cyc-1
C. elegans
Cytochrome c domain-containing protein
What the model saw
Gene: cyc-1 Organism: Caenorhabditis elegans Known functions: Cytochrome c domain-containing protein. electron transfer activity. heme binding.
View unredacted entry
Cytochrome c domain-containing protein. electron transfer activity. heme binding.
Solver output
cyc-1 encodes cytochrome c, a core component of the mitochondrial electron transport chain (ETC) that shuttles electrons from Complex III (cytochrome bc1) to Complex IV (cytochrome c oxidase) via its heme cofactor. Robust ETC activity drives efficient oxidative phosphorylation but also increases mitochondrial membrane potential and reactive oxygen species (ROS) production. In C. elegans, partial reduction of ETC function — including knockdown of cytochrome c — is well-established to extend lifespan, consistent with the mitohormesis and reduced insulin/IGF-1-like signaling models. Therefore, the normal (full) function of cyc-1 promotes high ETC flux, which opposes longevity relative to states of reduced mitochondrial respiration.
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 predicted anti_longevity for cyc-1 in C. elegans. The mechanistic reasoning is sound and well-articulated: cyc-1 encodes cytochrome c, a key ETC component, and its knockdown (reducing ETC function) is known to extend lifespan in C. elegans via mitohormesis. Therefore, the normal function of cyc-1 is anti-longevity. The model correctly identifies the relevant pathways (ETC, oxidative phosphorylation, mitohormesis) and the logic is consistent with established C. elegans aging biology. Confidence of 0.72 is appropriate given the complexity of the field.
Raw API responses
solver
{
"reasoning": "cyc-1 encodes cytochrome c, a core component of the mitochondrial electron transport chain (ETC) that shuttles electrons from Complex III (cytochrome bc1) to Complex IV (cytochrome c oxidase) via its heme cofactor. Robust ETC activity drives efficient oxidative phosphorylation but also increases mitochondrial membrane potential and reactive oxygen species (ROS) production. In C. elegans, partial reduction of ETC function — including knockdown of cytochrome c — is well-established to extend lifespan, consistent with the mitohormesis and reduced insulin/IGF-1-like signaling models. Therefore, the normal (full) function of cyc-1 promotes high ETC flux, which opposes longevity relative to states of reduced mitochondrial respiration.",
"confidence": 0.72,
"key_pathways": [
"mitochondrial electron transport chain (Complex III→IV electron shuttling)",
"oxidative phosphorylation / ROS production",
"mitohormesis / mitochondrial retrograde signaling"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for cyc-1 in C. elegans. The mechanistic reasoning is sound and well-articulated: cyc-1 encodes cytochrome c, a key ETC component, and its knockdown (reducing ETC function) is known to extend lifespan in C. elegans via mitohormesis. Therefore, the normal function of cyc-1 is anti-longevity. The model correctly identifies the relevant pathways (ETC, oxidative phosphorylation, mitohormesis) and the logic is consistent with established C. elegans aging biology. Confidence of 0.72 is appropriate given the complexity of the field.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}