of aging. The deregulated nutrient sensing hallmark best captures this gene's role, as phosphate availability is a key nutrient signal integrated by TOR and related pathways in yeast.
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 MIR1 as pro_longevity, but the ground truth is anti_longevity. The model's reasoning assumed that loss of mitochondrial phosphate transport would be harmful (impair ATP production), leading it to conclude MIR1 is pro_longevity. However, the actual GenAge classification is anti_longevity, meaning MIR1 deletion likely extends lifespan. This is consistent with the idea that reduced mitochondrial phosphate import may reduce OXPHOS efficiency and trigger beneficial mitochondrial stress responses (mitohormesis), or that MIR1 deletion reduces ROS production. The model's mechanistic reasoning was plausible on the surface but led to the wrong conclusion. The model had moderate confidence (0.62) but was still clearly wrong on both the answer and the underlying mechanism interpretation.
Raw API responses
solver
{
"reasoning": "MIR1 encodes the mitochondrial phosphate carrier (Mir1p) in S. cerevisiae, responsible for transporting inorganic phosphate across the inner mitochondrial membrane into the matrix, where it is essential for oxidative phosphorylation and ATP synthesis. Adequate mitochondrial phosphate import supports efficient OXPHOS and mitochondrial function, which is linked to healthy aging. Phosphate homeostasis is tightly coupled to nutrient sensing pathways, including TOR signaling; proper phosphate transport helps maintain the balance between anabolic and catabolic states that favors longevity. Loss of mitochondrial phosphate transport would impair ATP production and mitochondrial membrane potential, contributing to mitochondrial dysfunction—a recognized hallmark of aging. The deregulated nutrient sensing hallmark best captures this gene's role, as phosphate availability is a key nutrient signal integrated by TOR and related pathways in yeast.",
"confidence": 0.62,
"key_pathways": [
"mitochondrial phosphate transport / oxidative phosphorylation",
"TOR/nutrient sensing pathway",
"mitochondrial membrane potential maintenance"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted MIR1 as pro_longevity, but the ground truth is anti_longevity. The model's reasoning assumed that loss of mitochondrial phosphate transport would be harmful (impair ATP production), leading it to conclude MIR1 is pro_longevity. However, the actual GenAge classification is anti_longevity, meaning MIR1 deletion likely extends lifespan. This is consistent with the idea that reduced mitochondrial phosphate import may reduce OXPHOS efficiency and trigger beneficial mitochondrial stress responses (mitohormesis), or that MIR1 deletion reduces ROS production. The model's mechanistic reasoning was plausible on the surface but led to the wrong conclusion. The model had moderate confidence (0.62) but was still clearly wrong on both the answer and the underlying mechanism interpretation.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}