CYT1
S. cerevisiae
ubiquinol--cytochrome-c reductase catalytic subunit CYT1
What the model saw
Gene: CYT1 Organism: Saccharomyces cerevisiae Known functions: ubiquinol--cytochrome-c reductase catalytic subunit CYT1. electron transfer activity. heme binding. quinol-cytochrome-c reductase activity.
View unredacted entry
ubiquinol--cytochrome-c reductase catalytic subunit CYT1. electron transfer activity. heme binding. quinol-cytochrome-c reductase activity.
Solver output
CYT1 encodes the cytochrome c1 subunit of Complex III (ubiquinol–cytochrome c reductase) in the mitochondrial electron transport chain. Its quinol-cytochrome-c reductase activity is essential for efficient electron transfer from ubiquinol to cytochrome c, directly supporting mitochondrial membrane potential and ATP synthesis. Proper Complex III function minimizes electron leak and superoxide generation at this node of the ETC, thereby reducing oxidative damage. In yeast, loss of mitochondrial respiratory function (petite phenotype) is associated with shortened chronological and replicative lifespan, while intact OXPHOS supports longevity. The heme-binding property of CYT1 is critical for its catalytic role, and disruption of this activity impairs respiratory competence, a hallmark of mitochondrial dysfunction linked to 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 predicted pro_longevity with 0.72 confidence, but the ground truth is anti_longevity. The model's reasoning is plausible on the surface — CYT1 is indeed a key Complex III subunit, and loss of mitochondrial function is generally associated with shortened lifespan. However, the model failed to account for the fact that in yeast, CYT1 deletion (or dysfunction) can paradoxically extend lifespan through mechanisms such as mitohormesis or retrograde signaling. The anti_longevity classification suggests that CYT1 activity actually promotes aging (i.e., its presence shortens lifespan), possibly because Complex III activity generates ROS that accelerate aging, or because its deletion triggers compensatory longevity pathways. The model's reasoning was internally consistent but led to the wrong conclusion, and the mechanistic framing (intact OXPHOS supports longevity) is contradicted by the ground truth classification.
Raw API responses
solver
{
"reasoning": "CYT1 encodes the cytochrome c1 subunit of Complex III (ubiquinol–cytochrome c reductase) in the mitochondrial electron transport chain. Its quinol-cytochrome-c reductase activity is essential for efficient electron transfer from ubiquinol to cytochrome c, directly supporting mitochondrial membrane potential and ATP synthesis. Proper Complex III function minimizes electron leak and superoxide generation at this node of the ETC, thereby reducing oxidative damage. In yeast, loss of mitochondrial respiratory function (petite phenotype) is associated with shortened chronological and replicative lifespan, while intact OXPHOS supports longevity. The heme-binding property of CYT1 is critical for its catalytic role, and disruption of this activity impairs respiratory competence, a hallmark of mitochondrial dysfunction linked to aging.",
"confidence": 0.72,
"key_pathways": [
"mitochondrial electron transport chain (Complex III)",
"oxidative phosphorylation",
"reactive oxygen species homeostasis"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity with 0.72 confidence, but the ground truth is anti_longevity. The model's reasoning is plausible on the surface — CYT1 is indeed a key Complex III subunit, and loss of mitochondrial function is generally associated with shortened lifespan. However, the model failed to account for the fact that in yeast, CYT1 deletion (or dysfunction) can paradoxically extend lifespan through mechanisms such as mitohormesis or retrograde signaling. The anti_longevity classification suggests that CYT1 activity actually promotes aging (i.e., its presence shortens lifespan), possibly because Complex III activity generates ROS that accelerate aging, or because its deletion triggers compensatory longevity pathways. The model's reasoning was internally consistent but led to the wrong conclusion, and the mechanistic framing (intact OXPHOS supports longevity) is contradicted by the ground truth classification.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 3,
"ground_truth_questionable": false
}