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old-1

C. elegans

Tyrosine-protein kinase receptor old-1

What the model saw

Gene: old-1
Organism: Caenorhabditis elegans
Known functions: Tyrosine-protein kinase receptor old-1. ATP binding. protein kinase activity. protein tyrosine kinase activity. transmembrane receptor protein tyrosine kinase activity.
View unredacted entry
Tyrosine-protein kinase receptor old-1. ATP binding. protein kinase activity. protein tyrosine kinase activity. transmembrane receptor protein tyrosine kinase activity.

Solver output

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

old-1 (overexpressed in long-lived daf-2 mutants) encodes a transmembrane receptor tyrosine kinase in C. elegans. Its name derives from its upregulation in long-lived mutants, and it has been shown to be a positive regulator of lifespan when overexpressed. As a receptor tyrosine kinase, old-1 modulates downstream signaling cascades that intersect with the insulin/IGF-1 signaling (IIS) pathway — the central nutrient-sensing longevity axis in C. elegans. Overexpression of old-1 extends lifespan in a manner partially dependent on daf-16 (FOXO), suggesting it acts within or parallel to the IIS pathway to promote longevity. Unlike the canonical IIS receptor daf-2 (whose activity is anti-longevity), old-1 kinase activity appears to promote pro-longevity outputs, possibly by modulating DAF-16/FOXO nuclear localization or activity.

Key pathways
insulin/IGF-1 signaling (IIS) pathwayDAF-16/FOXO transcription factor regulationreceptor tyrosine kinase signaling
Longevity influence
Pro-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
Correct
Mechanism
Correct
Reasoning quality
4/5
Failure mode
Correct
Notes

The model correctly predicted pro_longevity for old-1. The reasoning is well-grounded: old-1 is indeed upregulated in long-lived daf-2 mutants, encodes a transmembrane receptor tyrosine kinase, and its overexpression extends lifespan in a daf-16-dependent manner. The mechanism class of "deregulated_nutrient_sensing" is reasonable given the connection to IIS/DAF-16 pathway, though old-1 is somewhat distinct from canonical nutrient sensing. The model correctly notes the contrast with daf-2 (anti-longevity) and old-1's pro-longevity role. Minor uncertainty about the exact mechanism class label, but overall the reasoning is accurate and well-supported.

Raw API responses

solver

{
  "reasoning": "old-1 (overexpressed in long-lived daf-2 mutants) encodes a transmembrane receptor tyrosine kinase in C. elegans. Its name derives from its upregulation in long-lived mutants, and it has been shown to be a positive regulator of lifespan when overexpressed. As a receptor tyrosine kinase, old-1 modulates downstream signaling cascades that intersect with the insulin/IGF-1 signaling (IIS) pathway — the central nutrient-sensing longevity axis in C. elegans. Overexpression of old-1 extends lifespan in a manner partially dependent on daf-16 (FOXO), suggesting it acts within or parallel to the IIS pathway to promote longevity. Unlike the canonical IIS receptor daf-2 (whose activity is anti-longevity), old-1 kinase activity appears to promote pro-longevity outputs, possibly by modulating DAF-16/FOXO nuclear localization or activity.",
  "confidence": 0.72,
  "key_pathways": [
    "insulin/IGF-1 signaling (IIS) pathway",
    "DAF-16/FOXO transcription factor regulation",
    "receptor tyrosine kinase signaling"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model correctly predicted pro_longevity for old-1. The reasoning is well-grounded: old-1 is indeed upregulated in long-lived daf-2 mutants, encodes a transmembrane receptor tyrosine kinase, and its overexpression extends lifespan in a daf-16-dependent manner. The mechanism class of \"deregulated_nutrient_sensing\" is reasonable given the connection to IIS/DAF-16 pathway, though old-1 is somewhat distinct from canonical nutrient sensing. The model correctly notes the contrast with daf-2 (anti-longevity) and old-1's pro-longevity role. Minor uncertainty about the exact mechanism class label, but overall the reasoning is accurate and well-supported.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}