eat-6
C. elegans
Sodium/potassium-transporting ATPase subunit alpha
What the model saw
Gene: eat-6 Organism: Caenorhabditis elegans Known functions: Sodium/potassium-transporting ATPase subunit alpha. ATP binding. ATP hydrolysis activity. P-type potassium transmembrane transporter activity. P-type sodium:potassium-exchanging transporter activity. nucleotide binding. sodium ion transmembrane transporter activity.
View unredacted entry
Sodium/potassium-transporting ATPase subunit alpha. ATP binding. ATP hydrolysis activity. P-type potassium transmembrane transporter activity. P-type sodium:potassium-exchanging transporter activity. nucleotide binding. sodium ion transmembrane transporter activity.
Solver output
eat-6 encodes the alpha subunit of the Na+/K+-ATPase, the primary ion pump responsible for maintaining electrochemical gradients across the plasma membrane. This pump consumes a large fraction of cellular ATP and is essential for neuronal excitability, nutrient uptake (e.g., amino acid co-transport), and cellular volume regulation. In C. elegans, eat-6 is critical for pharyngeal muscle function and feeding behavior; loss-of-function mutations cause reduced food intake, which mimics dietary restriction—a well-established pro-longevity intervention. Reduced Na+/K+-ATPase activity in eat-6 mutants leads to slowed pumping and caloric restriction-like states that activate nutrient-sensing pathways (e.g., reduced IIS/TOR signaling), extending lifespan. The normal function of eat-6 thus supports robust feeding and energy expenditure, and its partial reduction is associated with longevity through deregulated nutrient sensing rather than complete loss of ion homeostasis.
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 is internally coherent but leads to the wrong conclusion. eat-6 is classified as anti_longevity, meaning its normal function promotes longevity (or its loss shortens lifespan), not that its reduction extends life. The model's logic that eat-6 loss mimics dietary restriction and extends lifespan is incorrect - the gene is anti_longevity, meaning it works against longevity (i.e., its normal activity shortens lifespan, or loss-of-function extends life... wait, actually anti_longevity in GenAge means the gene's normal function promotes aging/shortens lifespan). Actually, in GenAge terminology, anti_longevity means the gene promotes aging (its activity is detrimental to longevity). So the model's reasoning that eat-6 reduction extends lifespan could be consistent with anti_longevity classification - but the model labeled it pro_longevity, which is the opposite of what GenAge says. The model confused the direction: if eat-6 loss extends lifespan, eat-6 would be anti_longevity (its normal function shortens life). The model's mechanistic story (reduced eat-6 → dietary restriction mimicry → longer life) would actually support anti_longevity classification, but the model incorrectly labeled it pro_longevity. Additionally, the mechanism_class of "mitochondrial_dysfunction" is incorrect for a Na+/K+-ATPase pump - this is an ion homeostasis/membrane transport mechanism, not mitochondrial dysfunction. The confidence of 0.65 is moderate but still wrong.
Raw API responses
solver
{
"reasoning": "eat-6 encodes the alpha subunit of the Na+/K+-ATPase, the primary ion pump responsible for maintaining electrochemical gradients across the plasma membrane. This pump consumes a large fraction of cellular ATP and is essential for neuronal excitability, nutrient uptake (e.g., amino acid co-transport), and cellular volume regulation. In C. elegans, eat-6 is critical for pharyngeal muscle function and feeding behavior; loss-of-function mutations cause reduced food intake, which mimics dietary restriction—a well-established pro-longevity intervention. Reduced Na+/K+-ATPase activity in eat-6 mutants leads to slowed pumping and caloric restriction-like states that activate nutrient-sensing pathways (e.g., reduced IIS/TOR signaling), extending lifespan. The normal function of eat-6 thus supports robust feeding and energy expenditure, and its partial reduction is associated with longevity through deregulated nutrient sensing rather than complete loss of ion homeostasis.",
"confidence": 0.65,
"key_pathways": [
"dietary restriction / caloric restriction mimicry",
"deregulated nutrient sensing (IIS/TOR)",
"Na+/K+-ATPase-dependent ion homeostasis"
],
"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 is internally coherent but leads to the wrong conclusion. eat-6 is classified as anti_longevity, meaning its normal function promotes longevity (or its loss shortens lifespan), not that its reduction extends life. The model's logic that eat-6 loss mimics dietary restriction and extends lifespan is incorrect - the gene is anti_longevity, meaning it works against longevity (i.e., its normal activity shortens lifespan, or loss-of-function extends life... wait, actually anti_longevity in GenAge means the gene's normal function promotes aging/shortens lifespan). Actually, in GenAge terminology, anti_longevity means the gene promotes aging (its activity is detrimental to longevity). So the model's reasoning that eat-6 reduction extends lifespan could be consistent with anti_longevity classification - but the model labeled it pro_longevity, which is the opposite of what GenAge says. The model confused the direction: if eat-6 loss extends lifespan, eat-6 would be anti_longevity (its normal function shortens life). The model's mechanistic story (reduced eat-6 → dietary restriction mimicry → longer life) would actually support anti_longevity classification, but the model incorrectly labeled it pro_longevity. Additionally, the mechanism_class of \"mitochondrial_dysfunction\" is incorrect for a Na+/K+-ATPase pump - this is an ion homeostasis/membrane transport mechanism, not mitochondrial dysfunction. The confidence of 0.65 is moderate but still wrong.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2
}