cua-1
C. elegans
P-type Cu(+) transporter
What the model saw
Gene: cua-1 Organism: Caenorhabditis elegans Known functions: P-type Cu(+) transporter. ATP binding. ATP hydrolysis activity. ATPase-coupled monoatomic cation transmembrane transporter activity. P-type monovalent copper transporter activity. copper ion binding. metal ion binding. nucleotide binding.
View unredacted entry
P-type Cu(+) transporter. ATP binding. ATP hydrolysis activity. ATPase-coupled monoatomic cation transmembrane transporter activity. P-type monovalent copper transporter activity. copper ion binding. metal ion binding. nucleotide binding.
Solver output
CUA-1 is a P-type Cu(+)-transporting ATPase, the C. elegans ortholog of ATP7A/ATP7B, responsible for intracellular copper trafficking and delivery to cuproenzymes. Proper copper homeostasis is essential for the function of cytochrome c oxidase (Complex IV) in the mitochondrial electron transport chain, which requires copper for its catalytic subunits. Loss of CUA-1 function would impair copper delivery to mitochondria, disrupting oxidative phosphorylation and increasing reactive oxygen species production. Additionally, CUA-1 supplies copper to superoxide dismutase (SOD-1/SOD-4), a key antioxidant enzyme; without adequate copper loading, SOD activity declines and oxidative damage accumulates. Maintaining copper homeostasis through CUA-1 therefore supports mitochondrial integrity and antioxidant defense, both of which are pro-longevity functions.
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 pro_longevity for cua-1. The mechanistic reasoning is sound and well-grounded: CUA-1 as a P-type copper transporter supports cytochrome c oxidase function and copper-dependent SOD activity, both of which are relevant to longevity. The mechanism class "mitochondrial_dysfunction" is a reasonable framing (loss of CUA-1 would cause mitochondrial dysfunction), though it's slightly indirect since the primary function is copper homeostasis rather than a direct mitochondrial gene. The reasoning is detailed and biologically plausible. Confidence of 0.72 is appropriate given the specificity of the gene.
Raw API responses
solver
{
"reasoning": "CUA-1 is a P-type Cu(+)-transporting ATPase, the C. elegans ortholog of ATP7A/ATP7B, responsible for intracellular copper trafficking and delivery to cuproenzymes. Proper copper homeostasis is essential for the function of cytochrome c oxidase (Complex IV) in the mitochondrial electron transport chain, which requires copper for its catalytic subunits. Loss of CUA-1 function would impair copper delivery to mitochondria, disrupting oxidative phosphorylation and increasing reactive oxygen species production. Additionally, CUA-1 supplies copper to superoxide dismutase (SOD-1/SOD-4), a key antioxidant enzyme; without adequate copper loading, SOD activity declines and oxidative damage accumulates. Maintaining copper homeostasis through CUA-1 therefore supports mitochondrial integrity and antioxidant defense, both of which are pro-longevity functions.",
"confidence": 0.72,
"key_pathways": [
"mitochondrial electron transport chain (cytochrome c oxidase copper delivery)",
"copper-dependent superoxide dismutase antioxidant defense",
"P-type ATPase copper trafficking pathway"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for cua-1. The mechanistic reasoning is sound and well-grounded: CUA-1 as a P-type copper transporter supports cytochrome c oxidase function and copper-dependent SOD activity, both of which are relevant to longevity. The mechanism class \"mitochondrial_dysfunction\" is a reasonable framing (loss of CUA-1 would cause mitochondrial dysfunction), though it's slightly indirect since the primary function is copper homeostasis rather than a direct mitochondrial gene. The reasoning is detailed and biologically plausible. Confidence of 0.72 is appropriate given the specificity of the gene.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}