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tax-6

C. elegans

Serine/threonine-protein phosphatase 2B catalytic subunit

What the model saw

Gene: tax-6
Organism: Caenorhabditis elegans
Known functions: Serine/threonine-protein phosphatase 2B catalytic subunit. calcium ion binding. calmodulin binding. calmodulin-dependent protein phosphatase activity. hydrolase activity. phosphoprotein phosphatase activity. protein binding. protein serine/threonine phosphatase activity.
View unredacted entry
Serine/threonine-protein phosphatase 2B catalytic subunit. calcium ion binding. calmodulin binding. calmodulin-dependent protein phosphatase activity. hydrolase activity. phosphoprotein phosphatase activity. protein binding. protein serine/threonine phosphatase activity.

Solver output

Predicted influence
Pro-longevity
Confidence
72%
Mechanism
Deregulated nutrient sensing
Reasoning

tax-6 encodes the C. elegans ortholog of calcineurin (PP2B), a calcium/calmodulin-dependent serine/threonine phosphatase. In C. elegans, calcineurin (tax-6) has been shown to act downstream of calcium signaling to dephosphorylate and regulate transcription factors including NFAT-like factors and components of the DAF-16/FOXO pathway. Loss-of-function of tax-6 extends lifespan in C. elegans, suggesting that calcineurin activity normally suppresses longevity. The pro-longevity effect of tax-6 loss is linked to its role in modulating DAF-16/FOXO nuclear localization and activity — calcineurin dephosphorylates substrates that antagonize DAF-16, so when tax-6 is active it dampens the insulin/IGF-1-like signaling (IIS) longevity pathway. Additionally, tax-6 integrates calcium-dependent signals that influence stress response and metabolic regulation, placing it within the deregulated nutrient-sensing hallmark. Thus, the normal function of tax-6 is anti-longevity (its activity shortens lifespan), but the gene itself, when functioning normally, opposes longevity.

Key pathways
DAF-16/FOXO insulin/IGF-1 signalingcalcium/calmodulin-dependent calcineurin signalingstress response and proteostasis regulation
Longevity influence
Anti-longevity
Lifespan effect
Increase

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

Answer
Incorrect
Mechanism
Correct
Reasoning quality
3/5
Failure mode
Right answer, wrong reasoning
Notes

The model correctly identifies the mechanism: tax-6/calcineurin loss-of-function extends lifespan, meaning the gene's normal activity is anti-longevity. The mechanistic reasoning is accurate. However, the model then contradicts itself in its final classification. It states "the normal function of tax-6 is anti-longevity (its activity shortens lifespan)" but then classifies the gene as "pro_longevity" — the opposite of what the ground truth says (anti_longevity). The model seems confused about the directionality convention: it correctly understands the biology but mislabels the longevity influence. The final answer is wrong despite the reasoning being largely correct, making this a case of right reasoning but wrong answer output.

Raw API responses

solver

{
  "reasoning": "tax-6 encodes the C. elegans ortholog of calcineurin (PP2B), a calcium/calmodulin-dependent serine/threonine phosphatase. In C. elegans, calcineurin (tax-6) has been shown to act downstream of calcium signaling to dephosphorylate and regulate transcription factors including NFAT-like factors and components of the DAF-16/FOXO pathway. Loss-of-function of tax-6 extends lifespan in C. elegans, suggesting that calcineurin activity normally suppresses longevity. The pro-longevity effect of tax-6 loss is linked to its role in modulating DAF-16/FOXO nuclear localization and activity — calcineurin dephosphorylates substrates that antagonize DAF-16, so when tax-6 is active it dampens the insulin/IGF-1-like signaling (IIS) longevity pathway. Additionally, tax-6 integrates calcium-dependent signals that influence stress response and metabolic regulation, placing it within the deregulated nutrient-sensing hallmark. Thus, the normal function of tax-6 is anti-longevity (its activity shortens lifespan), but the gene itself, when functioning normally, opposes longevity.",
  "confidence": 0.72,
  "key_pathways": [
    "DAF-16/FOXO insulin/IGF-1 signaling",
    "calcium/calmodulin-dependent calcineurin signaling",
    "stress response and proteostasis regulation"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model correctly identifies the mechanism: tax-6/calcineurin loss-of-function extends lifespan, meaning the gene's normal activity is anti-longevity. The mechanistic reasoning is accurate. However, the model then contradicts itself in its final classification. It states \"the normal function of tax-6 is anti-longevity (its activity shortens lifespan)\" but then classifies the gene as \"pro_longevity\" — the opposite of what the ground truth says (anti_longevity). The model seems confused about the directionality convention: it correctly understands the biology but mislabels the longevity influence. The final answer is wrong despite the reasoning being largely correct, making this a case of right reasoning but wrong answer output.",
  "failure_mode": "right_answer_wrong_reasoning",
  "answer_correct": false,
  "mechanism_correct": true,
  "reasoning_quality": 3,
  "ground_truth_questionable": false
}